HEART MURMURS1–3 June 2009

Dr Jim Hall, Secretary of theCardiology SAC, discusses settingthe standards for higher specialistcardiology training through the cur-riculum and its assessment. 2

David Hackett, Vice President(Clinical Standards), BritishCardiovascular Society, outlines therevalidation of UK cardiologists.

4

Dr Stephen Wheatcroft, Universityof Leeds, says that despite recentadvances patients with diabetesmellitus continue to have alarming-ly high rates of morbidity. 6

The Programme Committee andthe Affiliated Groups have creat-ed a superb education and scien-

tific programme including some newadditions to the meeting structurewhich you should look out for. Wehave concentrated the HRUK sessionon Wednesday to create an “arrhyth-mia day” although there are manyother interests catered for as well.

Do make sure you visit theExhibition: not only is there a widespectrum of exhibitors but there arequite a few educational activities in theExhibition area. Today and tomorrow,the PCI simulators will be in full flightand there are opportunities ofTransoesophageal Echo simulation andto test your clinical skills with “Harvey”.Cardiac rhythm management basedsimulators will be here on Wednesday.Do not miss Valentin Fuster, one of thegreat names in Cardio-vascular researchdeliver the Paul Wood lecture at 16.00on Monday in the Auditorium.

I hope to see you all at the annualdinner on Tuesday evening. It should

be magic! Having feasted on the edu-cation on the opening day, you mightbe attracted by some wine andcanapés during the Moderated PosterSessions in Exhibition Hall later onMonday.

Another highlight will be the displayof artwork from local schools on thetheme “Health lives – Healthy heart”, acompetition supported by the BritishHeart Foundation. Great work and spotthe budding Hockneys of the future.Prize winners announced on Tuesday,but they are all winners and don’tworry if you miss them. We will beposting a selection at www.bcs.com

Our roving reporters are alreadyactive and if you cannot make a ses-sion, why not read a summary of it onthe website www.bcs.com

Finally, a particular thanks to theProgramme Committee, the AffiliatedGroups and our Exhibitors and spon-sors for helping to deliver such a highquality and diverse international educa-tional event. Can’t stop! I am off to theOpening Ceremony.

A very warm welcome to ExCeL, London, and theBCS Annual Conference & Exhibition 2009. I hopeyou enjoy the Conference and the venue. It hasbeen a long time since the BCS has held anAnnual Conference in London and it is good to bereturning to such an excellent facility.

Welcome to the87th Meeting

Chronic stable angina

The ability to mechanically dilate

obstructive coronary artery

stenoses has fundamentally

altered our approach to manag-

ing patients with CAD. 2

Pathologicalinvestigation

Mary N Sheppard

Royal Brompton and Harefield

NHS Trust, undertakes a patho-

logical investigation of sudden

cardiac death 6

Omega-3

Professor Julian Halcox, Cardiff

University, dicusses the signifi-

cance of omega-3 6

AuditUlf Stenestrand reports on RIKS-

HIA 7

Chronic pulmonarythromboendarterectomy

Dr Joanna Pepke-Zaba discuss-

es treatment outcomes 9

Ablation for atrialfibrillation

Tim Betts asks whether ablation

is the treatment of choice or the

final option. 12

What patients want

Richard Schilling asks why are

patients with heart rhythm prob-

lems particularly anxious?

12

Molecular imaging

Molecular and cellular process-

es of atherosclerosis,

thrombosis and vascular inflam-

mation. 13

Suduko and answers12 & 14

Exhibitors and floorplan 14 & 15

BCS Conference News

Professor David NewbyBritish Heart Foundation Chair ofCardiology, University of Edinburgh

The endothelium plays a vital role inthe control of blood flow, coagula-tion, fibrinolysis and inflammation.

To date, clinical studies have focused onthe assessment of vasomotion and thereis now extensive evidence of abnormalendothelium-dependent vasodilatation inpatients with atherosclerosis and its asso-ciated risk factors. Indeed, abnormal vaso-motor responses, whether in the coronary

or peripheral circulations, independentlypredict adverse cardiovascular outcomes.However, whilst endothelium-dependentvasomotion is important, it may not berepresentative of other important aspectsof endothelial function. Under normal circumstances, the

endothelium prevents thrombus forma-tion through a number of mechanisms.Thrombomodulin, protein S, heparan sul-fate proteoglycans and tissue factor path-way inhibitor are all endothelium-derivedinhibitors of coagulation, while prostacy-

clin and nitric oxide inhibit platelet aggre-gation. However, when the endotheliumis perturbed, it can rapidly become proco-agulant by down regulating its anticoagu-lant functions, inducing tissue factorexpression and increasing secretion of fac-tors such as fibronectin, von Willebrandfactor and platelet activating factor. The endogenous fibrinolytic system pro-

tects the circulation from intravascular fib-rin formation and thrombosis that wouldotherwise result in vessel occlusion and

Strickland Goodhall Lecture: Intravascularthrombosis- new frontiers in endothelial function

Dear colleaguesWelcome to ExCeL,London and the87th BritishCardiovascularSociety’s AnnualConference andExhibition. This isthe first year thatBCS has had a con-ference newspaper -it’s a new venturedesigned to keepyou up-to-date withevents and hot top-ics of the three days,whether they beclinical, scientific, educational or industry based.We would welcome any feedback you may haveabout the newspaper (please emaileditor@bcs.com).

This Conference marks the end of my tenure asBCS President. I would like to thank theMembers of the Society for making my tenure apleasant and rewarding experience. I believe theSociety and its Conference and Exhibition have agreat future and will continue to thrive in thecapable hands of your next President, ProfessorKeith Fox.

I hope you have a wonderful conference andenjoy your time with us at ExCeL.

Nicholas Boon, President of BCS

Iain A Simpson Chairman of the Programme

CommitteeBCS Vice President, Education &

Research

CONTENTS

Sarah Clarke, BCS Chair ofCommunication and Education

MONDAY - Auditorium 11.30–12.30

David NewbyContinued on page 4

2 1–3 June 2009 Heart Murmurs

Monday’s timetableMonday 1 June 2009

Platinum 309.00 Multi-management of ischaemic heart disease:

Do we have the COURAGE of our convictions?Sponsored Symposia: CV Therapeutics

10.00 Exhibition opens

10.30 Opening ceremony

Auditorium10.45 Imaging in coronary artery disease

Platinum 1 & 210.45 SAC

Platinum 310.45 Paradoxical Embolism

Platinum 410.45 Revalidation in cardiology. Where are we and

where are we going?

Platinum 510.45 Medical and holistic management of congenital

heart disease12.15 Exhibition break

Auditorium

Exhibition Hall (Boulevard Theatre)12.30 How to assess and manage carotid disease in

cardiac patients

Platinum 1 & 2

Exhibition Hall (Waterfront Theatre)12.30 How to manage the pregnant patient with valve

disease

Platinum 3

Exhibition Hall (Waterfront Theatre)12.30 How to be a successful academic cardiologist

Auditorium13.30 Assessing chest pain in A&E by imaging

Platinum 1 & 213.30 Reperfusion therapy in STEMI

Platinum 313.30 Medical, surgical and interventional

management of coarctation of the aorta

Platinum 413.30 The way forward in cardiac pathology

Platinum 513.30 Fits, faints and flops15.00 Exhibition break

Meet the Experts

Exhibition Hall15.15 Magnetic resonance imaging in Acute Coronary

Syndromes; provenance and pitfalls15.15 Dilemmas and escapes in primary PCI

Auditorium16.00 Promotion of cardiovascular health: From risk

factors to imaging and genomics17.00 Moderated posters in exhibition

Platinum 318.00 Omega-3s, challenging hearts and minds

Platinum 418.00 Optimal Treatment of CAD: Are we addressing

all the risk factors?19.00 Exhibition ends

William E Boden, MD, FACCProfessor of Medicine and PreventiveMedicine, University at BuffaloSchools of Medicine and PublicHealth; Medical Director, CardiovascularServices, Kaleida Health; Chief of Cardiology, Buffalo Generaland Millard Fillmore Hospitals,Buffalo, NY

Since the advent of percutaneouscoronary intervention (PCI) in 1977,the ability to mechanically dilate

obstructive coronary artery stenoses hasfundamentally altered our approach tomanaging patients with coronary arterydisease (CAD). Over these decades, theremarkable and sustained evolution ofthis catheter-based technology has shift-ed treatment largely away from an initialpharmacologic approach to one thatemphasized an anatomically-driven man-agement strategy. Importantly, over thissame time period, significant advancesoccurred in our understanding of thepathophysiologic basis for acute coronarysyndromes and the important role thatplaque rupture or fissure plays in thegenesis of MI, which clearly indicate thatnon-flow-limiting coronary stenoses arethe principal progenitors of most “hard”clinical events.1–3 We now recognize thattotal or subtotal coronary occlusion fol-lowing plaque rupture or fissuring is acardiovascular emergency that cannot beoptimally managed pharmacologically.Abundant trials data support the beliefthat urgent/emergent PCI in patientswith ST-segment elevation myocardialinfarction (STEMI) or high-risk non-STEMIderive a prognostically-important reduc-tion in death or subsequent MI.4–9

Because performing PCI in patientswith chronic angina and stable electiveCAD is virtually identical procedurally tothat performed in ACS patients, manyhave accepted the broader (butunproven) premise that PCI would confera more durable clinical benefit (i.e.,beyond mere angina relief or improvedexercise performance) in this populationof patients as well. Accordingly, themanagement of stable angina has beenbased largely on the “conventional wis-dom” that the triad of angina, objectiveevidence of myocardial ischemia, and thepresence of one or more flow-limitingcoronary stenoses necessitated revascu-larization as the sine qua non of optimaltreatment.

The Clinical Outcomes Utilizing

Revascularization and Aggressive druGEvaluation (COURAGE) Trial wasdesigned to determine whether PCI cou-pled with optimal medical therapy (OMT)reduces the risk of death or non-fatal MIin patients with stable coronary arterydisease (CAD), as compared with optimalmedical therapy alone.10 Such a “strate-gy trial” had never been conducted pre-viously. COURAGE enrolled 2,287patients with objective evidence ofmyocardial ischemia and significant CADfrom 50 U.S. and Canadian centers.Between 1999 and 2004, 1,149 patientswere assigned to PCI with optimal med-ical therapy and 1,138 to optimal med-ical therapy alone. The primary outcomewas all-cause mortality or non-fatalmyocardial infarction (MI) during a 2.5 to7.0 year (median 4.6 year) follow-up.There were 211 primary events in thePCI group and 202 events in the medicaltherapy group. The 4.6-year cumulativeprimary event rates were 19.0% and18.5% in the PCI and medical therapygroups, respectively (hazard ratio [HR] inthe PCI group compared with the med-ical therapy group, 1.05; 95% confi-dence interval [CI], 0.87 to 1.27;P=0.62). Comparing PCI and medicaltherapy groups, there were no differ-ences in death, MI, or stroke (20.0% vs19.5%, HR, 1.05; 95% CI, 0.87 to 1.27;P=0.62); hospitalization for acute coro-nary syndrome (12.4% vs. 11.8%, HR,1.07; 95% CI, 0.84 to 1.37; P=0.56); orMI (13.2% vs. 12.3% HR, 1.13; 95% CI,0.89 to 1.43; P=0.33). Thus, the mainstudy findings indicate that, as an initialmanagement strategy in patients withstable CAD, PCI did not reduce death,MI, or other major cardiovascular eventswhen added to optimal medical therapy.

Importantly, the Kaplan-Meier life-table curves for the primary outcome

measure of death or MI were virtuallysuperimposable for the two randomizedgroups over the initial 4.5 years of fol-low-up (hazard ratio, 1.05, 95% confi-dence interval [CI], 0.87-1.27). In fact,the 95% CI excludes a potential benefitof PCI of greater than 13%, whichmeans that there is only a 5% chancethat a death or MI reduction with PCI is13% or greater.

Perhaps the singular achievement inCOURAGE that is the most importantand least controversial is the profoundimpact that intensive medical therapyand lifestyle intervention had on mitigat-ing clinical events in both randomizedarms of the trial during long-term fol-low-up. While many have attempted toportray COURAGE as an epic battle ofwhich management strategy in stableCAD patients with chronic angina issuperior, the overarching take-homemessage from the trial is that optimalmedical therapy as an initial manage-ment strategy in such patients is bothsafe and effective. The COURAGE resultsdo not indicate that PCI is inherentlyworthless or that PCI is ineffective orinappropriate as an initial managementstrategy in stable CAD patients; it meansthat PCI is not the only viable and clini-cally-defendable initial strategy and thatOMT alone may be suitable and appro-priate for many patients (and physicians)

who may decide to defer PCI until afteran assessment of the efficacy of OMTcan first be made. Importantly,COURAGE does not inform us that pri-mary PCI for STEMI or PCI for high-riskACS should be delayed or deferred.

The clinical implications of COURAGEare potentially profound. Simply stated,CAD is a systemic problem that requiressystemic treatment. Flow-limiting lesionscause angina and ischemia but may notnecessarily be the lesions predisposing todeath, MI, and ACS. OMT is directedtoward stabilizing so-called vulnerableplaques that are frequently mild angio-graphically and non-obstructive, suchthat OMT should rightfully be regardedas the preferred therapeutic approach toreducing clinical events in patients withchronic coronary syndromes and as com-plementary to focal revascularizationapproaches directed toward angina andischemia relief, if needed. Achieving andmaintaining multiple treatment targetsmay be a difficult challenge, but is wellworth the effort.

COURAGE should change clinical prac-tice not only in the U.S., but worldwide.While no one trial is likely to result in pro-found change, there is reason to believethat COURAGE will re-orient our clinicalthinking away from what has been alargely procedural approach to initialpatient management for stable CAD.

COURAGE confronts conventional wis-dom and an existing belief system thatchronic angina, objective evidence ofischemia, and significant obstructiveCAD may not inevitably require myocar-dial revascularization as an initial man-agement strategy. The results are conso-nant with currently published ACC/AHAclinical practice guidelines that OMTshould be considered an appropriate andfavored first approach in stable CADpatients.11 COURAGE may well alter thebelief systems of many physicians whowill synthesize the trial results and seekto achieve equipoise in their clinical deci-sion-making between PCI plus OMT ver-sus OMT alone.

Chronic stable angina: Pills, pipework, or both?

Dr Jim HallSecretary of the Cardiology SAC The James Cook University Hospital Middlesbrough

Each year at the BCS annual confer-ence and exhibition the CardiologySAC has an open meeting with

trainees. We aim to use this opportunity toinform trainees and trainers of develop-ments in cardiology training and to hearthe views of a broad spectrum of traineeson these or other training issues.

The Cardiology SAC, under the chair-manship of Prof Stuart Cobbe, has theresponsibility of setting the standards forhigher specialist cardiology trainingthrough the curriculum and its assessment.This year we will give some short presenta-tions on the current ‘hot topics’ of qualitymanagement of training programmes, theassessment strategy, the knowledge basedassessment for trainees and the sub-spe-cialty curricula.

These topics cover the most importantchanges in the rules, regulations and struc-tures of cardiology training. These havebeen made in response to new directivesfrom PMETB (the postgraduate medicaleducation and training board) which is thestatutory regulatory body responsible foroverseeing postgraduate medical educa-tion.

I will give the presentation on the sub-specialty training curricula and will reviewthe background to sub-specialisation, out-line the current curricula and introduce theplans for selection into sub-specialties.

Sub-specialties within cardiology (consid-ered as sub-sub-specialties by PMETB) arereflections of the realities of current clinicalpractice. Over the past ten to twenty yearsit has become increasingly common forconsultants to focus exclusively on particu-lar spheres of cardiac work e.g. advancedechocardiography or electrophysiology.This sub-specialisation has been reflectedin the job market with cardiac depart-

ments increasingly advertising for consult-ant cardiologists with specific areas ofexpertise.

The cardiology curriculum 2007 indi-cates that sub-specialty training will takeplace after the completion of core training(ST3, ST4 and ST5). The training will con-sist of a combination of discrete modules.In order to guide trainees and trainers indeciding what is an achievable mix oftraining in the final two years the follow-ing provisos should be met: traineesshould achieve 4-5 “credits” before com-pletion of training, CCT; the modules mustbe taken in full; the modular weightingsare coronary Intervention 4, interventionalEP + devices 4, device therapy 2; echocar-diography 3, nuclear cardiology 2, CMR 2,heart Failure 2, ACHD 2 or 4; heart diseasein pregnancy 1 (must be attached toACHD), academic cardiology (only availableto NTN(a) holders) up to 4, general internal(acute) medicine 2.

The process for determining which sub-

specialty modules are undertaken by anindividual trainee in their ST6 and ST7years will largely take place at Deanerylevel. The following guidelines have beenset: allocation should be organised atdeanery/cluster level; sub-specialty trainingcapacity should be explicit; vacant trainingslots can be made available to out-of-deanery trainees; some small sub-special-ties (e.g. ACHD) will need to be organisedat a national level; competitive selectionprocess could be necessary for over-sub-scribed sub-specialties. Any competitiveprocesses will need to be robust andshould be modelled on current arrange-ments for ST2-3 allocation with appropri-ate person specifications; ARCP reviewsshould guide trainees to appropriate mod-ular combinations.

It is hoped that this presentation willclarify the current state of play in this areaof the curriculum. As part of the SAC ses-sion with trainees there will be the oppor-tunity for questions from the floor.

Subspecialty curriculum and selection

Jim Hall

References:1 Naghavi M, Libby P, Falk E, et al.

From Vulnerable Plaque toVulnerable Patient: A Call for NewDefinitions and Risk AssessmentStrategies: Part I. Circulation 2003;108:1664-72.

2 Ambrose JA, Tannenbaum MA,Alexopoulos D, et al. Angiographicprogression of coronary artery dis-ease and the development ofmyocardial infarction. J Am CollCardiol 1988; 12:56-62.

3 Little WC, Constantinescu M,Applegate RJ, et al. Can coronaryangiography predict the site of asubsequent myocardial infarction inpatients with mild-to-moderate coro-nary artery disease? Circulation1988; 78:1157-66.

4 Antman EM, Anbe DT, ArmstrongPW, et al. ACC/AHA guidelines for

the management of patients with ST-elevation myocardial infarction--exec-utive summary: a report of theAmerican College ofCardiology/American HeartAssociation Task Force on PracticeGuidelines (Writing Committee toRevise the 1999 Guidelines for theManagement of Patients With AcuteMyocardial Infarction). Circulation2004;110: 588-636.

5 Keeley EC, Boura JA, Grines CL.Primary angioplasty versus intra-venous thrombolytic therapy foracute myocardial infarction: a quanti-tative review of 23 randomised trials.Lancet 2003; 361:13-20.

6 Invasive compared with non-invasivetreatment in unstable coronary-artery disease: FRISC II prospectiverandomised multicentre study.FRagmin and Fast Revascularisation

during InStability in Coronary arterydisease Investigators. Lancet 1999;354:708-15.

7 Cannon CP, Weintraub WS,Demopoulos LA, et al. Comparisonof early invasive and conservativestrategies in patients with unstablecoronary syndromes treated with theglycoprotein IIb/IIIa inhibitor tirofiban.N Engl J Med 2001; 344:1879-87.

8 Fox KA, Poole-Wilson PA, HendersonRA, et al. Interventional versus con-servative treatment for patients withunstable angina or non-ST-elevationmyocardial infarction: the BritishHeart Foundation RITA 3 randomisedtrial. Randomized Intervention Trial ofunstable Angina. Lancet 2002;360:743-51.

9 Mehta SR, Cannon CP, Fox KA, et al.Routine vs selective invasive strate-gies in patients with acute coronary

syndromes: a collaborative meta-

analysis of randomized trials. JAMA

2005; 293:2908-17.

10 Boden WE, O'Rourke RA, Teo KK,

et al. Optimal medical therapy with

or without PCI in stable coronary

disease. N Engl J Med 2007; 35:

1503-16.

11 Gibbons RJ, Abrams J, Chatterjee K,

et al. ACC/AHA 2002 guideline

update for the management of

patients with chronic stable angina--

summary article: a report of the

American College of

Cardiology/American Heart

Association Task Force on practice

guidelines (Committee on the

Management of Patients With

Chronic Stable Angina). J Am Coll

Cardiol 2003; 41:159-68.

MONDAY - Platinum 1&2: 10.45–12.15

MONDAY - Platinum 3: 09.00–10.00

William Boden

4 1–3 June 2009 Heart Murmurs

David HackettVice President (Clinical Standards),British Cardiovascular Society

Revalidation for doctors registered withthe General Medical Council (GMC) inthe UK is coming! The purpose of

revalidation is to demonstrate and confirmthat licensed doctors practise according tothe GMC’s generic standards (relicensure),and that specialists meet the standardsappropriate for their specialty (recertifica-tion). The GMC has stated that the processof revalidation for doctors should be sup-portive rather than punitive, there shouldbe patient & carer involvement, the resultshould be to raise standards, and remedia-tion and rehabilitation should be included.Revalidation should be a continuingprocess, not a 5-yearly event, should ensureconsistent standards across practices, bebased on evidence from local practice, anddepend on the quality of appraisal.

There are several problems when devel-oping a process for revalidation of doctors.There are logistical issues with large num-bers of doctors, in diverse practices & set-tings; methodological concerns to ensurevalid, reliable, proportionate & fair systems;connectivity issues with different systems &organisations, and avoidance of duplication;quality of information with accurate & veri-fiable clinical outcomes; and cultural issuesto develop continuous quality improvementprograms.

Revalidation of doctors in the UK will bebased on structured annual appraisal, andfive satisfactory consecutive appraisals willlead to revalidation. The GMC, theAcademy of Royal Medical Colleges, andthe Royal College of Physicians have devel-oped an agreed framework for genericappraisal based on “Good MedicalPractice”, with the following four domains:n Knowledge, Skills, Performancen Safety & Qualityn Communication & team work

n Maintain TrustThe Health and Social Care Act 2008 estab-lished the post of Local Responsible Officer(LRO); this is likely to be the Medical Directorof NHS Trusts, and similar roles in otherhealthcare organisations. The responsibilitiesof the LRO include liaison between the localhealthcare organisations and the GMC; andimplementation of medical revalidation. Theclinical governance responsibilities of the LROwill include contracts of employment fordoctors or provision of services; monitoringconduct and performance; ensuring appro-priate action when necessary; and havingregard to guidance from regulators.

The GMC has stated that the revalidationprocess must have objective standards,assessment schemes, arrangements for mon-itoring and delivery, and quality assurance inplace; ensure that decision making processesand procedures for recertification must befair, objective, transparent, and free fromunfair discrimination; recertification will coin-cide with relicensing (one process); schemesfor recertification must be monitored and theassessment methods kept under review,amended and updated; and that doctors donot need to be members of Colleges toundertake recertification.

The GMC has agreed that the standardsfor remaining on the Specialist Register andthe GP Register will be the same as the stan-dards currently required for entry to thoseregisters. However, the range of competen-cies and evidence to be demonstrated forrecertification will relate to the doctor’s actu-al practice, rather than their original training.

The British Cardiovascular Society (BCS)has discussed revalidation for cardiologistsin numerous forums and meetings since2007. We have held two workshops to fur-ther develop our plans for revalidation: inJuly 2008 we agree the broad outlines of asystem and process for revalidation of cardi-ologists in the UK. This workshop agreedthat cardiologists should be revalidated inthe three domains of knowledge, skills and

professional behaviour. In late 2008 wepublished our proposals for revalidation onour website, and undertook consultationand sought feedback from our member-ship. Approximately 68-90% of respon-dents agreed or strongly agreed with theseproposals. In April 2009 we held a secondworkshop to discuss and agree the contentof a portfolio to lead to revalidation of car-diologists. This content will be discussedand debated at various BCS meetings dur-ing this meeting. It is intended that if thereis agreement, then BCS will use this contentto develop pilot systems for revalidation ofcardiologists.

Some advantages of the educational(rather than regulatory) approach adoptedby the BCS as the basis for revalidation,include: foundation based on the core andsubspecialty curriculum in cardiology; link-ing of knowledge based assessment withassessment of competency in procedures;linking clinical practice with actual job plan;allowing the credentialing of individual clini-cians in procedures and in healthcare

organisations; and has the potential fordevelopment as a system for revalidation ofcardiologists in Europe.

The European Board for the Speciality ofCardiology (a joint initiative by theEuropean Union of Medical Specialties andthe European Society of Cardiology) hastasked Orzone AB www.orzone.se, aSwedish medical simulation companyfounded in 2008 with a focus on patientsafety, to develop a knowledge-basedassessment process for trainees in cardiolo-gy. The first pilot assessment will take placeduring this meeting. BCS is exploring thepotential for Orzone to develop a web-based platform for the electronic content ofa revalidation portfolio for cardiologists. It ispossible that such a system could be usedfor other specialties in the UK, and for car-diologists in other European countrieswhere regulatory systems for revalidationwill be developed in the future. If such aweb based platform is developed, weintend that it would be accessed throughthe BCS website, could be populated from

a number of sources, both automaticallyfrom web based documentations or ondemand from personal sources, and couldbe used for personal appraisal each year,and for revalidation every five years.

The original GMC timescale for revalida-tion of doctors in the UK was to beginpilots in late 2009, with the first cycle ofrevalidation of doctors in 2010. It is nowexpected that the GMC will issue licencesto practice in late 2009, that local responsi-ble officers will be appointed during 2010,and the first revalidation of doctors willnow take place in early 2011. If our devel-opment plans bear fruit, BCS hopes thatthere would be a first version of a webbased system ready for pilot use in late2009, and we would pilot revalidation forvolunteers in 2010. If all was successful,cardiologists would be ready for the firstwave of revalidation of doctors in 2011.

Revalidation SessionDo come to the BCS session on“Revalidation in Cardiology. Where are weand where are we going?” on Monday 1June 2009 at 10:45 to 12:15 in Platinum 4 inthe ExCeL Centre. There will be presentationsfrom Dr Peter Mills of EBCS with a Europeanperspective; Dr David Hackett of BCS with aUK perspective; Dr Ian Starke of RCP with aperspective from the Royal College ofPhysicians; and Dr Una Lane of the GMCwith a GMC perspective. As well as plenty oftime for discussion afterwards where you canhave your questions about revalidation forcardiologists in the UK answered.

Revalidation Centre, stand 380There will be a stand in the Exhibition Hallholding details of Revalidation initiatives inboth UK and Europe. You will be able tosee an example of the software for aRevalidation portfolio that is currently beingdeveloped and try your hand at a fewKnowledge Based Assessment questions.The stand is number 380.

Revalidation of cardiologists – UK perspectiveMonday - Platinum 4: 10.45–12.15

Cardiology Review Course Dr Alun Harcombe

The inaugural joint ‘British Cardiovascular Society and Mayo ClinicCardiology Review Course’ ran from 2 to 6 March 2009 at the RoyalCollege of Physicians in London and proved to be a great success,

according to feedback from the 77 delegates and 26 faculty. The coursewas co-directed by Dr Peter Brady, from the Mayo Clinic, Rochester,Minnesota, USA, and Dr Alun Harcombe, from Nottingham UniversityHospitals NHS Trust, representing the BCS. Work on this concept had beenongoing for more than two years, initiated by Professor David Crossmanand latterly supported by Dr Iain Simpson. Drs Brady and Harcombe werejointly responsible for course content and faculty selection and the BCS,expertly led by Kirsten Bradbury, was responsible for administration. Thecourse organisers were grateful to have received unrestricted educationalgrants from St Jude, via Radi Medical, as well as Cordis Johnson andJohnson/ Biosense-Webster, and Sanofi-Aventis.

The course aimed to cover the cardiology curriculum comprehensively;

with an expert faculty recognised for educational excellence drawn fromthe Mayo Clinic as well as the UK, to meet the educational needs oftrainees planning to sit the forthcoming Knowledge Based Assessmentexamination. The target audience was trainees at or around ST5 level, butwas also intended to include European colleagues and indeed anyonewishing to review cardiovascular medicine, including consultants. Themajority of delegates proved to be cardiology trainees (77%), with theremainder being cardiologists from outside the UK, Associate Specialistsand Staff Grades. Delegates attending from Sweden, Hong Kong, Qatar,USA and Cuba emphasised the universal appeal of the programme.

Hosting an intensive 5 day lecture series from 9am to 5pm each daywas no problem for the Royal College of Physicians, whose staff wereexemplary in their courtesy and service throughout the week. There wasan excellent audience response system, ably supported the audio-visualstaff headed by Barry Lewis, which allowed continuous lecture evaluations- each speaker was assessed immediately on content, duration, practicalvalue and overall rating. Presenters could run multiple choice case scenar-ios and other questions, increasing audience engagement and participa-tion. Subjects ranged from ECG interpretation and continued via complica-

tions of myocardial infarction, ablation for atrial fibrillation and many othertopics, all the way through to complex congenital heart disease. Delegatesovercame their initial ‘stunning’ at the variety and depth of subjects tointeract with presenters via many excellent questions, with further probingat break times.

Evaluation was by paper form for the course as a whole and via theaudience response systems for each talk: 100% of delegates said theywould recommend the course to others, 99% rated the course overallexcellent or good and the mean rating of individual lectures was 90%excellent or good. Some delegates commented:

“I had high expectations coming to this course and it far surpassed myexpectations. I think the course was really excellent, very practically usefuland it made me feel excited to be a trainee in cardiology.”

“The course has been excellent. The best educational event I've attend-ed since becoming a cardiology trainee. Thanks for the hard work of allthe faculty.”

Plans are at an advanced stage for the next course in 2010, from 8 to 12March – reserve your place now by emailing courses@bcs.com becausedemand is likely to be very high after the success of this year’s event. v

David Hackett

tissue ischemia. Following the initiation ofintravascular thrombus formation, the endotheli-um acutely releases tissue plasminogen activatorin response to a range of factors that are predom-inantly related to the coagulation cascade, espe-cially factor Xa and thrombin. Once released, tis-sue plasminogen activator catalyses the conver-sion of plasminogen to plasmin and thereby facili-tates thrombus dissolution through the proteolyt-ic degradation of fibrin to soluble fibrin degrada-tion products. The efficiency with which tissueplasminogen activator converts plasminogen toplasmin is markedly increased in the presence offibrin, thus ensuring efficient and localizedintravascular activation. The onset and efficacy offibrinolysis is principally determined by the rapidi-ty and magnitude of tissue plasminogen activatorrelease from the endothelium. The initiation, modification and resolution of

thrombus associated with eroded or unstablecoronary plaques is critically dependent on theefficacy of endogenous fibrinolysis that is itself

dependent upon the cellular activation and func-tion of the surrounding endothelium and vascularwall. In particular, the acute release of tissue plas-minogen activator from the endothelium makesan important contribution to the defence againstintravascular thrombosis. Professor Newby hasexplored fundamental aspects of vascular injuryand repair including his work looking at the regu-lation of endogenous fibrinolytic capacity. In boththe peripheral and coronary circulations, impairedtissue plasminogen activator release is a promi-nent feature of cigarette smokers; a cardiovascu-lar risk factor with a particularly prominent pro-thrombotic phenotype. However, impaired tissueplasminogen activator release is not a feature ofall endothelial dysfunctional states since othercardiovascular risk factors, including hypercholes-terolaemia, are associated with normal endothe-lial tissue plasminogen activator release. In anattempt to get closer to the physiological andpathophysiological mediators activated by acuteatherosclerotic events, Professor Newby’s grouphas explored the vascular actions of thrombinusing specific thrombin receptor activating pep-

tides. Stimulation of the endothelial cell thrombinreceptor causes arterial vasodilatation, venousconstriction, platelet activation and tissue plas-minogen activator release. This work has beenfurther extended to look at the mechanisms ofthrombin receptor activation and to demonstrateeven more marked vascular and fibrinolyticabnormalities in smokers. Thus the nature of theinsult and the specific signalling pathwaysinvolved appear to have important and diverseeffects on endothelial and vascular function.These major effects are highly relevant to the clin-ic and, in a prospective cohort study; his grouphas shown that the capacity to release t-PA acute-ly predicts future adverse cardiovascular events inpatients with coronary heart disease.Air pollution is increasingly recognised as an

important and modifiable determinant of cardio-vascular disease in urban communities. Acuteexposure has been linked to a range of adversecardiovascular events including hospital admis-sions with angina, myocardial infarction, andheart failure, and long-term exposure increaseslifetime risk of death from coronary heart disease.

The main arbiter of these adverse health effectsappears to be combustion-derived nanoparticu-late generated by road traffic. Through the induc-tion of cellular oxidative stress and pro-inflamma-tory pathways, this nanoparticulate matterappears to augment the development, progres-sion and destabilisation of atherosclerosis. Indeed, consistent with effects described in cig-

arette smokers (self-induced air pollution), ourgroup has demonstrated that controlled expo-sures to traffic-derived air pollutants causeimpaired vascular effects and in particular,reduced endothelial tissue plasminogen activatorrelease. This dysfunctional state is apparent inpatients with coronary heart disease who alsohave evidence of exacerbated myocardialischaemia during periods of exposure. Theseadverse cardiovascular effects appear to underpinthe atherothrombotic consequences of acute andchronic exposure to air pollution. A greater under-standing of the mediators and mechanisms is nec-essary if we are to develop strategies to protectindividuals at risk and reduce the impact of airpollution on cardiovascular disease.

Continued from page 1

Strickland Goodhall Lecture: Intravascular thrombosis- new frontiers in endothelial function

6 1–3 June 2009 Heart Murmurs

Professor Julian Halcox, Cardiff University

Fatty acids may be saturated, monounsaturated orpolyunsaturated fatty acids (PUFAs). PUFAs containtwo or more double bonds in their hydrocarbon

backbone and two nomenclatures exist describing theposition of the first double bond in the hydrocarbon.

Either “omega” or “n” are used to denote the posi-tion of the first double bond relative to the methylgroup; for example in the “omega-3” or “n-3” family,the first double bond occurs three carbons from thefirst methyl group. PUFAs are classed as essential fattyacids as they cannot be made by the body and must bederived from the diet.

There is increasing evidence that omega-3 as well asomega-6 PUFAs play important roles in mediating andregulating inflammatory processes, immune functionand blood clotting within the body.

Recently, strategies for the secondary prevention ofMI have focused on the omega-3 family of PUFAs (n-3

PUFAs), and several studies have provided evidence forthe anti-atherogenic, anti-thrombotic and anti-arrhyth-mic effects of n-3 PUFAs1,2,3.

Cardiovascular disease (CVD) remains the biggestkiller in the UK, accounting for 238,000 deaths eachyear.4 Approximately half (48%) of these CVD deathsare from coronary heart disease (CHD).4

Interest in the possible cardio-protective effects of n-3 PUFAs have existed since the late seventies. There isgrowing evidence to suggest that n-3 PUFAs offer pro-tection against CHD and this benefit appears most pro-nounced on CHD mortality and sudden cardiac death,which is 50% lower in men who consume oily fish atleast once a week.5

The results of the landmark GISSI-Prevenzione6 trial(involving 11,324 patients within 3 months of an MI)showed that the addition of n-3 PUFAs (one capsuledaily of 860mg in the form of EPA and DHA) to stan-dard therapy for post-MI patients further reduces therelative risk of:

n All-cause death by 20%n Cardiovascular death by 30%n Sudden death by 45%Combined mortality was reduced within four monthsof treatment, supporting the hypothesis of an earlyanti-arrhythmic mechanism.

The National Institute for Health and ClinicalExcellence have recently recommended that survivors ofan acute myocardial infarction consume at least 1g perday of n-3 PUFA either as (oily) fish or as a licensed,highly purified n-3 preparation.

N-3 PUFAs have also been shown to reduce levels oftriglycerides in the body. EPA and DHA act at severalpoints in the pathway of triglyceride metabolism in the

liver (so reducing TG levels). They inhibit triglyceridesynthesis and also reduce secretion of very low densitylipoprotein (VLDL) which may have antiatheroscleroticconsequences.7

More recently the JELIS8 study (evaluating 1,800mgEPA or placebo in 18,645 Japanese patients alreadybeing treated with statins for primary or secondary pre-vention) showed that the cumulative rate of majorcoronary events were reduced by 19% in the EPAgroup (RRR, p=0.011).

The biology and clinical trial data of n-3 PUFA andtheir potential for improving outcomes in patients withand at risk of CVD will be discussed in a satellite sym-posium held on Monday 18.00–19.00, Platinum 3.

Relevance of omega-3

Monday - Platinum 4: 13.30–15.00

Monday - Platinum 3: 18.00–19.00

References1. Simopoulos AP. Omega-3 fatty acids in

health and disease and in growth and devel-opment. American Journal of ClinicalNutrition 1991;54(3): 438–463

2. Simopoulos AP. Omega-3 fatty acids in theprevention-management of cardiovasculardisease. Canadian Journal of Physiology andPharmacology 1997;75(3): 234–239

3. Marchioli R and Di Pasquale A. [The bio-chemical, pharmacological and epidemiologi-cal reference picture of the GISSI-Prevention.The Gruppo Italiano per lo Studio della

Streptochinasi nell’Infarto Miocardico].Giornale Italiano di Cardiologia 1993; 23(9):933–964

4. British Heart Foundation. Heart Stats. HeartStats 2008 August 1Available from:www.heartstats.org

5. Marckmann P, Gronbaek M. Fish consump-tion and coronary heart disease mortality. Asystematic review of prospective cohort stud-ies. Eur J Clin Nutr 1999;53:585-90

6. Gruppo Italiano per lo Studio dellaSopravvivenza nell'Infarto miocardico. Dietarysupplementation with n-3 polyunsaturated

fatty acids and vitamin E after myocardialinfarction: results of the GISSI-Prevenzionetrial. Lancet 1999 Aug 7;354(9177):447-55.

7. Thies F et al. Association of n-3 polyunsatu-rated fatty acids with stability of atheroscle-rotic plaques: a randomised controlled trail.The Lancet 2003; 361: 477-485.

8. JELIS. Effects of eicosapentaenoic acid onmajor coronary events in hypercholestero-laemic patients: a randomized open-label,blinded endpoint analysis. Lancet2007;369:1090-1098.

Mary N SheppardRoyal Brompton and Harefield NHS Trust“My fine healthy son dropped dead atsixteen” so runs a recent headline in one ofour daily papers. Such sudden, inexplicabledeaths are more common than you mightthink. For families this is probably one of themost devastating and traumatic events thatcan happen in their lives. Families arehorrified when they are left without anexplanation as to the cause or there is adelay in the coronial report or inquest. Thisentity has grabbed the headlines since theperson is often young and has beenpreviously healthy. The term sudden cardiac(SCD) or sudden arrhythmic death (SAD) isused and refers to the presumed mode ofdeath in all cases as a lethal cardiacarrhythmia. It has also been called suddenadult death to distinguish it from suddeninfant death but it can occur at any age, notjust in adulthood. The incidence of thisentity has been unknown/underestimated inthe past.

I became involved with sudden cardiacdeath in 1994 when I was asked to partici-pate in a research project sponsored by theBritish Heart Foundation looking into thisentity. In all ages the majority not surpris-ingly (82%) are due to coronary artery dis-ease, but we found in 5.3% other cardiaccauses, including potentially inheritable car-diomyopathies and in 4.1% the deaths

were totally unexplained despite detailedexamination by three cardiac pathologists.1

Non–ischaemic causes of sudden cardiacdeath are of major importance becausethey include genetic diseases, such ashypertrophic cardiomyopathy, dilated car-diomyopathy and arrhythmogenic right ven-tricular cardiomyopathy. We showed anestimated frequency of sudden unexpecteddeath due to cardiac or unidentified causesof 11/100,000 which translates into 3481

annual deaths. A further prospectivestudy showed they had a mean age of 32years and 63% were male. This nationalsurvey was the first to characterize SADSvictims through informant interviews and tocompare the mortality for this syndromewith official ONS mortality statistics. Theestimated incidence rate is 0.16 per100,000 per annum and is twice that regis-tered officially by The Office of NationalStatistics. Importantly the survey revealed an18% prevalence of a family history of otherpremature sudden or unexplained accidentsemphasizing the heritable aspect of cardiac

disease. This study recommended theterm Sudden Arrhythmic Death Syndrome(SADS) as the officially certified cause ofdeath to facilitate systematic populationbased research through a national registerinto the environmental and genetic causesof these unexplained deaths with evaluationof families2. In a further study of families of

SADS victims, 53% screened were diag-nosed with inheritable heart disease.Therefore accurate pathological examina-tion and clinical examination is vital forappropriate prophylaxis amongst relatives,guided and confirmed by mutation analysis3

The concept of the morphologically nor-mal heart in sudden death is of majorimportance with the emergence of themolecular channelopathies such as Long QTor Brugada syndrome giving rise to lethalcardiac arrhythmias in the last 15 years.4

Following the initial BHF study many coro-ners in the UK have sent cases of suddencardiac death to me and I now have a valu-able database which we use extensively forresearch. The coroner/pathologist sends theheart for examination by our departmentwith the full consent of the relatives and weprovide a detailed examination and report.

At a time of intense anxiety for a familywe can provide a detailed report of the casewithin two weeks. We are a multidiscipli-nary team using the skills and expertise ofpathologists, biomedical scientists, laborato-

ry assistants and secretarial staff. Recentadverse publicity has led to a trend towardsrefusing retention and further investigationof organs and tissues from autopsiesbecause of the perceived distress to familiesthat this may cause. This is totally erroneousin view of the fact that tissue examination isessential in determining many familial caus-es of sudden cardiac death and thus in pre-venting sudden death in other members of

the family. We published our results of theinvestigation of over 600 sudden deaths inEngland indicating that electrical faults inthe hearts are becoming a frequent causeof sudden death.7

From examining post mortem reports inthis cardiac sudden death study (1) Ibecame aware of the variable quality ofautopsies and in particular the way the car-diovascular system was examined. This vari-able quality in coronial autopsies has sincebeen reiterated by the NCEPOD study whichemphasised that sudden cardiac deathcases are poorly investigated especiallywhen the question of cardiomyopathy orcardiac hypertrophy arises.4 This is despitepublished guidelines for pathologists investi-gating sudden death.5,6

Now we have established a nationaldatabase under CCAD guidelines to gaugethe true incidence of sudden non ischaemiccardiac deaths in England and will publishour first year results soon. Pathologicalimput and a thorough and well investigatedautopsy with detailed macroscopic andmicroscopic examination of the heart areessential in sudden cardiac death.Pathologists and coroners need support andappropriate infrastructure to carry out thisimportant duty for families and the cardiol-ogists who will screen them.

The pathological investigationof sudden cardiac death

Reference1 Bowker TJ, Wood DA, Davies MJ,

Sheppard MN, Cary NR, Burton JD et al.Sudden, unexpected cardiac or unex-plained death in England: a nationalsurvey. QJM 2003; 96(4):269-279.

2 Behr ER, Sheppard MN, Wright M,Bowker TJ, Davies MJ, McKenna WJ etal. Sudden Arrhythmic Death Syndrome(SADS) - a national survey of suddenunexplained cardiac death. Heart 2007;

93(5):601-605.3 Behr ER, Dalageorgou C, Christiansen

M, Syrris P, Hughes S, Tome Esteban MTSheppard,M.N. et al. Sudden arrhythmicdeath syndrome: familial evaluationidentifies inheritable heart disease inthe majority of families. Eur Heart J2008; 29(13):1670-1680.

4 Ranson D. Coroners' autopsies: qualityconcerns in the United Kingdom. J LawMed 2007; 14(3):315-318.

5 Sheppard MN. Sudden adult death andthe heart. Kirkham NSN, editor. [6],185-202. 2003. London, GreenwichMedical Media. Progress in Pathology.1-1-2003.

6 Lucas S, Burnett RCCLSMJ, Moore ISR.The Royal College of PathologistsWorking Party on the autopsy.Guidelines on autopsy practice-Scenario1: Sudden death with likely car-diac disease. 2005. London, Royal

College of pathologists. The RoyalCollege of Pathologists working partyon the autopsy.

7 Fabre A, Sheppard MN. Sudden adultdeath syndrome and other non-ischaemic causes of sudden cardiacdeath. Heart 2006; 92(3):316-320.

Mary N Sheppard

ArrhythmiaAwareness Week & World HeartRhythm Week 8–14 June 2009Arrhythmia Alliance will hold its sixth annual ArrhythmiaAwareness Week (AAAW) with a parliamentary launch on June8 in the House of Commons. The international organisation ofArrhythmia Alliance (A-A) will celebrate World Heart RhythmWeek (WHRW) with the official launch of A-A Sweden.

The theme of the week is 'Know Your Pulse'(www.knowyourpulse.org). Materials for hosting an aware-ness event are available free of charge by emailingjoannag@stars.org.uk

PublisherHeart Murmurs - BCS Conference News is published by DendriteClinical Systems LtdEditorOwen Haskins: owen.haskins@e-dendrite.comManaging EditorMelissa Griffithsmelissa.griffiths@e-dendrite.comAdvertising:Mary Kennedy: mary.kennedy@e-dendrite.com

Managing DirectorPeter K H Waltonpeter.walton@e-dendrite.com

Head Office59A Bell Street,Henley-on-ThamesOxfordshire RG9 2BA, United KingdomTel: +44 (0) 1491 411 288Fax:+44 (0) 1491 411 399Wesite: www.e-dendrite.com

Heart Murmurs - BCS Conference NewsCopyright ©2009: Dendrite Clinical Systems Ltd and the British Cardiovascular Society. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, transmitted in any form or by any other means, electronic,mechanical, photocopying, recording or otherwise without prior permission in writing of the editor. The content within does not reflect the views or opinion ofDendrite Clinical Systems or the Britsh Cardiovascular Societyay be reproduced, stored in a retrieval system, transmitted in any form or by any other means,electronic, mechanical, photocopying, recording or otherwise without prior permission in writing of the editor. The content within does not reflect the viewsor opinion of Dendrite Clinical Systems or the Britsh Cardiovascular Society

Heart Murmurs 1–3 June 2009 7

Tuesday’s timetableTuesday 2 June 2009

Auditorium08.30 Who should manage cardiac patients in the

modern NHS

Platinum 1 & 208.30 Guidelines and guidance

Platinum 308.30 Anti-thrombotic update

Platinum 408.30 YRWP clinical

Platinum 508.30 Pulmonary thrombo-embolism10.00 Moderated Posters in Exhibition Hall

Auditorium11.00 Assessing LV function

Platinum 1 & 211.00 Coronary atherosclerosis – new insights in

diagnosis and therapy

Platinum 311.00 BCS Audit

Platinum 411.00 Inequalities in cardiac care in the UK

Platinum 511.00 YRWP – Basic12.30 Exhibition break

Auditorium

Exhibition Hall (Boulevard Theatre)12.30 How to assess cardiovascular risk before non

cardiac surgery

Platinum 1 & 2

Exhibition Hall (Waterfront Theatre)12.30 How to assess the evidence

Platinum 312.30 How to assess risk in acute coronary

syndromes

Auditorium13.30 Controversial decision making in percutaneous

intervention

Platinum 1 & 213.30 Heart Failure

Platinum 313.30 Diabetes&atherosclerosis – new concepts and

emerging therapeutic targets

Platinum 513.30 Atrial fibrillation in primary care and beyond15.00 Exhibition break

Meet the Experts

Exhibition Hall15.15 PFO and ASD closure; why, when and how15.15 Pressure wire: use and misuse

Auditorium16.00 Investing in your arteries!

Lifetime management of atherosclerosis17.00 Moderated posters in exhibition

Platinum 318.00 Improving outcomes for the ACS (acute

coronary syndromes) patient: The way forward?

Platinum 418.00 Anticoagulation in ACS –

The theory and the practice19.00 BCS ACE Cocktail Party @ ExCeL

Ulf Stenestrand, Associate professor ofcardiologySenior consultantinterventional cardiologistDeptartment of Cardiology, University HospitalSE 58185 Linköping, Sweden

President SWEDEHEARTChairman RIKS-HIAstenestrand@riks-hia.se

When the local cardiacintensive care registerwas started in

Linköping, Sweden, 1991 wehad no idea that it would leadto a world wide known registerone day. In 1995 the Register ofInformation and Knowledgeabout Swedish Heart Intensivecare Admissions, RIKS-HIA,became a national quality assur-ance register. The participatingnumber of hospitals grew grad-ually to 72 in 2001 and since2007 all 74 hospitals participate.Sweden is a country of 9 million

people and twice the size of UKthat gives a population densitythat is 1/10 of UK.

RIKS-HIA has contributed toenhance adherence to nationaland ESC guidelines. Open com-parisons on-line and an annualreport publishing quality indexand complications for every hos-pital stimulate the media debateand the reformation in Swedishhospitals.

Even though there stillremains differences betweenhospitals in adherence to guide-lines these differences are muchsmaller compared to 10 yearsago, and in general the adher-ence is substantially improvedtogether with lower complica-tion rates and improved survivalafter myocardial infarction. Thishas saved both money andunnecessary suffering inSweden.

On-line reports in RIKS-HIAgive immediate feedback to thehospital how it treats its patientswith acute coronary syndrome

compared to guidelines and alsocompared to the 20 best per-forming hospitals.

The register has also con-tributed to study treatmenteffects of therapy in subpopula-tions and also evaluated differ-ent treatment strategies such asearly statin therapy in myocar-dial infarction and early revascu-larization in non-ST-elevationmyocardial infarction. In ST-ele-vation myocardial infarctionthrombolysis in elderly wereproven to be safe and in a laterstudy primary PCI proved superi-or to thrombolysis. Cost benefitstudies have been conducted.Several other studies have beenconducted on the basis of RIKS-HIA resulting in new knowledgepresented in medical journals.As well as supporting adherenceto guidelines the register’s studyresults have contributed to cur-rent knowledge and writing ofinternational guidelines.

The greatest problem withRIKS-HIA is that it still requiresdata entering into the internetbased system separate frommedical records. Today electron-

ic records are becoming moreprevalent in Sweden and thecurrent important task for thedevelopers of the 3rd genera-tion of quality register is theintegration with electronicpatient records. Once this isachieved all the benefits of thequality register will be therewithout the extra labor.

The first years all softwarewas developed by me on myfree time. Today it is done byprofessional programmers andstatisticians running an annualbudget of 500.000 Euro. Allfinancial support is provided bythe Swedish government. Thegovernment also uses the quali-ty index as an instrument todecide which of competing hos-pitals in larger cities will begiven the right to treat cardiolo-gy patients.

In 2009 RIKS-HIA is entering anew era when the four qualityregisters on ischemic heart dis-ease are going to be convertedinto one register. The SwedishCoronary Angiography andAngioplasty Registry (SCAAR),the Heart Surgery Register, RIKS-

HIA, and the SecondaryPrevention Register (SEPHIA) alljoin to one common register theSWEDEHEART (Swedish Web-system for Enhancement andDevelopment of Evidence-basedcare in Heart disease EvaluatedAccording to RecommendedTherapies). New challenges arebeing faced while several advan-tages will come with this newregister. The goal is to furtherimprove the quality of care inpatients with heart disease inSweden. Well, not only Swedensince the country of Iceland anda part of Finland is already partof our Swedish register.

Audit: RIKS-HIA

David HackettVice President (Clinical Standards),British Cardiovascular Society

The British Cardiovascular Society(BCS) has been concerned for sometime about inequalities in provision

of and access to cardiac care in the UK.International comparisons show that theprovision of services for the managementof heart disease in the UK remains farbelow that of comparable Europeancountries. The BCS commissioned aninequalities report in 2004, which waspublished in the British Journal ofCardiology in 2005. This study examinedand reported on substantial differencesin the provision of cardiac care in thefour countries in the UK. The secondBCS Inequalities Report published inHeart in 2006 highlighted some strikingdisparities between spending, activityand the burden of disease, and includedmany examples of the inverse care law:‘‘the availability of good medical caretends to vary inversely with the need forit in the population served.”

The third BCS inequalities report pub-lished on the BCS website emphasisedthe phenomenon of postcode prescrib-ing, also known as the postcode lottery,

that has been well publicised and reflectsmany variables, particularly the availabili-ty and expertise of staff, which especiallyinfluence small health care units. Thegeographical variation in activitydescribed in this third report related tomuch larger service blocks and could beconstrued as a national lottery. Theinequalities are therefore more likely toreflect differences in health care policyand planning.

These BCS reports into inequalities incardiac care did not systematically allowfor variations in the local burden of dis-ease, or for differences in populationstructure now or projected into thefuture. Nor did they take into accountthe rapidly declining mortality from car-diovascular disease, nor for the conse-quent increase in prevalence and burdenof disease in the population. Indeed, theNational Heart Foundation of Australiapredicts a 50% increase in the preva-lence of cardiovascular disease in thepopulation by 2050.

With this background, BCS togetherwith British Heart Foundation (BHF) andthe Cardio-Vascular Coalition (CVC)together commissioned a report from DrStephen Green and Dr Rebecca Miles ofOxford Healthcare Associates, a respect-

ed and independent healthcare serviceconsultancy. It was agreed that the studywould examine the current and project-ed future need for various specific car-diac procedures, including cardiaccatheterisation and angiography, revas-cularisation including PCI and CABG, theneed for valve surgery, cardiac deviceimplants including pacemakers, defibrilla-tors and re-synchronisation devices, andfor cardiac electrophysiology studies andablations. The agreed brief was:

To assess current levels of service pro-vision for specific cardiac procedures inthe UK, for specific population groupsand identify variations in provision; byobtaining and synthesising the most up-to-date data on current numbers & ratesfor specified cardiac procedures on apopulation basis; for the UK as a whole,for each of the four UK countries, foreach English SHA, and for each LocalAuthority in the UK; and to produce areport on current levels of service provi-sion.

To review current estimates of ‘proxyneed’ for specific cardiac procedures,based on local burden of cardiovasculardisease and local population structure;and to estimate current variationsbetween provision and estimated need,

and thus describe current inequalities inprovision of cardiac care.

To calculate the future levels of needup to 2020 for the various cardiac proce-dures; to review the model and ifrequired re-assess the current levels of'proxy-need' for these specific cardiacprocedures, based on local burden ofcardiovascular disease and populationprojections from the Office of NationalStatistics; and to estimate growthrequired for each of the various cardiacprocedures to ensure equality by 2020for each of the four UK countries, foreach English SHA, and for each LocalAuthority in the UK.

The key findings of the study will bepresented to the conference on Tues 02June 2009. It is expected that the studywill demonstrate a marked increase inprovision of the main cardiac treatmentsin all parts of the country, with year-on-year increases in provision of cardiac careinterventions in all regions, since 2000.Despite these significant improvements,the UK is likely to remain near the bot-tom of the international league for themain cardiac interventions when com-pared to other similar European coun-tries.

It is expected that the study will give aclear indication as to where more servicesmay be required to improve equity of

Inequalities in cardiac care in the UK

Ulf Stenestrand

Hugh Montgomery, UCL Insitute, London

For those cardiologists work-ing in general hospitals,scarcely a day will go past

without a variety of irritatingcalls. A request to look at anECG in casualty to help deter-mine if it showed AF of VFsprings to mind. Much morecommon, however, is therequest to come and see apatient to help determine if theyare ‘for for surgery’. Whatshould be our response?

Firstly, we should demon-strate a degree of humility. Fewof us are anaesthetists, and wethus lack an understanding of

the cardiac burden imposed bythe surgical procedure. Nor dowe understand the choices andeffects of the diverse drugswhich might be used- whichcross the spectrum of negativeand positive inotropes andchronotropes, hypertensiveagents and those which willlower coronary perfusion pres-sure. Even less do we under-stand the possibilities for local orregional analgaesia, and specifi-cally the (contra)indications andphysiological effects or epiduralor spinal anaesthesia. It is forthis reason that the UK anaes-thesia governing bodies stateclearly that surgical risk assess-ment should only be performed

by those trained in such assess-ment.

Secondly, we must under-stand that ‘risk’ and ‘hazard’ arenot the same thing. The risk(likelihood of an event happen-ing) may be very low, but thehazard (‘how bad it is when itdoes happen’) may be great. Ingeneral terms, whilst the rangeof possible hazards may beclear, the individual risk of eachmay be very hard to define.Further, such data as exist maybe acceptable across a popula-tion, but offer very limited infor-mation about an individual.Imagine, then, that you are 83and have an early oesophagealmalignancy amenable to surgi-

cal intervention. The data whichexist suggest that you have a50% chance of dying. Youmight say ‘I’d rather die on thetable than obstructed in a year’.But few deaths are ‘on thetable’: most result from pneu-monia or anastamotic break-down, with mediastinal drainsand a slow slide of sufferinginto multiorgan failure. Is thatworth it?

Which brings us to the nextpoint: we are usually asked toopine on the ‘risk’ of surgery- bywhich ‘cardiac risk’ is generallyinferred. However, the vast bulkof perioperative mortality andmorbidity is not due to a pri-mary cardiac event. In fact, a

multitude of comorbiditiesimpact upon outcome.Amongst these, cardiac diseaseclearly plays a significant role:impaired ventricular function(and a corresponding inabilityfor the heart to meet the meta-bolic demands resulting fromsurgery) may be the major con-tributor to whether youroesophageal anastamosis willbreak down. But how good arewe at assessing this risk? And ifthere were great data withwhich we were fully familiar,would there be anything wecould do about it?

So what is the cardiologistsrole? Firstly, cardiovascular physi-ologists (for that is what we are)

may be welcomed in periopera-tive risk services. Taking an inter-est in this field may save a greatnumber of lives. In addition, wecan streamline investigationalpathways: echocardiography for‘LV function’ has little to con-tribute to risk and hazard assess-ment in the individual, and bet-ter options might be available.As importantly, we can indeedadvise on areas of specialistknowledge: we might discusscases of HCM, aortic stenosis,mitral stenosis and so forth withour anaesthetic colleagues andintensivists to lay a plan. Wemight look at the patient withtrifascicular disease and decidewhether we want to preopera-tively pace with a temporarywire. Finally, we shouldn’t forgetour holistic role: a patient withcardiac disease facing a big

operation is scared. Knowingthat ‘their heart doctor’ isinvolved should reassure.

This session will discuss suchissues, such that the cardiologistcan offer real value in improvingoutcome and avoid many of thetiresome calls through establish-ing some form of process inperioperative assessment.

Cardiovascular risk: The intensivist’s view

Tuesday - Platinum 4: 11.00–12.30

Tuesday - Platinum 3: 11.00–12.30

Tuesday - Exhibition Hall: 12.30–13.30

Hugh Montgomery

Continued on page 8

8 1–3 June 2009 Heart Murmurs

Dr Stephen Wheatcroft, University of Leeds

Despite recent advances inthe prevention and man-agement of cardiovascular

disease, patients with diabetesmellitus continue to have alarm-ingly high rates of morbidity andmortality secondary toatherothrombotic complications.The increased risk in a patientwith diabetes is equivalent to 10-15 years of aging in a personwithout diabetes and around80% of patients with diabetescurrently die from vascular dis-eases. In day to day practice, around a

quarter of patients admitted withacute coronary syndromes havediabetes – this proportion is likelyto increase in line with the pre-dicted rise in diabetes globallyover the next two decades.Diabetes and cardiovascular dis-ease in combination pose severalimportant challenges to the cardi-ologist. Patients with diabetesderive less protection from pri-mary and secondary preventionstrategies than their counterpartswithout diabetes, as well as expe-riencing worse outcomes follow-ing acute coronary syndromesand coronary revascularisation. At the University Leeds, we

recently investigated the impactof diabetes on 18 month out-comes in patients admitted tohospitals in our region with acutecoronary syndromes in 1995 and2003. Increased provision of sec-ondary prevention measures andgreater delivery of early revascu-larisation between these time

points were associated with asubstantial improvement in sur-vival in patients without diabetes.However, survival remainedunchanged in patients with dia-betes sustaining an acute coro-nary syndrome despite similarimprovements in care. These wor-rying statistics suggest that con-temporary risk reduction strate-gies are failing to benefit ourhighest risk group of patients.Although diabetes-specific guide-lines for cardiovascular risk reduc-tion were published jointly by theEuropean Society of Cardiologyand the European Association forthe Study of Diabetes in 2007,cardiologists continue to be facedby unresolved controversies overhow best to manage theirpatients with diabetes.

Clinical studiesA close association betweenblood glucose concentrations andcardiovascular mortality in epi-demiological studies has beenrecognised for many years.However, whether intensivelylowering blood glucose levelsprotects against macrovasculardisease remains controversial. Therecently published ADVANCE andVADT studies, which comparedintensive with conventional treat-ment strategies in patients withdiabetes at high risk of cardiovas-cular disease, showed nomacrovascular benefit from inten-sive glucose control. Furthermore,the large ACCORD trial indicatedincreased all-cause and cardiovas-cular mortality with intensive con-trol. In contrast, in the long-termfollow up of patients with type 2

diabetes in the UKPDS study,there was a significant reductionin myocardial infarction and allcause mortality in the intensivetreatment group. Taken together,these studies suggest that inten-sive blood glucose control early inthe disease process may translateinto long term clinical benefits,but that other strategies are nec-essary in older populations withlongstanding diabetes or estab-lished cardiovascular disease, inwhom aggressive glucose-lower-ing may cause harm. The possibility that intensifying

treatment early in patients withdiabetes might improve long-term cardiovascular outcomesraises the question of whetherpatients with diabetes shouldroutinely be screened for coro-nary artery disease. This is another area of contro-

versy which has been debatedfor many years. In their mostrecent guidance, the AmericanDiabetes Association did notadvocate a policy of widespreadscreening. One key issue integral

to this decision, however, iswhether patients with diabetesgain a greater clinical benefitfrom early detection of coronaryartery disease with subsequentrevascularisation than thatafforded by intensive medicaltherapy alone. In the myocardialperfusion imaging sub-study ofthe COURAGE trial, revascularisa-tion did confer a prognostic ben-efit in patients in whom signifi-cant inducible ischemia had beendemonstrated. The BARI-2D studytested this hypothesis in patientswith diabetes, by comparing theeffects of optimal medical thera-py with optimal medical therapyplus revascularisation on cardio-vascular outcomes. The resultswill presented at the AmericanDiabetes Association meeting onthe 7 June. In patients with diabetes and

coronary artery disease who arereferred for revascularization,the choice between PCI andcoronary artery bypass surgeryremains contentious. A recentlypublished Lancet collaborative

analysis supports the long heldview, initially proposed by theoriginal BARI study, that surgeryconfers a survival advantageover angioplasty in patientswith diabetes. More recent ran-domized trials, including CARDiaand SYNTAX, however, revealedno difference in mortality fol-lowing PCI compared to surgeryin patients with diabetes,although more patients under-going PCI required repeat proce-dures.

Insulin resistance Insulin resistance is a major playerin the pathogenesis of both type2 diabetes and atherosclerosis,suggesting that insulin-sensitizingstrategies should be highly effec-tive in reducing cardiovascularrisk. However, continuing contro-versy surrounds the cardiovascu-lar profile of the insulin-sensitis-ing drugs thiazolidinediones. Inthe ProACTIVE study of pioglita-zone in patients with type 2 dia-betes and cardiovascular disease,the primary composite endpointwas not significantly improved,although analysis of secondaryendpoints and post-hoc analysesof patients with established vas-cular disease indicate a protectiverole of pioglitazone. In the IVUS-based PERISCOPE

trial, coronary plaque regressionwas demonstrated when pioglita-zone was added to a sulphony-lurea. The influence of rosiglita-zone on cardiovascular risk is lessclear. A pivotal meta-analysis sug-gesting an increased risk ofmyocardial infarction with rosigli-tazone had substantial limitationsand has been widely criticized.The controversy surrounding thepotential cardiovascular risk ofrosiglitazone has, however, initi-ated a landmark change in theregulatory approval of novel dia-

betes drugs. Guidance from theFDA now places stringent require-ments on the pharmaceuticalindustry to undertake rigorousphase 2 and phase 3 trials ofemerging diabetes drugs, with anindependent cardiovascular end-points committee. Regardless of their effects on

athero-thrombotic risk, both cur-rently marketed thiazolidine-diones induce fluid retention,largely by increasing sodium reab-sorption in the renal collectingduct. The risk of heart failure issignificantly increased with thia-zolidinediones although, some-what surprisingly, not mortality –perhaps because myocardial func-tion is not impaired (and in factmay be improved) by this class ofdrug. Again, the forthcomingresults of the BARI-2D will help toclarify whether an insulin sensitis-ing strategy (metformin + thiazo-lidinedione) offers a cardiovascu-lar risk reduction advantage overan insulin providing strategy(sulphonylurea + insulin).The limited impact of current

treatment strategies on cardio-vascular outcomes in individu-als with diabetes places agrowing impetus on cardiovas-cular researchers to identifynovel therapeutic targets toreduce diabetes-related cardio-vascular disease. In our labora-tory, for example, we are exam-ining the potential for insulin-like growth factor binding pro-teins to reduce susceptibility toobesity, insulin resistance andvascular disease. Developmentof novel therapies which targetnot only glucose homeostasisbut also the molecular and cel-lular pathways promotingatherothrombosis may ulti-mately reverse the adverseeffect of diabetes on the risk ofcardiovascular disease.

Controversies in diabeticvascular risk management

Stephen Wheatcroft

Professor David Fitzmaurice,University of Birmingham

Warfarin belongs to a class of drugsknown as coumarins which arevitamin K antagonists and cause

reduced biological activity of the vitamin Kdependent factors II, VII, IX and X (clottingfactors) as well as protein C and S (anticoagu-lant factors). The action of warfarin is unpre-dictable and, along with issues such as foodand drug interactions, leads to the necessityfor therapeutic monitoring with the INR. Thetrue clotting mechanism is complicated interms of both warfarin’s mechanism of actionhowever for newer products it is the finalcommon pathway which illuminates most).

New AgentsMany of the requirements for a drug toreplace warfarin, including not having tomonitor, have now been met by new agents.There are a large number of drugs currentlyunder development targeting different stagesin the pro-coagulant pathway. Figure 1 showsthe properties of some of the more advancedanticoagulants.

The first of the new order of oral anticoagu-

lants to be licensed for orthopaedic thrombo-prophylaxis was Ximelagatran. Despite largeclinical trials programmes abnormalities in theliver enzyme ALT began to emerge with morethan a three-fold increase in this enzyme notedin around 9% of patients. More than 20,000patients received this agent, however, a smallnumber of patients were identified with hepat-ic failure on extended use. The company tookthe unexpected step shortly thereafter to haltfurther studies and withdraw the drug for all itslicense indications from the market. The causeof the idiosyncratic hepatic drug response hasnot to date been identified, and therefore,remains a concern for all new anticoagulantsunder trial, particularly the direct thrombininhibitors. It has, however, served to enhancethe surveillance of similar agents currentlyunder trial.

Dabigatran EtixalateDabigitran Etixalate is a pro-drug that is con-verted to Dabigitran a potent reversible directthrombin inhibitor. It is currently licensed forprimary prevention of venous thromboem-bolism in adult patients who have undergoneelective total hip replacement or total kneereplacement surgery. The drug is also under

investigation for the treatment of venous andarterial thromboembolic disorders, particularlyatrial fibrillation. The drug is active orally withthe mean terminal half-life of approximately 12– 14 hours in volunteers and 14 – 17 hours inpatients undergoing major orthopaedic surgery.The drug is largely (85%) excreted by renalpathways and patients with moderate renalimpairment or elderly patients that require adose reduction to 75mgs for the first dosepost-operatively followed by 150mgs per day. Itcurrently meets many of the criteria for an idealanticoagulant, in particular it has a low level ofdrug interactions. Cytochrome P450 pathway isnot involved in the formation or metabolism ofDabigitran. The drug has a fast onset and offset of action and is not affected by interactionswith food. Due to its wide therapeutic windowthe drug does not require laboratory monitor-ing of coagulation tests.

RivaroxabanRivaroxaban is an oral direct and highly selec-tive inhibitor of activated Factor Xa. In thephase III trial programme for the prevention ofVTE after orthopaedic surgery from theRECORD studies, it was shown to be superiorin the efficacy for the composite end point of

DVT, non-fatal PE and all-cause mortalitywhen compared with Enoxaparin when givenat 40 mgs subcutaneously per day or 30mgssubcutaneously twice per day. Rivaroxabanhas a high oral bio availability with a peakplasma concentration 2 – 4 hours after oraladministration. It is primarily excreted by therenal (66%) and faecal / biliary routes (28%).Drug interactions are much less commonlyseen than with warfarin although agents thatare strong inducers or inhibitors of CYP3A4and P glycoprotein such as ketoconazole andRifampicin may modify anticoagulant effect.Overall, however, the safety profile is promis-ing with low bleeding incidence similar tothat of Enoxaparin.

ConclusionIt does finally appear that a new era of oralanticoagulant management has arrived. Thepotential for these agents to alter the deliveryof anticoagulant services with no laboratorymonitoring and less concern about seriousdrug interaction should make extendedthromboprophylaxis and extended treatmentmore readily achievable. The rate of changeand uptake of the new agents is, however,impossible to predict. Overall, the change inmanagement of oral anticoagulation fromSecondary to Primary Care will be facilitatedas these agents gain wider license for throm-boprophylaxis and treatment.

New AF oral anticoagulant drugs References

1 Eriksson, BI, Berqust D, Kalebo P et al.

Ximelagatran and Melagatran compared

with Dalteparin for prevention of venous

thromboembolism after total hip or knee

replacement: the METHRO II randomised

trial. Lancet 2003; 360: 1441-7

2 Eriksson BI, Agnelli G, Cohen AT et al. The

direct thrombin inhibitor malagatran fol-

lowed by oral Ximelagatran compared with

Enoxaparin for the prevention of venous

thromboembolism after total hip or knee

replacement: the EXPRESS study. J Thromb

Haemost 2003; 1 (12): 2490-6

3 Shulman S, Wahlander K, Lundstrom et al.

Secondary prevention of venous throm-

boembolism with the oral direct thrombin

inhibitor Ximelagatran. N Eng J Med; 349

(18): 1713-21

4 Eriksson BI, Dahl OE, Rosencher N et al. Oral

Dabigitran Etexilate vs. subcutaneous

Enoxaparin for the prevention of venous

thromboembolism after total knee replace-

ment: the RE-MODEL randomised trial. J

Thromb Haemost 2007; 5: 2178-2185

5 Eriksson BI, Dahl OE, Rosencher N et al.

Dabigitran Etexilate vs, Enoxaparin for pre-

vention of venous thromboembolism after

total hip replacement: a randomised, dou-

ble-blind, non-inferiority trial. Lancet 2007;

370: 949-956

6 Friedman RJ, Caprini JA, Comp PC et al.

Dabigitran Etexilate vs. Enoxaparin in pre-

venting venous thromboembolism following

total knee arthroplasty (the RE-MOBILIZE

trial). Abstract O-W-051 presented at the

XXIst Congress of the International Society

on Thrombosis and Haemostasis, July 6-12

2007, Geneva. J Thromb Haemost 2007; 5

(suppl 1): O-W-051

7 Eriksson BI, Borris L, Friedman RJ et al.

Rivaroxaban vs. Enoxaparin for thrombopro-

phylaxis after hip surgery. N Engl J Med

2008; 358: 2765-75

Tuesday - Platinum 5: 13.30

Tuesday - Platinum 3: 13.30–15.00

Figure 1Drug Argatroban Hirudin Bivalirudin Ximelagatran Fondaparinux Idraparinux Dabigatran RivaroxabanType of Action Bivalent DTI BivalentDTI Active site DTI Active site DTI Indirect Xa-inh Indirect Xa-inh Direct Thrombin Direct Xa

inhibitor inhibitorAdministration IV IV IV Oral IV / SC SC Oral OralHalf-life 45 mins 80 mins 25 mins 4 hrs 15 hrs 130 hrs 12–14 hrs 5.2–9.2 hrsClearance Hepatic Renal Proteolysis Renal Renal Renal Renal Renal 66%/ faecal

28%/ biliaryReversible Yes Slow Rapid Yes No No No No

Dr Joanna Pepke-ZabaConsultant Chest PhysicianDirector of National Pulmonary Vascular DiseasesUnit, Papworth Hospital, Cambridge, UK

Chronic thromboembolic pulmonary hypertension(CTEPH) is one of the leading causes of severepulmonary arterial hypertension (PAH). CTEPH

patients treated only with anticoagulation have a poorprognosis with more than 50% of patients with a meanpulmonary artery pressure >50 mmHg not survivingbeyond one year from diagnosis.

CTEPH currently represents the only form of PH withthe prospect for cure with PEA, which is therefore thetreatment of choice for selected patient population.However, PEA is a complex surgical procedure and10–50% of patients present with an unacceptableoperative risk due to inaccessible material, distal arteri-opathy and/or comorbid diseases.

All patients have to be treated with life long antico-agulation. Although some patients may benefit fromconventional medical treatments (diuretics, digitalis,oxygen), these are generally considered to be support-ive. The evidence from several small, non-placebo-con-trolled studies have shown improvements in diseasecharacteristics in CTEPH patients when treated withprostacyclin analogues (Eur Respir J 2004:23:594-600),or sildenafil (CHEST 2008:134:229) and one multi-cen-ter RCT with bosentan (J A Coll Cardiol 2008:52;2127-34)which showed a significant reduction in PVR.Therefore pharmacotherapy with PAH specific treat-

ments may be beneficial in certain contexts: (1) inpatients with predominantly distal disease that is notsurgically accessible; (2) when surgery is contraindicat-ed due to prognostically significant co-morbidity; (3) inpatients who are “high-risk” due to extremely poorhemodynamics prior to PEA (bridging to PEA); (4) inpatients with persistent or residual PH after PEA.

Since 2001 the diagnosis, treatment and follow-upof all adult CTEPH patients in the United Kingdom(UK) has been designated to seven PH centres (RoyalBrompton, Hammersmith, Royal Free Hospitals inLondon, Royal Hallamshaire in Sheffield, Freeman inNewcastle, Golden Jubilee Hospital in Glasgow andPapworth Hospital in Cambridge). Papworth Hospitalhas also been designated as the single national centrefor pulmonary endarterectomy (PEA) surgery. This hasresulted in a unique opportunity to study the naturalhistory of the disease and to test the hypothesis thatthe outcome of patients with CTEPH has improvedsince the introduction of surgical and medical treat-ment in the UK.

Baseline information for incident 469 CTEPH patientsdiagnosed in the UK pulmonary hypertension servicebetween January 2001 and June 2006 were collectedof which 148 (32%) had distal, non-surgical disease(Am J Respir Crit Care Med 2008;177:1122-7) . Oneand three year survival from the date of diagnosis overthe whole period was 88% and 76% for those treat-ed with PEA and 82 % and 70% for those with non-surgical disease (p=0.023). As the first oral disease-modifying therapy became available in the UK in

December 2002, we therefore separately analysed thesurvival of distal, non-surgical patients who entered thecohort during 2001/02 and 2003 onwards. As a learn-ing effect is well recognised in PEA programmes sur-vival in patients with surgical disease was also analysedseparately during these two periods. Of those undergo-ing PEA, 29% of the earlier group received PH disease-modifying therapy before surgery, compared with 65%of the later group (p<0.001). In patients with non-sur-gical disease, 70% of the earlier group received dis-ease-modifying therapies compared with 90% of thelater group (p=0.005).

In the current study the survival beyond one year ofboth non-surgical and surgical patients was better inthose diagnosed from 2003 onwards. In patients withnon-surgical disease one and three year survival in thisperiod was 83% and 76%.

An important finding of our study is that survival inpatients with persistent PH three months followingPEA, who were treated with disease-modifying therapyin selected cases, was excellent.

In 2005 the incidence of diagnosed and treatedCTEPH in the Pulmonary Hypertension Centers in UKwas 1.75 cases/yr/million. The observed incidenceincreased by 75% over a period of 5 years which ismost likely to be due to increased awareness of thecondition over studied period.

In this large national cohort, predictors of outcome inpatients with operable and non-operable CTEPH havebeen identified (Eur RespirJ 2009;33:332-8). The gastransfer and exercise capacity independently predicted

pulmonary endarterectomy peri-operative mortality.Cardiac index and exercise capacity independently pre-dicted outcome in patients with non-operable disease.A previous splenectomy was noted in 6.7% of patients,being significantly more common in patients with non-operable rather than operable disease (p<0.001).

Establishing predictors of outcome may be useful inplanning patient management. The improvements inoutcome during the modern treatment era, highlightthe importance of identifying patients with this increas-ingly treatable condition.

Heart Murmurs 1–3 June 2009 9

Chronic Thromboembolic Pulmonary Hypertension: treatment outcomes

Joanna Pepke-Zaba

Non-surgical patient’s survival Patients at risk2003- 115 81 45 18 12001/2002 33 24 18 17 13 4

Surgical

Sugically treated

Non-surgical

Years from diagnosis

Cum

mul

ativ

e su

rviv

al

1.0

0.8

0.6

0.4

0.2

01 2 3 4 5 6

Patients with CTEPHSurgically treated 236 190 146 89 53 28Non-surgical 148 105 63 35 14 4

Non-surgical

2003

2001/2002

Years from diagnosis

Cum

mul

ativ

e su

rviv

al

1.0

0.8

0.6

0.4

0.2

01 2 3 4 5 6

S

Mr David JenkinsPapworth Hospital

The surgical treatment of chronicthromboembolic pulmonary hyperten-sion (CTEPH) – pulmonary thromboen-

darterectomy (PTE or PEA) – is the onlyproven treatment to offer significant symp-tomatic and prognostic benefit and is cura-tive for many patients. The PTE operationwas developed mainly by Jamieson at theUniversity of California in San Diego (UCSD)and this unit retains the largest patientseries, having now completed over 2,500procedures. Experience at Papworth hospi-tal began in 1997, and we were commis-sioned as a single provider to run thenational service in 2000. We are now per-forming 60–80 procedures per year and todate have completed 490 operations. In2001, the national commissioning groupalso designated national adult pulmonaryhypertension centres at Glasgow, London,Newcastle, Papworth and Sheffield. Manyreferrals for pulmonary endarterectomyarise through this network of specialist cen-tres, but as awareness of the diseaseincreases more direct referrals arrive fromcardiologists and chest physicians.

CTEPH is the result of intraluminal throm-bus organisation and fibrous stenosis and/orcomplete obliteration of the pulmonaryartery lumen, and as a result of the hyper-tension there may be an adaptive responsein the non-obstructed arteriolar bed withmedial hyperplasia further increasing vascu-

lar resistance. This two compartment modelexplains why some CTEPH patients havesevere pulmonary hypertension out of pro-portion to the degree of vascular obstructionvisible in imaging investigations. Decisionson the risk/benefit ratio of PTE may be diffi-cult in some patients with high pulmonaryvascular resistance (PVR) and relatively distaldisease on imaging and at Papworth allpatients are evaluated in a weekly multidisci-plinary meeting. Ultimately the ease of dis-section and true extent of clearable diseasecan only determined at operation. The dis-ease has been classified into four subgroupsbased on the operative findings withpatients with more central types 1 and 2 dis-ease deriving more benefit from endarterec-tomy at less perioperative risk.

Overall, the key determinant of operabili-ty is the correlation between the degree of

visible disease in imaging studies and thehaemodynamic dysfunction (absolute PApressure, cardiac output and the function ofboth – PVR). Operative risk is almost totallydependent on PVR as discussed above, andconcomitant procedures (CABG, valvereplacement etc) can be performed as nec-essary during the rewarming phase of theoperation without additional risk to thepatient. The only comorbidity that mayinfluence the decision to operate is severeparenchymal lung disease.

It is important to distinguish operationsfor acute pulmonary embolism – embolec-tomy, from the true endarterectomy proce-dure for CTEPH. The fundamental aim ofthe surgery is to perform a full endarterec-tomy (not embolectomy or thrombectomy)of both pulmonary vascular beds. The oper-ation is performed via a median sternotomy

with hypothermic cardiopulmonary bypassand right and left pulmonary arteriotomieswithin the pericardium. The dissection planeis in the superficial media and a cast isremoved by gentle traction and eversionprogressing peripherally to include subseg-mental vessel ‘tails’ (see figure). Adequatevisualisation for distal dissection necessitatesreduction in bronchial arterial collateralreturn to the pulmonary arteries.Traditionally this has been overcome byperiods of complete deep hypothermic cir-culatory arrest (DHCA) for periods of 20minutes at 200C and this techniqueremains the standard teaching. At Papworthwe have devised a method of antegradecerebral perfusion (ACP) to avoid total circu-latory arrest. My personal view is that dis-section is technically easier with completeDHCA, but that it is not necessary in allpatients and ACP appears to be technicallyfeasible in the majority of patients. We haverecently completed randomisation in a trial(PEACOG) designed to compare ACP withDHCA with full functional, haemodynamicand neuropsychological follow up to oneyear.

Following surgery, patients are trans-ferred to the intensive care unit and remainsedated and ventilated over the first night.There is usually an early dramatic reductionin PA pressure and PVR after weaning frombypass. Many patients can be extubated bythe first post operative day. Most of thegeneral principles of postoperative cardiacsurgical care apply and in addition we aimto avoid any factors that may increase PVR.

Many units have reported excellent earlyresults after pulmonary endarterectomy inthe last few years. It is accepted that alearning curve exists with this procedure,

but with experience the in- hospital mortali-ty is reduced to approximately 5% in lead-ing centres including our own. As with allseries of surgical patients, outcome is oftendetermined by case mix once a learningcurve for the procedure has been overcome.

As well as the general complicationsoccurring after cardiothoracic surgery, thereare problems specific to pulmonaryendarterectomy patients. The most seriousproblem is residual PH (usually due to ahigher proportion of microvascular diseasethan anticipated) and/or reperfusion lunginjury. Often a combination of both prob-lems is present as residual PH exacerbatesreperfusion damage and the resultinghypoxia and hypercarbic acidosis furtherincreases PVR so a vicious cycle develops.When severe this accounts for the majorityof the fatalities in the post operative period.There may be some benefit in supportingseverely compromised patients in the earlypost operative period with extra corporealmembrane oxygenation (ECMO) providedan adequate endarterectomy has beenobtained. We have used veno-arterialECMO in approximately 5% of our recentpatients in the last three years with six of11 patients surviving to discharge from hos-pital.

Little international data is available onlonger term follow up. In the UK we havetried to correct this by routinely reviewing allsurvivors at three months and one year afterendarterectomy. The unique nature of thededicated PH service and single centre forpulmonary endarterectomy surgery in the UKhas facilitated comprehensive patient followup. Last year we reported the most completeevaluation following PTE in 230 patients sur-

Pulmonary thromboendarterectomy for chronicthromboembolic pulmonary hypertension

David Jenkins PTE specimen

Continued on page 10

Tuesday - Platinum 5: 08.30–12.30

Tuesday - Platinum 5: 08.30–10.00

Patients with CTEPH Non-surgical

10 1–3 June 2009 Heart Murmurs

In July 2009, the Society for Cardiothoracic Surgery iinGreat Britain and Ireland (SCTS) will release the SixthNational Adult Cardiac Surgical Database Report,

which will report on the outcomes from more than400,000 cardiac surgery cases from England, Scotland,Wales and Ireland. As well as reporting mortality out-comes, the publication will highlight: changes to thepatient population; the evolution of surgical tech-niques; the factors influencing surgical outcomes; five-year survival; post-op stroke rate; post-op renal failure;re-explorations for bleeding; and other process meas-ures. This latest report will be the most comprehensivepublic documentation of adult cardiac surgical practicepublished anywhere in the world.

“The NHS is a nationally funded service and theremust be accountability and transparency, and this hasbeen achieved in cardiac surgery,” said Mr BenBridgewater, Consultant Cardiac Surgeon, SouthManchester University Hospitals Trust, and Chair of theSCTS database committee. “Clinical governance is notjust about reporting mortality rates or outcomes, it isabout the wider spectrum of quality.”

The first nationally pooled cardiac data was collected in1977, with the aim of providing surgeons with a meansof comparing cases. This voluntary registry developedover time as people realised that in order to achieve use-ful comparisons you need to include more sophisticateddata including age, sex, cardiac function etc.

However, it was the major scandals such as theevents at Bristol Royal Infirmary that created great con-cern about governance within healthcare, and in partic-ular cardiac surgery. As a result, the SCTS acceleratedthe whole clinical governance debate and requestedthat every adult cardiac unit collected data, therebyproviding accountability and transparency.

Data collectionAlthough, the SCTS decides the dataset and steers thedirection of the audit, the responsibility for data collec-tion and validation is down to the local unit. This isachieved in a variety of ways from using commercialorganisations to developing an in-house database sys-tem. The mechanism for collating that data and provid-ing some superficial analysis sits with the CentralCardiac Audit Database (CCAD), part of the NHSInformation Centre. Surgeons submit encrypted dataonline and it all gets pooled together. All the processescomply with data protection legislation.

“Clinical audit does not cost the earth and in someways we are only seeing the tip of the iceberg in regardto the themes we have extracted from the data so far,”explained Bridgewater. “We should not underestimatethe power of numbers. We have data from every NHShospital in the UK, as well as some private hospitals anddata from Ireland. Overall, we have data on some114,000 coronary artery bypass graft (CABG) proceduresbetween 2004–2008 and long-term follow-up on themajority. The data give us confidence because we knowthat we are stating factual evidence.”

BenefitsFor example, one can see how cardiac surgery haschanged over time with an increase in valve surgerybut a decrease in CABG and increases in ablationfor atrial fibrillation. All these changes have signifi-

cant implications on resources, training, commis-sioning etc. Furthermore, the case-mix in cardiacsurgery has become more complex with time, yetdespite that; there have been significant reductionsin operative mortality over the past few years.

“A commonly cited concern regarding self-audit isthat surgeons may turn down the high-risk cases toensure that their results are good. In reality, this is anoverstated phenomenon and I think we have reacheda position now in the SCTS where we want to be asopen and transparent as possible,” he commented.“From time to time this may ruffle a few feathers inthe profession, but we have been successful as aSociety in supporting our members to change andimprove their practice.”

Governance and improvementsAccording to the Society, the coverage and the qualityof data submitted by cardiac surgeons are of such astandard that this improves the understanding of dataand assists in the clinical analysis. This allows surgeonsto have confidence when benchmarking their resultswith those of their peers, thereby driving improvementsin the quality of care they provide.

“In other areas of medicine people have been tryingto provide improvements in the quality of care but haveshied away culturally from open clinical governanceand comparisons. But the two are parallel partners, youmust have complete coverage to have quality data, inorder to perform effective comparisons and driveimprovements.”

International standardsUnfortunately, Great Britain and Ireland are the onlycountries in the world to have such in-depth coverage.In places where they do have sufficient databases, thedata is not analysed or published to allow internationalcomparisons. Therefore it is difficult to make interna-tional comparisons, however, the mortality of cardiacprocedures in the UK is within pre-determined confi-dence intervals, so the overall mortality is low.Moreover, when the data is used with a risk-modelling

tool, such asthe EuroScorebenchmarkingtool, the overallmortality in theUK is less thanhalf than waspredicted.

“We knowthat associatedwith collectingand bench-marking dataon adult car-diac surgerythere has beena 50% reduc-tion in risk-adjusted mor-tality over thelast seven or eight years. We also know to someextent from North American data that collectingbenchmarking data drives quality. So if we acknowl-edge that such initiatives work, whether the data ismade public or not, failure to provide a process/s isdenying the patient the right to the associated bene-fits.”

Conclusions“In some ways I think it has been easy for cardiac sur-gery to perform self-audit because we perform a rela-tively small number of operations and mortality used tobe an outcome measure that happens sufficiently fre-quently to be useful, interesting and meaningful.Because of improvements in quality mortality is now solow that I am not sure this remains true. But no matterthe specialty, if you have an appropriate culture withina surgical profession and a culture between profession-als and policy makers and other stakeholders, you cancreate a resource that has many potential benefits tomany people. Failure to provide ongoing benchmarkingis a betrayal of professional responsibilities.”

Cardiac specialty demonstrateseffective self-governance

Ben Bridgewater

Wednesday’s timetableWednesday 3 June 2009

Auditorium09.00 Atrial Fibrillation: Improving treatment through

understanding mechanisms

Platinum 1 & 209.00 Aortic stenosis

Platinum 309.00 New frontiers in myocardial protection

Platinum 409.00 Heart Failure or Heart Success

Platinum 509.00 Early diagnosis & management10.30 Moderated Posters in Exhibition Hall

Auditorium11.30 Intravascular thrombosis: new frontiers in

endothelial function

Platinum 511.30 Risk intervention – what works?12.30 Exhibition break

Auditorium12.30 AGM (BCS Members Only)

Auditorium

Exhibition Hall (Waterfront Theatre)12.45 How to use pacemakers & defibrillators in

congenital heart disease

Platinum 1 & 2

Exhibition Hall (Waterfront Theatre)12.45 How to assess and manage Marfans Syndrome

Auditorium13.45 Devices-pacemakers ICD & CRT

Platinum 1 & 213.45 Aortic interventions

Platinum 313.45 Imaging vascular pathophysiology

Platinum 413.45 What patients want

Platinum 513.45 Established disease15.15 Exhibition break

Meet the Experts

Exhibition Hall15.15 Ablation; last ditch option in atrial fibrillation or

first line therapy15.15 Inappropriate shocks – Horror stories from the

ICD clinic

16.00 Exhibition closes

Platinum 1 & 215.45 Delivering arrhythmia care

Platinum 315.45 Read with the experts

Platinum 415.45 Advanced heart failure: An evidence-based

approach or a need for evidence?

Platinum 515.45 Co-morbidities and end of life care17.15 Closed

Dr Philip MacCarthyConsultant Cardiologist, King’s College Hospital, London, UK

The limitations of thecoronary angiogramhave been appreciated

for a long time, primarilybecause it is a ‘lumenogram’giving a 2D representation ofcomplex, moving 3D struc-tures – the coronary arteries.The angiogram gives usanatomical, not physiologicalinformation, yet it is physiol-ogy we aim to alter (correct)when we treat our patients.Many studies have shownthat it is myocardialischaemia that predictsadverse outcome in patientswith coronary artery disease(not angiographic atheroma)and it is therefore myocardialischaemia which we must cor-rect when we perform coro-nary revascularisation (of anyform). The intracoronary pres-sure wire helps us to do justthat, in a simple and scientificway.The evidence base for the

use of the pressure wire wasaccrued in the 1990s, with anumber of elegant studiescomparing it to non-invasivetests for myocardialischaemia. One of the princi-pal problems with thisendeavour was defining a‘Gold Standard’ for myocar-dial ischaemia, in large partbecause all non-invasive testshave their faults and nonehave 100% sensitivity orspecificity. The index that ismeasured with the pressurewire is the Fractional FlowReserve (FFR), which is a pres-

sure-derived index of coro-nary flow. The FFR has a nor-mal value of 1.0 and is notsubject to the influence ofsalient haemodynamics,unlike the older CoronaryFlow Reserve (CFR).Essentially, the FFR is the pro-portion of blood flowingthrough the stenosed coro-nary artery as compared tothe amount of blood thatshould be flowing through itif it were unobstructed. TheFFR is always measured inconditions of maximal hyper-aemia, which is ideallyachieved with centrallyadministered, iv adenosine.When the FFR is <0.75, theflow reduction in the vessel issufficient to produce myocar-dial ischaemia.The pressure wire and the

measurement of the FFRtherefore allow us to definecoronary stenoses capable of

inducing ischaemia and treatthem at the same sitting. Thisapproach also allows us toleave non-significant stenosesalone. The DEFER studyshowed us that it was safeand appropriate to do thiswith single vessel disease(with results beyond 5 years)and this has now beenextended to the setting ofmultivessel disease with thepublication of the FAMEstudy earlier this year. FAMErecruited patients with ARTS-type criteria for cornarystenoses in 2 or more coro-nary arteries and randomisedthem to angiographically-guided or pressure-wire-guid-ed intervention. It showedthat use of the pressure wiresignificantly reduced majoradverse cardiac events withan absolute difference inMACE-free survival of 5.3% at1 year. This was done with areduction in cost and contrastvolume and no increase inprocedural time. It thereforeseems highly preferable toperform physiological inter-vention wherever possible. Itmay even be that such anapproach to multivessel inter-vention will narrow the gapthat still exists between PCIand coronary surgery in termsof target lesion revascularisa-tion.Use of the pressure wire is

now widespread in the UKand most catheter labs havethe ability to measure FFR,although there remains areluctance to use it in somequarters. Many more scientif-ic studies are needed andindeed are underway, butfew would deny that thepressure wire and the meas-urement of FFR have openeda new, more scientific era inpercutaneous intervention –the era of ‘physiologicalrevascularisation’.

The pressure wire –FAME at last!

Philip MacCarthy

Wednesday - Platinum 1&2: 13.45–15.25

viving to three month follow up. We demonstrated a signifi-cant increase in six-minute walk distance compared with preoperation (276.3 ± 17 to 375.8 ± 14 m, p < 0.001). At 12months, there was a further increase in six-minute walk dis-tance (375.8 ± 14 to 394.7 ± 15 m, p = 0.004). At threemonths, 30.9% were in NYHA class I, 55.9% were in NYHAclass II, 12.3% were in NYHA class III and 0.5% were inNYHA class IV (p < 0.001 vs pre-op). At 12 months there wasfurther improvement in NYHA class: 40.7% were in NYHAclass I, 50.3% were in NYHA class II, 8.5% were in NYHAclass III and 0.5% were in NYHA class IV (p < 0.001 vs threemonths). We have also been able to investigate medium termsurvival in this same group of 230 patients who completedthree month follow up. Conditional survival was 94% atthree years, 92.5% at five years and 88.3% at 10 years fol-low-up (see figure). This is the largest PTE series to report out-come after discharge from hospital and the first to reportextended follow up of a complete national patient cohort.

In summary there is now widespread acceptance that themortality from PTE surgery can be reduced to 5% in experi-enced units reflecting improved perioperative care and bet-ter understanding of patient selection. Patients derive signif-icant reduction in PA pressure and PVR immediately follow-ing complete endarterectomy. This early haemodynamicimprovement is sustained at three months and translatesinto improved exercise capacity and reduced symptoms atone year following surgery. Medium term survival (to fiveyears at least) is substantially better than that expected inuntreated patients with CTEPH.

Conditional survival after PTE

Years

Number at risk

Cum

mul

ativ

e su

rviv

al

1.0

0.8

0.6

0.4

0.2

020 4 6 8 10

162230 91 31 6 1

92.5% 88.3%

Pulmonarythromboendarterectomy for chronic thromboembolicpulmonary hypertension

Continued from page 9

12 1–3 June 2009 Heart Murmurs

Richard Schilling, ConsultantCardiologist and Reader, Barts and theLondon NHS Trust and Queen MaryUniversoty London

Why are patients with heartrhythm problems particularlyanxious?When patients present to their doctor witha medical problem they will often havesome preconceived ideas of what the prob-lem might be. Public information cam-paigns and messages from the news andentertainment media means that thosepatients presenting with chest pain or pal-pitation are often concerned that theymight have a serious heart condition.Palpitation may often be more frighteningto the patient than chest pain because it isa symptom that is much less frequently dis-cussed within the general public. Althoughvery serious ischaemic heart disease is socommon almost every family have hadmembers live with angina or even experi-enced myocardial infarction. Even thoughcardiac arrhythmia is relatively common it isless common for patients to be aware offamily members suffering similar symptomssuch as atrial fibrillation. For this reason the patient has no referencepoint other than dramatic scenes fromshows like the US drama “ER” where theysee patients being resuscitated (or not)from “VTach” by glamorous hospital staff.

The patient’s perceptions of heart rhythmsymptoms are that they are likely to causeby a potentially life threatening cardiaccondition which may need urgent hospitaladmission.

Why do heart rhythm patientsneed specific health careprovision?Happily the vast majority of consultationsfor palpitation relate to benign problems.The first point of contact with the medicalprofession for patients is the general practi-tioner (GP). Appropriately, most patientshave great trust in their GPs but it is oftendifficult for the GP to give a definitive diag-nosis to the patient during the first consul-tation because of lack of time, access toinvestigations, and they may also feel outof their depth advising on potential cardiacarrhythmia. This is often apparent to patients duringthe consultation. If the patient is referredfor an outpatient investigation (many GPsnow have access to Holter monitoring forexample) they may then be reassured if thistest is normal. Despite a normal test many continue to beconcerned that the GP may have missed aserious condition if insufficient time hasbeen spent on explaining the cause of thesymptoms and the test results. Alternativelyif the GP decides to refer the patient eitherbecause of the results of investigations or

the patients’ history or continued worriesthe patient may see a junior doctor whohas no specialist training in arrhythmia.They may then be dissatisfied with theexperience.

What does the patient want?I believe that when patients present withsymptoms that may be related to heartrhythm problems, they want to know threethings in order of priority:n Is the problem going to kill me?n What is the problem?n What are the treatment options?

Question one can often be easily answeredby anyone with an interest in heart rhythmmanagement if they have access to cardiacinvestigations. For example an ECG andechocardiography. Question two can alsobe answered in many cases, either by tak-ing a careful clinical history or by recordingthe ECG during symptoms. For symptomsthat occur less than once a week thenmost forms of ambulatory ECG monitoringare of little use and consideration may haveto be given to implantation of a looprecorder (if the symptoms are severeenough to warrant it). The answer to ques-tion three is often dependent on the resultsof question two but the correct answer isoften more likely to be given by someonewith an interest and current knowledge ofarrhythmia management.

How to answer the patient’squestionsIn the previous paragraph I have beencareful not to stipulate who answers thepatients’ questions. The reasons for this isthat I believe that the job title of the per-son consulting with the patient (nurse, GP,consultant) is not important. What isimportant is that they have an interest inarrhythmia management with regular sup-port and collaboration with other heartrhythm specialists. The reason for this isthat heart rhythm management hasevolved so quickly over the last few yearsthat regular updating and interaction isnecessary to remain current.Furthermore, in order to reassure patientsit is important to be able to speak withjustified authority on a subject, otherwiseeven simple problems like benign ectopicbeats can become a source of recurrentworry for the patient. Finally it is impor-tant to have the time to spend with thepatient explaining the diagnosis and whatthe prognosis and treatments are. If thepatient does not understand the problemthey will not be able to rationalise thetreatment plan in their own minds andmay lose faith in it.

Where to answer the patient’squestions?In almost every survey of patients’ views onthe health service, having access to local

health care is listed as the number one prior-ity. However, if one delves deeper into thepatients’ wishes and desires, they also wantexpert care. Clearly it cannot be possible tohave internationally recognised expertsworking in every local hospital and so howcan one rationalise these conflicting desires?One approach might be to have a healthcare model whereby local experts have closelinks to tertiary care so that when the threekey questions cannot be answered there areappropriate links to move the patient on toan appropriate specialist. This could be provided by GPs with specialinterests or nurse arrhythmia specialists. Thekey however is that they do not get isolatedand regularly interact with other “localexperts” and tertiary care. This allows con-tinual updating of investigation and treat-ment protocols as clinical research evolves. Italso means that the “local experts” knowwhat is and is not possible in terms of treat-ment in tertiary care and that patients getaccess to this treatment without unneces-sary delay.

ConclusionConsidering what patients want and deliv-ering it using the approaches described inthe above model should allow the timelyinvestigation and treatment of heart rhythmsymptoms. Considerable anxiety and unnec-essary suffering should be avoided as aresult.

What patients want – expert advice and treatment

Dr Tim Betts MDConsultant Cardiologist & ElectrophysiologistDept of Cardiology, John Radcliffe Hospital, Oxford

Atrial fibrillation (AF) affects more than 1% of the populationand is the most common tachyarrhythmia encountered in clini-cal practice. Although it may be asymptomatic and discovered

coincidentally, in many individuals it results in debilitating symptomsand impaired quality of life. Until recently the mainstay of treatmentwas drug therapy, either for ventricular rate control or in an oftenfutile attempt to restore and maintain sinus rhythm. The low efficacyand potential proarrhythmic effects of antiarrhythmic drugs in trialssuch as AFFIRM and RACE has cast doubts on the merits of a rhythm-control strategy, yet close examination of these studies shows thatwhen sinus rhythm can be achieved and maintained, quality of lifeimproves. Thus, the ideal therapy would be one that restores andmaintain sinus rhythm with a high success rate in a simple and cost-effective manner and has no side effects. Is left atrial ablation thattherapy?

Left atrial ablation, or more specifically pulmonary vein isolation,was first described in the mid-late 1990s by Michel Haissaguerre andcolleagues from Bordeaux. The principle behind the technique is theabolition of focal triggers (ectopics or tachycardia) that arise from thepulmonary vein musculature and initiate and maintain AF.This approach evolved rapidly from focal ablation in singleveins to empirical ablation at the ostium of all four pul-monary veins. The paradigm has subsequently expanded toinclude additional targeting of rotor sites and autonomicganglionic plexi throughout the atria. Persistent as well asparoxysmal AF can be ablated and experienced centres willnow take on patients with structural heart disease as wellas those with normal hearts. In Oxford we undertook over200 AF ablation procedures in 2008, half of which were forpersistent AF.

One of the challenges with left atrial ablation is that ahigh bar has already been set with ablation of supraventric-ular tachycardias and atrial flutter. Whereas those simplearrhythmias enjoy a >95% success rate, a re-do rate of<10%, low complication rates and are usually day-case pro-cedures, AF is a more complex arrhythmia requiring exten-sive treatment. Overall, in experienced hands, patients withparoxysmal AF should expect an 80-85% success rate, albeitwith a 30-40% chance of multiple procedures. Those withpersistent AF have a lower success rate, approximately70-75%, with at least 50% requiring more than oneablation. Perhaps the most important concept is that

the aim is not to cure, but to control. Complete abolition of AF israre, however good rhythm control, meaning patients are satisfiedwith the reduction in AF burden and symptoms (ideally off drug ther-apy), is an admirable goal and from a patient’s and physician’s per-spective, a success.

Success or failure is not a simple, binary outcome either. It can taketime for atrial electrophysiological remodelling to occur, early recur-rences do not necessarily mean treatment failure and a 6-12 monthAF-free period doesn’t necessarily mean a life-long cure. Many of thefactors that predispose to AF, such as hypertension, age and diabetes,will continue to develop over time. AF may be abolished, only to allowscar-related atrial flutters to emerge, necessitating further treatment.Although a true “cure” may be achieved in a lucky few, it would bebetter to consider ablation as a form of palliation, much in the sameway we palliate rather than cure coronary artery disease.

In common with all invasive procedures, ablation carries some risk.Although serious femoral bleeding and cardiac tamponade may occurin 1-2% of patients it is almost never fatal. The reported mortalityfrom ablation is just under 0.1%. Peri-procedural stroke is the mainconcern, affecting 1% of patients to varying degrees. It is likely thatcomplications increase in the elderly and serious consideration shouldbe given to the alternative approach of AV node ablation and pace-maker for drug-refractory symptoms in this group.

So, who is the ideal candidate and when should ablation beoffered? The golden rule is that patients must be symptomatic. Thereis no evidence that ablation reduces thromboembolic risk and the cost,complexity and complications mandate that patients should be highlysymptomatic (and motivated) to go through the potentially arduousprocess. Drug therapy should have been attempted and ablation candi-dates are those in who a rate or rhythm control strategy is ineffectiveor causes unacceptable side effects. Current NICE guidelines put abla-tion on a level with Amiodarone therapy, a second or third-line drug

that many patients and physicians would prefer to avoid. Asexpected, ablation candidates tend to be younger, physicallyactive people in whom good rhythm control, off drug therapycan make a significant improvement to their quality of life, yetit is also subgroups such as those with heart failure whosesymptoms deteriorate dramatically with the onset of AF whohave much to benefit.

When reading about an expensive procedure that has nomortality benefit, is palliative rather than curative, has a 75-85% success rate, a high re-do rate and comes with a risk ofserious complications, one can see why there may be a degreeof skeptisism in the cardiology community regarding its utilityand value. It should not be forgotten however that just over adecade ago this would be an accurate description of plain oldballoon coronary angioplasty. That particular interventionaltechnique has gone on to benefit from technological advancesas well as extensive pharmacological adjuncts such as statinsand antiplatelet therapy. It is likely that in a similar time periodablation treatment for AF will make the same progress.Although AF ablation is not yet a first line approach neither isit a last ditched resort and it should be considered for everysymptomatic, drug-refractory patient under 75 years of age.

Ablation for atrialfibrillation: first lineor last resort?

Wednesday - Exhibition Hall: 10.45–11.00

Wednesday - Platinum 4: 13.45–15.15

Tim Betts

NavX navigation system measures and calculates the electrode position in 3D space.

Heart Murmurs 1–3 June 2009 13

Robin Choudhury, University of Oxford

Appreciation of themolecular and cellularprocesses of atheroscle-

rosis, thrombosis and vascularinflammation opens the way forcommensurately sophisticatedapproaches to disease character-ization through imaging. Thecommon goals of molecularimaging approaches are toaccelerate and refine diagnosis,provide insights that reveal dis-ease diversity, guide specifictherapies and monitor theeffects of those therapies. Tothese ends, a range of contrastmethodologies are in develop-ment across a number of modal-ities. Vascular disease is relatively

privileged compared, forinstance, to neurological imag-ing since many of the targetsare accessible to the blood andblood-borne reagents. There arealso specific impediments. Bloodvessels are often deeply locatedstructures, which can restrict theapplication of low penetrancetechniques, such as fluorescenceimaging or ultrasound unlessintravascular imaging systemsare developed. In addition,there challenges of movementdue to cardiac and respiratorymotion and high sheer stresses

of blood in large arteries, whichcan be challenging to particu-late contrast agents.Funded by the Wellcome Trust

and the British HeartFoundation, our laboratory hasfocused on the development andapplication of micron-sized parti-cles conjugated to a variety ofligands, which recognizeendovascular molecules that aredifferentially expressed in ather-osclerosis, thrombosis and vascu-lar inflammation. The mircoparti-cles of iron oxide (MPIO) in apolymer shell (0.9–4.5�microme-tres). For imaging endovascularstructures, MPIO possess severalpositive attributes. Firstly, theparticles convey a high payloadof iron. Secondly, the effects ofMPIO on local magnetic fieldhomogeneity, and thereforedetectable contrast, extend for adistance ~50 times the physical

diameter of the microparticle.Thirdly, unlike USPIO, the rela-tively large size of MPIO meansthat they are less susceptible toextravasation or non-specificuptake by endothelial cells andtherefore retain specificity formolecular targets expressed onthe vascular endothelium. Usingthese approaches, it has beenpossible to image vascularinflammation (including‘ischaemic memory’), by target-ing VCAM-1 or P-selectin andactivated platelets using particlesarmed with ligands directedagainst the activated conforma-tion of glycoprotein IIbIIIa. In collaboration with col-

leagues in the Chemistry,Pharmacology andNeuroimaging, we are seekingto develop biodegradable parti-cles that might prove safe andefficacious in clinical practice.

An approach to molecularimaging in vascular disease

Richard Charles, EmeritusConsultant Cardiologist,Liverpool Heart & ChestHospital.Chairman, Network DevicesSurvey Group

Cardiac rhythm disorders andheart failure are major causesof sudden death and disabili-

ty, but for many sufferers a modernpacemaker, defibrillator or cardiacresynchronisation device can savelife and reduce symptoms whenimplanted by a simple operation.The indications for device implanta-tion are supported by agreednational and international guidelineswhich are now essentially identical.

The Network Devices SurveyGroup has recently made public itssecond systematic survey of the NHSin England and Wales , documentingthe volume and equity of provisioncardiac pacemakers, implantabledefibrillators (ICDs) and cardiacresynchronisation therapy (CRT)compared to local relative need,using methodology which allowsvalid direct comparison amongstCardiac Networks and Primary CareTrusts (PCTs). The report is availableat www.devicesurvey.com.

The findings continue to pose amajor challenge to the NHS. Whilstincreasing numbers of patients arebenefiting, implantation rates in theUK remain amongst the lowest inWestern Europe and there is evi-

dence of real local inequity of serv-ice provision.

The relative paucity of deviceimplants in the UK was first high-lighted 25 years ago, yet in 2009we still need to increase the pace-maker implant rate by 13% per yearto achieve parity with Europeanimplant rates by 2015 and the cur-rent increase is just under 4%.

No single or simple reason forthe low and inequitable provisionof these devices in the UK emergesfrom the survey, but evidence isaccumulating for several possibleculprits. Robust international datadiscount the possibility of excessiveprescribing of devices in Europe orthe US. Blocks in the referral chainremain a prime suspect. Lowawareness of the significance of rel-evant symptoms amongst patientsand general practitioners, insuffi-cient appreciation in secondary careof which patients conform to con-sensus guideline indications , and

inadequate investment in resourcesfor diagnosis, screening ‘at-risk’populations, device procurement,implantation centres and educationare all likely to play a part.

Innovative and enlightened com-missioning policies must play adecisive role in rectifying the underprovision and inequities identified inthe report. Coordinated by theDepartment of Health through NHSImprovement and implementationof Chapter 8 of the NationalService Framework for CoronaryHeart Disease the provision ofdevice services by Cardiac Networksand PCTs is now receiving enthusi-astic support. Arrhythmia Alliancewww.heartrhythmcharity.org.ukactively promotes public educationand awareness, whilst best practice,identified by the Survey, must beshared and implemented widely.

Rising implant rates for each ofthe three device categories must beencouraged and welcomed, andtheir funding planned for. Goodpractice now can realise savings later.Commissioners must be convinced toinvest in technologies which providedownstream savings - compellingevidence exists for the cost effective-ness of cardiac pacing, ICDs and CRTwhich reduce hospitalisations as wellas mortality and morbidity.

Our progress can be monitoredonly by recurrent audit; theSurvey Group’s 2008 review iswell advanced.

Cardiac implantable devices – why arethey not reaching all who need them?

Wednesday - Platinum 3: 13.45–15.15 Wednesday - Auditorium: 13.45–15.15

Wednesday - Platinum 4: 13.45–15.15

Microparticles of iron oxide (green) bound to activated endothelial cells (red) in vitro.

Imag

e: Dr MA M

cAteer

Richard Charles

Dr Matthew FayWestcliffe Medical Practice, Shipley

Introduction

Over the past few years the NHS hassuffered from poor press as regardsthe time patients need to wait for a

diagnosis and interventions. This can clearlybe related to an increase in morbidity andmortality as pathology goes un-diagnosedand untreated. However the other issuesrelate to the anxiety caused to patients andcarers by these delays.

The NHS has seen a variety of approach-es to this dilemma, with rapid access chestpain clinics, fast track malignancy referralsand 18 week waits developed to try andresolve this issue. However we remain in a

service where these issues still make head-lines and patients still complain to their GPsabout the problems.

We have seen Primary Care respond tothe challenge in a variety of ways howeverdata regarding true system change issketchy.

With the improvement in technology wehave seen a move of investigations thatwere previously the remit of the hospital-based specialist move in to primary care.This is usually under the pretence that thiswill improve triage of referrals and thusreduce the demand on the systems.

It is thought that the use of natureticpeptides will assist in the selection ofpatients for echocardiography. This simpleblood test which can be performed either

through a hospital lab or with near patienttesting is used in some areas. However itsuse is still not widespread and the dilemmaof the course of action for the elevatedpeptide and the acceptable echo appear-ance not resolved. Its’ assistance in thediagnosis of LVSD is not disputed, that factthat it has made a reduction in referral isnot proven.

The use of cardiac event recorders andHolta monitoring in the community isincreasing. The advent of Practice BasedCommissioning and the potential develop-ment of revenue stream for primary carepractices is clearly an incentive. Howevermany of these services have stringentaccess protocols, restricting access topotentially only very simple dysrhythmia,

meaning that many people are still referredon. The concern frequently heard by spe-cialists is around the governance and safe-ty in the system if the recording is notreviewed in a hospital setting. If a signifi-cant dysrhythmia is diagnosed who isresponsible to take this forward?

The development of GPwSI services incardiology continues, many based with orvery close to the hospital based service. Thebelief that this will assist in triaging thesimpler cases out of the consultant’s case-load is yet to be proven. These tend to mir-ror hospital practice being based on GPreferral for consultation and opinion, someof the onus being on the GeneralPractitioner to select appropriate patients tothe ‘heart failure’ service or the ‘atrial fibril-lation’ service.

These solutions however have notresolved many of the issues that the delay-ing step is the movement of the patient

through the system, from symptoms to GPto test to GPwSI, to secondary care to terti-ary care. The information of how you areprogressing through the system remainsunclear; assistance, support and informa-tion of possible disease states remains atthe end of the path; The paradigm remainsunchanged.

The solution may require bolder stepsand involve the self-referral of the patientto the open access service publicised in alocality. A service with a plethora of patientand clinician led support. The clinic staffedwith a clinician with the options to breakfree of the normal chain of events andrefer from presentation in primary care tothe interventionist in tertiary care.

Such a service is to be piloted in Shipleynorth of Bradford during the arrhythmiaawareness week. A presentation of howthis solution has been reached is given byDr Fay.

Rapid access

Sudoku - Each block of nine small squares and each vertical and horizontal line of squares must contain the numbers 1 to 9. This requires no

mathematical prowess, just every ounce of logic you possess. They start off easy, but get more difficult... (answers on page 15).

14 1–3 June 2009 Heart Murmurs

Organisation Stand Number

3M Health Care 207

Abbott Vascular 314

AGA Medical Limited 312

Bayer Schering Pharma 153

Biosensors Europe SA 310

BIOTRONIK 250

BMJ Group – Heart Journal 309

Borm Bruckmeier Verlang GmbH 293

Boston Scientific Corporation 320

Bracco UK Ltd 254

Bristol-Myers Squibb and Sanofi-Aventis 360

British Heart Foundation 266

British Society for Heart Failure C3

British Society of Echocardiography C8

Cambridge Theranostics Ltd 261

Cardiac Risk in the Young C6

Cardiac Science (UK) Holdings Limited 252

Cardiology News 280

Cardiomyopathy Association C2

CeloNova BioSciences 150

Cordis, Johnson & Johnson Medical 308

Coronary Heart Publishing Ltd 286

CV Therapeutics Europe/A MENARINI PHARMA UK SRL 245

Daiichi Sankyo 210

DAIICHI SANKYO and Eli Lilly and Company 220

Datascope Medical Co Ltd 100

Dendrite Clinical Systems 190

Elitech UK Limited 191

Enverdis GmbH 195

Fukuda Denshi UK 255

GE Healthcare 145

Genzyme Therapeutics 322

GlaxoSmithKline 206

Grown Up Congenital Heart Patients Association C10

Guys and St Thomas’ Hospital NHS Foundation Trust 285

HCL Healthcare 258

Heart Manual Programme 110

HeartWorks by Inventive Medical Ltd 278

IHS and SSC 313

Instrumentation Laboratory 196

Inverness Medical UK 257

IROKO 198

Lab21 253

Life Stream Healthcare Limited 152

Lilly UK 135

Medcon UK Ltd 268

MedicAlert Foundation C4

Medicines Company 305

MediMax Global UK Ltd 267

Medtronic Ltd 105

Merck, Sharp & Dohme 265

MHRA 270

Millbrook Medical Conferences Ltd 209

National Heart and Lung Institute, Imperial College 284

NHS Evidence – cardiovascular collection 264

NHS Improvement – Heart 318

Oxford Biosystems Ltd 274

Pfizer Ltd 155

Philips Healthcare (formerly TOMCAT Clinical Systems) 208

Physiological Measurements Ltd 259

PULSE 262

Pri-Med Educational Programmes 260

Radi Medical Systems Ltd 115

Randox Laboratories Ltd 290

Revalidation stand 380

SADS UK C1

Servier Laboratories Ltd 140

Shire Human Genetics Therapies 256

Society for Cardiological Science and Technology (SCST) C9

Solvay Healthcare 205

Spacelabs Healthcare 154

Syner-Med (Pharmaceutical Products) Ltd 103

Takeda UK Ltd 146

Terumo UK Ltd 301

Vitabiotics Ltd 263

World Heart Federation C5

Your World Recruitment Ltd 276

6 7 85 9 23 4 1

9 1 34 8 65 7 2

2 4 51 3 78 9 6

4 6 78 3 91 2 5

1 2 96 5 73 4 8

3 5 84 1 26 7 9

2 8 47 5 39 1 6

7 9 18 6 42 3 5

5 6 39 2 17 8 4

6 2 1 35 6 74 8 9

7 9 43 1 86 2 5

6 8 59 2 41 3 7

9 3 41 5 67 2 8

2 5 68 3 71 4 9

7 1 82 4 93 5 6

6 7 18 4 23 9 5

5 8 39 6 14 7 2

8 9 25 7 38 6 1

3 1 5 86 2 73 4 9

9 2 41 3 56 7 8

3 6 74 8 95 1 2

4 6 58 9 27 1 3

7 8 14 5 32 6 9

9 2 31 7 68 5 4

5 7 42 3 19 8 6

8 9 25 4 63 1 7

6 3 17 9 82 4 5

8

SUDOKU ANSWERS

Forthcoming Events 2009

List of Exhibitors

12 June

The Moller Centre, CambridgeTel: 01480 364448Email: anne.scott@papworth.nhs.ukWebsite: http://www.papworthhospital.nhs.uk

2–3 July

The Moller Centre, CambridgeImperial College LondonTel: 02088461258Email: m.kudyba@imperial.ac.uk

10–12 September

Queen’s CollegeTel: 020 8979 8300 Email: alafond@hamptonmedical.com Website: http://www.artery.uk.net

21 September

Royal College of Physicians, LondonTel: 020 7935 1174 ext. 252 Email: conferences@rcplondon.ac.uk Website: http://www.rcplondon.ac.uk/event/details.aspx?e=1409

14 October

Queen Elizabeth II Conference Centre, LondonTel: 020 8652 9557 Email: jmoore@pri-medupdates.co.uk Website: www.pri-medupdates.co.uk

26–27 November

Queen Elizabeth II Conference Centre01865 391215 Email: info@bsh.org.uk Website: www.bsh.org.uk

Heart Murmurs 1–3 June 2009 15

Exhibition floor plan