2015 Asia Pacific conference on cardiometabolic diseases management · 2015-10-26 · 2015 Asia Pacific conference on cardiometabolic diseases management EXCEMED live educational

2015 Asia Pacific conference oncardiometabolic diseases management4 - 5 July 2015 - Mumbai, India

FINAL PROGRAMME AND ABSTRACT BOOK

General information

VenueThis live educational conference takes at the:Holiday Inn Mumbai International AirportSakinaka Junction, Andheri Kurla Road, Andheri East, 400072Mumbai, India

LanguageThe official language of this live educational conference is English.

Scientific secretariatEXCEMED - Excellence in Medical EducationSalita di San Nicola da Tolentino, 1/b00187 Rome, Italy

Associate Programme Manager: Francesca CucciollaT: +39 06 420413 315F: +39 06 420413 677E-mail: [email protected]

EXCEMED is a Swiss Foundation with headquarters in 14, Rue du Rhône, 1204 Geneva, Switzerland

Organising secretariatMeridiano Congress InternationalVia Sapri, 6 - 00185 Rome, ItalyCongress Coordinator: Debora UrbinelliT +39 06 88 595 232 - F +39 06 88595 234 E-mail: [email protected]

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2015 Asia Pacific conference on cardiometabolic diseases management

EXCEMED live educational conference:

2015 Asia Pacific conference on cardiometabolic diseases management4 - 5 July 2015 - Mumbai, India

AimsOne of the biggest problems in modern patient care is to correctly manage “complexity”. In medicine the term “complexity” refersnot only to difficult cases, but quite often to co morbidities. Hypertension, diabetes and thyroid disorders represent the most commonpathologies in our daily clinical practice. According to the Global Burden of Disease study (Lancet 2012), high blood pressure is stillthe leading cause of death in the world and remains an unsolved problem in cardiovascular medicine despite the effort of scientificsocieties. Diabetes Mellitus, especially type 2, is a growing epidemic in Asia, as the population is increasingly adopting western lifestyles. A particular genetic predisposition in these populations is also present. The 6th Edition of the International DiabetesFederation Atlas indicates that 8.2% of the population (75 million people) in South-East Asia countries and 8.5% of the population(138 million people) in Western Pacific countries have diabetes. Management of this disease and its complications and co morbiditiesare big challenges, especially for the healthcare community, especially when considering the low level of funding dedicated todiabetes. Finally, thyroid disorders are also very common in Asia Pacific countries, mostly due to iodine deficiency combined withgenetic factors.

EXCEMED is involved in a comprehensive educational programme to increase knowledge in hypertension, diabetes and thyroiddisorder, and is proud to organize the 2015 APAC conference on cardiometabolic diseases management. This live educationalconference will address the most recent advancements of research in these three areas of cardiometabolic medicine and, inparticular, will discuss the best approaches for clinical management of such diseases in daily practice. Possibility for the exchangeof ideas and knowledge will be facilitated by direct interaction with participants through the use of clinical case studies.

Learning objectivesAfter attending this live educational conference, participants will be able to:• Manage hypertension and related cardiovascular complications• Update the issue of heart rate as a primary cardiovascular risk factor• Use the right diagnostic and therapeutic strategies in clinical practice to face difficult cases• Manage diabetes or thyroid disorders and related complications• Improve the proper use of oral anti diabetic agents in different conditions• Manage the complexity of the relationship between hypertension, diabetes and thyroid disorders and heart failure

Target audienceGeneral practitioners, junior cardiologists, internists and all other health care professionals managing cardiometabolic diseases.

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AccreditationEXCEMED (www.excemed.org) is accredited by the European Accreditation Council for Continuing Medical Education (EACCME®) toprovide the following CME activity for medical specialists. The EACCME® is an institution of the European Union of MedicalSpecialists (UEMS), www.uems.net

The CME “2015 Asia Pacific conference on cardiometabolic diseases management” held on 4 - 5 July 2015 in Mumbai, India, isdesignated for a maximum of 10 (ten) hours of European CME credits (ECMEC). Each medical specialist should claim only thosecredits that he/she actually spent in the educational activity.

Through an agreement between the European Union of Medical Specialists and the American Medical Association, physicians mayconvert EACCME® credits to an equivalent number of AMA PRA Category 1 Credits™. Information on the process to convertEACCME® credit to AMA credit can be found at www.ama-assn.org/go/internationalcme.

Live educational activities, occurring outside of Canada, recognized by the UEMS-EACCME® for ECMEC credits are deemed to beAccredited Group Learning Activities (Section 1) as defined by the Maintenance of Certification Program of The Royal College ofPhysicians and Surgeons of Canada.

EXCEMED adheres to the principles of the Good CME Practice Group (gCMEp)

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Scientific organiserStefano TaddeiDepartment of Clinical and Experimental MedicineUniversity of PisaPisa, Italy

Share your opinion with usWe are always looking for ways to bring oureducational activities to the next level and meet yourneeds as a healthcare practitioner. You will be asked to answer a real-time surveyduringthis event, followed by a post-event online survey tofind out if the experience met your educationalexpectations. Your views also help us tailor futureinitiatives.

Thank you for taking the time to participate.

Faculty membersSaifuddin M. BandukwalaLilavati Hospital and Research Centre Bandra WestMumbai, India

Claudio Borghi Department of Internal MedicineUniversity of BolognaBologna, Italy

Manoji Chadha Hinduja Hospital & Research CentreMumbai, India

Jamshed J. DalalCentre for Cardiac SciencesMumbai, India

Patricia GatbontonDepartment of Medicine Our Lady of Lourdes HospitalManila, Philippines

Shirish M.S. HiremathRuby Hall ClinicPune, India

Shashank Joshi Joshi Clinic, Lilavati & Bhatia Hospital Grant Medical College & Sir JJ Group of Hospitals Mumbai, India

Athanasios J. Manolis Cardiology DepartmentAsklepeion HospitalAthens, Greece

Roberto Mirasol St. Luke’s Medical CenterSection of Endocrinology, Diabetes and MetabolismQuezon City, Philippines

Mafauzy Mohamed Health CampusUniversity Sains MalaysiaKelantan, Malaysia

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Nemecio A. NicodemusUniversity of the PhilippinesCollege of MedicineAteneo School of Medicine & Public HealthEndocrinology, Diabetes & MetabolismManila, Philippines

Paolo Palatini Department of Medicine DIMEDUniversity of PadovaPadova, Italy

Bipin SethiDepartment of EndocrinologyCARE HospitalsHyderabad, India

Sanjiv ShahDiabetes Action CentreMumbai, India

Piyamitr SritaraCardiology UnitDepartment of MedicineFaculty of MedicineRamathiobodi HospitalMahidol University Bangkok, Thailand

Stefano Taddei Department of Clinical and Experimental MedicineUniversity of PisaPisa, Italy

Brian Tomlinson Department of Medicine and TherapeuticsThe Chinese University of Hong KongHong Kong SAR, China

Scientificprogramme

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Saturday, 4 July 2015

09.00 Welcome and introduction

Chairs: J.J. Dalal (India); A.J. Manolis (Greece)

Real-time survey

09.15 L1: Pre-hypertensionC. Borghi (Italy)

09.35 L2: High heart rate and the CV risk inHypertensionP. Palatini (Italy)

09.55 L3: Coronary artery diseaseA.J. Manolis (Greece)

Real-time survey

10.15 Questions and answers

10.30 Coffee break

11.00 - 12.30 Parallel workshops *

WS1: Hypertension managementS.M.S. Hiremath (India)

WS2: Coronary heart diseaseP. Sritara (Thailand)

12.30 Back to plenary, take home message fromclinical cases

12.45 Lunch

HypertensionSession I

Problem based learning approach workshops onhypertensionSession II

Chairs: P. Palatini (Italy); B. Tomlinson (Hong Kong, China)

Real-time survey

13.45 L4: Hypertension and risk of heart failureB. Tomlinson (Hong Kong, China)

14.05 L5: Diabetes as a promoter of heart failureS.M. Bandukwala (India)

14.25 L6: Heart failure and co-morbiditiesS. Taddei (Italy)

Real-time survey


16.00 Coffee break

16.30 - 18.00 Parallel workshops *

WS3: Heart failure managementB. Tomlinson (Hong Kong, China)

WS4: Heart rate managementJ.J. Dalal (India)

18.00 Back to plenary, take home messages andconcluding remarks

End of the first day

Heart failureSession III

Problem based learning approach workshops on heart failureSession IV

* The workshops will involve participants in an interactive discussion, giving them the chance to share opinions and test theirunderstanding of different topics based on clinical cases presentations. There will be two parallel workshops, each lasting 45minutes. The audience will be divided into two groups and each participant will attend both workshops in rotation. Take-homemessages from the speakers will be delivered at the end of the session in the plenary room.

Legend: L : Lecture; WS : Workshop; D : Debate

Sunday, 5 July 2015

Chairs: C. Borghi (Italy); M. Chadha (India)

Real-time survey

09.00 L7: International guidelines for the managementof diabetes: evidence based medicine vspersonalized medicineM. Mohamed (Malaysia)

09.20 L8: Thyroid nodules in clinical practice: frommedical therapy to ultrasonically-guideintervention N.A. Nicodemus (Philippines)

Real-time survey


10.00 Coffee break

Chairs: S. Joshi (India); N.A. Nicodemus (Philippines)

D1: Management of pre-diabetes: lifestyle vs drug therapy

10.30 Lifestyle S. Shah (India)

10.45 Drug therapy P. Gatbonton (Philippines)

11.00 Discussion

D2: Subclinical hypothyroidism: to treat or not to treat?

11.15 To treat R. Mirasol (Philippines)

11.30 Not to treat M. Chadha (India)

11.45 Discussion

12.00 Lunch

DiabetesSession V

Debates on hot topicsSession VI

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Chair: S. Taddei (Italy); C. Borghi (Italy)

Real-time survey

13.00 L9: Diabetes in pregnancyB. Sethi (India)

13.20 L10: Hypothyroidism and hyperthyroidism in pregnancyM. Mohamed (Malaysia)

13.40 L11: Hypertension in pregnancyJ.J. Dalal (India)

14.00 L12: Thyroid cancer guidelinesS. Joshi (India)

Real-time survey

14.20 Take home message

14.30 Closing remarks from the scientific organizer

End of the conference

ComplicationsSession VII

Disclosure of faculty relationships

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EXCEMED adheres to guidelines of the European Accreditation Council for Continuing Medical Education (EACCME®) and all otherprofessional organizations, as applicable, which state that programmes awarding continuing education credits must be balanced,independent, objective, and scientifically rigorous. Investigative and other uses for pharmaceutical agents, medical devices, and otherproducts (other than those uses indicated in approved product labeling/package insert for the product) may be presented in theprogramme (which may reflect clinical experience, the professional literature or other clinical sources known to the presenter). We askall presenters to provide participants with information about relationships with pharmaceutical or medical equipment companies thatmay have relevance to their lectures. This policy is not intended to exclude faculty who have relationships with such companies; it isonly intended to inform participants of any potential conflicts so that participants may form their own judgements, based on fulldisclosure of the facts. Further, all opinions and recommendations presented during the programme and all programme-relatedmaterials neither imply an endorsement nor a recommendation on the part of EXCEMED. All presentations represent solely theindependent views of the presenters/authors.

The following faculty provided information regarding significant commercial relationships and/or discussions of investigational ornon-EMEA/FDA approved (off-label) uses of drugs:

Saifuddin M. Bandukwala Declared receipt of honoraria or consultation fees from Abbott Lab., Novartis, Johnson & Johnson.Declared to participate in a company sponsored speaker’s bureau in Aristo Pharmaceuticals LTD India.

Claudio Borghi Declared receipt of honoraria or consultation fees from Menarini, Sanofi, Servies, MSD. Declared tobe member of a company advisory board, board of director or other similar groups o: Sanofi, Amgen,Menarini, MSD.

Manoji Chadha Declared no potential conflict of interest.

Jamshed J. Dalal Declared no potential conflict of interest.

Shirish M.S. Hiremath Declared no potential conflict of interest.

Athanasios J. Manolis Declared no potential conflict of interest.

Roberto Mirasol Declared to be member of a company advisory board, board of directors or other similar groups:Merck, Merck Sharpe and Dohme.

Mafauzy Mohamed Declared no potential conflict of interest.

Nemecio A. Nicodemus Declared receipt of honoraria or consultation fees from Novartis, Merck, Eli Lilly. He declared also tobe member of a company advisory board, board of directors or other similar groups: Merck, AstraZeneca.

Paolo Palatini Declared receipt of honoraria or consultation fees from Merck Serono and Takeda.

Bipin Sethi Declared no potential conflict of interest.

Piyamitr Sritara Declared receipt of grants and contracts from GSK, Pfizer and Sanofi Aventis. Declared also receiptof honoraria or consultation fees from GSK, Pfizer and Sanofi Aventis. Declared to be member of acompany advisory board, board of directors or other similar groups of GSK, Pfizer and Sanofi Aventis.

Stefano Taddei Declared receipt of grants and contracts from Novartis, Servier, Boehringer. Declared participation ina company sponsored speakers’ bureau of Servier, Stroder, Pfizer,Bayer, Msd and Boehringer.

Brian Tomlinson Declared receipt of grants and contracts from Astra Zeneka, Glaxo Smith Kline, Merck Serono, MerckSharp & Dhome. Declared also receipt of honoraria or consultation fees from Astra Zeneka, Janssenand Merck Serono. Declared to be member of a company advisory board, board of directors or othersimilar groups of Astra Zeneka and Merck Serono.

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The following faculty have provided no information regarding significant relationship with commercial supporters and/or discussionof investigational or non-EMEA/FDA approved (off-label) uses of drugs as of 00 Xxx 2015.

Patricia Gatbonton

Shashank Joshi

Sanjiv Shah

Abstracts

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L1. Pre-hypertension

Arterial hypertension is one of the most important risk factors for cardiovascular disease: a blood pressure (BP) reading above140/90 mmHg is associated with a significant increase in the relative risk of coronary artery disease, stroke or heart failure.Conversely, when elevated BP values are reduced with lifestyle changes and drug treatment, a substantial decrease in the rate ofmajor cardiovascular events and an improvement in long-term prognosis is observed.

Pre-hypertension – a typical condition of increasing prevalence – is also known as high-normal blood pressure or borderlinehypertension and is defined as a BP value that is higher than normal but below the diagnosis of overt hypertension. The prevalenceof pre-hypertension is increased in male subjects, particularly those in the second and third decades of life, and the absolute numberof pre-hypertensive subjects is 4-5 times higher than the number of people with established hypertension. Consequently, pre-hypertension is likely associated with a huge number of cardiovascular complications, despite its lower relative risk of myocardialinfarction or stroke.

The management approach for pre-hypertension remains a matter of strong debate, particularly in terms of treatment strategies.In particular, despite the significantly increased risk of all major cardiovascular complications in people who have BP values in thepre-hypertensive range, current guidelines limit treatment to lifestyle changes. One of the major problems with this peculiarcondition is how to identify those people with pre-hypertension who are at heightened risk of developing cardiovascularcomplications. The basic approach should be applied in exactly the same manner as it is in the hypertensive population, in terms ofcalculating the overall risk profile by combining the level of BP pressure increase and the presence of additional risk factors.

In addition, many people with pre-hypertension exhibit early development of target-organ damage. Indeed, such damage may bepre-existing. This suggests that a pathogenic mechanism may be responsible for cardiac or vascular damage before any overtincrease in BP values is observed. Elevated levels of uric acid in serum are purported to be among the factors responsible for anearly (and probably) reversible increase in BP to pre-hypertensive levels. Serum uric acid levels are markers of the vascular oxidativestress that is associated with activation of xantine-oxido-reductase. This oxidative mechanism is involved in the development ofhypertension and metabolic syndrome, starting in childhood or adolescence as a consequence of an excessive fructose intake. Thesame oxidative mechanism may also elicit early-stage cardiac, vascular or renal pathologies and may explain the target-organdamage observed in some patients with pre-hypertension, despite only having a mild increase in BP values. This evidence supportsthe possibility of a heterogeneous interpretation of pre-hypertensive conditions. In some people (especially those with a geneticpredisposition), an elevated serum uric acid level could be the first indication of future hypertension. In others, such a finding couldbe a marker of underlying vascular or renal disease, induced by neurohumoral or metabolic disorders and possibly associated withmore extensive target organ involvement and more severe cardiovascular prognosis than would usually be expected. Theidentification of characteristics that differentiate these two populations might help us to understand more appropriately whichpatients with pre-hypertension might benefit from additional treatment, and may also indicate which therapeutic measure is mostappropriate (i.e., antihypertensive drugs, or metabolic or urate-lowering strategies), given that the present generalized approachmay be too reductive in terms of cardiovascular disease prevention.

Claudio Borghi Department of Internal Medicine, University of Bologna, Bologna, Italy

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L2. High heart rate and the CV risk in

Measurement of heart rate (HR) is a medical tradition that dates back to the days when the doctor often relied on this medicalmanoeuvre to check the health status of the patient. But the first data about HR as a predictor of morbid events only emerged in the1980s, when epidemiologists in leading studies (such as the Framingham and Chicago cohorts) noticed a quite unexpected andstrong association between resting HR and mortality, especially in men. However, the information remained sparse and neglectedby doctors, who at that time did not realize the potential clinical importance of HR. In subsequent years, several leading studies wereperformed in general populations, such as the Paris Prospective study, which showed that HR was related to both total andcardiovascular (CV) mortality rates. This relationship between HR and mortality was observed in people of all ages.

One may wonder whether the relationship between HR and risk is linear across the HR range, or whether there is a J-shapedrelationship. According to the Framingham data and many other studies, the relationship is linear in the general population. Thisholds true for congestive heart failure, CV-related and all-cause death. A review published in Hypertension listed 11 studies,encompassing a large number of patients, which showed a positive association between high HR and adverse outcome. In the Syst-Eur study (a multicentre European study conducted in elderly patients) the mortality rate was rather flat from the first to the thirdHR quintile, but then sharply increased in men and women, with a doubled risk of mortality for subjects with HR >79 bpm, comparedwith those with lower HR.

A relationship between HR and adverse outcome was also found in hypertensive patients with coronary artery disease whoparticipated in the INVEST study. In this clinical trial, both baseline HR and HR after treatment were associated with the compositeendpoint of death, myocardial infarction and stroke. Interesting results were also published in a reanalysis of the VALUE study. Thisanalysis divided patients according to whether their HR was high or low and their blood pressure (BP) was, or was not, controlled bytreatment. The highest risk of events was found in those with uncontrolled BP and high HR. However, the risk was also high in thosewith controlled BP if HR was elevated. Thus, these data underscore the clinical importance of high HR in hypertension.

In all populations high HR has a non-normal distribution, being skewed to the right. Using mixture analysis, in several populationswe could identify two subpopulations: a larger one with normal HR and a smaller one with tachycardia. By comparing the clinicalcharacteristics of the two subpopulations we found that the subpopulation of patients with tachycardia also had higher BP values,which were associated with metabolic abnormalities. A relationship between HR and hypertension was also found in longitudinalstudies. In the Harvest study, which involved young to middle-aged patients with stage 1 hypertension, subjects with persistenttachycardia had an increased likelihood of developing sustained hypertension over time, compared with those with normal HR orwith high HR only at baseline. A recent analysis in this population also found that both baseline HR and HR measured in the clinicduring the follow-up period were predictive of future obesity. Similar results were observed in Asian populations. Thus, a largeamount of data consistently show that a high HR predates hypertension, obesity, metabolic syndrome and diabetes.

HR can be considered as a marker of sympathetic activity, as shown by Grassi et al., who in a large sample demonstrated that HRwas correlated with two measures of sympathetic activity: plasma norepinephrine and muscle sympathetic nervous activity. If oneconsiders HR as a marker of sympathetic activity it is easier to understand why people with tachycardia develop hypertension, obesityand metabolic disturbances. In fact, several laboratory studies have demonstrated that stimulation of beta-receptors, either acuteor chronic, and of alpha-receptors can result in insulin resistance through different mechanisms. The sympathetic overactivityunderlying tachycardia can lead to CV events through a variety of intermediate endpoints. However, tachycardia also has a directaction on the CV system, producing many detrimental effects. It increases oxygen consumption and facilitates ventriculararrhythmias, which is deleterious especially in the coronary patient. In addition, the low shear stress and high circumferential stressexerted on the arterial wall promote the coronary plaque and plaque disruption, leading to coronary disease and sudden death. HighHR also can cause left ventricular stiffness and dysfunction.

The role of high HR has also been investigated with ambulatory monitoring. In the ABP-International study we found that, inmultivariate models including all risk factors, night-time HR was the strongest predictor of CV events; daytime HR lost statisticalsignificance.

Due to the large body of evidence, HR is now included in the risk charts by some scientific authorities, such as the Cooper ClinicBoard. The importance of HR as a predictor of risk has also been reinforced by the latest European guidelines, which recommendthat HR should always be measured, together with BP, in the overall assessment of the hypertensive patient.

Evidence has been provided that HR reduction improves prognosis in patients with acute myocardial infarction and heart failure. Inhypertension, indirect evidence for a beneficial effect of pharmacological cardiac slowing with atenolol or verapamil has beenprovided by the INVEST study, in which a tendency to a J-shape relationship between HR and outcome was observed.

Paolo PalatiniDepartment of Medicine DIMED, University of Padova, Padova, Italy

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Tachycardia is a frequent finding in hypertension. In the Tensiopulse and Harvest studies, ~30% of the hypertensive participants hadtachycardia (defined as HR >80 bpm). According to the latest European Society of Hypertension guidelines, beta-blockers are stillconsidered as first-line antihypertensive agents, and remain as suitable as other drug classes for initiating therapy. In my opinion,beta-blockers should be the preferred agents for patients with high HR. In addition, beta-blockers are recommended for secondaryprevention in patients with previous cardiac events.

It should be pointed out that most data in hypertension were obtained with atenolol, a beta-blocker that may have undesirable side-effects. Highly beta1-selective beta-blockers may have several advantages over nonselective or modestly selective beta-blockers,especially in patients with broncho-obstructive disease or peripheral artery disease. In addition, beta1-selective beta-blockers havea better metabolic profile and cause sexual dysfunction less frequently than other types of beta-blocker.

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L3. Coronary artery disease

Coronary artery disease (CAD) constitutes the leading cause of death and is a major cause of morbidity and impaired health-relatedquality-of-life, worldwide. Compared with normotensive people, hypertensive people exhibit a two- to threefold higher prevalence ofCAD. Moreover, 60% of patients with CAD have hypertension, suggesting a close association between hypertensive disease and thepathophysiology of CAD.

CAD has a long asymptomatic latent period. Many patients with CAD – even those with advanced forms of the disease – do not showsymptoms before experiencing a major event such as sudden cardiac death, unstable angina, myocardial infarction, or congestiveheart failure. In the setting of asymptomatic hypertensive individuals, a diagnosis of CAD should be guided by total cardiovascularrisk. According to the European Society of Hypertension guidelines, high-risk hypertensive patients are defined as those with systolicBP ≥180 mmHg and/or diastolic BP ≥110 mmHg, diabetes (type 1 or 2), a severely elevated single risk factor or more than threecardiovascular risk factors, a history of previous cardiovascular or concentric left ventricular hypertrophy. Such patients shouldundergo further diagnostic testing for the presence of CAD, even if they are asymptomatic.

Although the physical risks of exercise testing are negligible, false-positive test results may result in inappropriate further testingand may increase patients’ anxiety levels, along with either work- or insurance-related problems. Thus, if a hypertensiveasymptomatic individual is considered low-risk after careful assessment, no further investigation of CAD is needed. If, however, ahypertensive asymptomatic patient is stratified as being of average or high/very high risk, a functional stress-test is recommended.

An isolated fall in BP with treatment does not completely reduce the risk of CAD in essential hypertension. This confirms thecomplexity of the relationship between CAD and hypertension, since numerous factors other than hypertension are implicated, aspreviously discussed. Antihypertensive treatment in patients with CAD must be more aggressive than antihypertensive treatmentconducted in the absence of coronary disease. Indeed, the risk of a recurrent coronary event in this population is very high and allefforts should be expended in order to lower BP, especially since we may expect a better level of antihypertensive treatmentcompliance after a coronary event.

As to which drugs are better in hypertensive patients, there is evidence for greater benefits from beta-blockers after a recentmyocardial infarction, a condition in which angiotensin-converting enzyme inhibitors have also been successfully tested. Later on,all classes of antihypertensive agents can be used. Beta-blockers and calcium antagonists are to be preferred, at least forsymptomatic reasons, in cases of angina.

Athanasios J. Manolis Cardiology Department, Asklepeion Hospital, Athens, Greece

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L4. Hypertension and risk of heart failure

Hypertension is one of the major risk factors for the development of heart failure (HF), including both HF with reduced left ventricularejection fraction (HFREF) and HF with preserved ejection fraction (HFPEF). Hypertension contributes to HF development in severalways, including being a major risk factor for atheromatous coronary artery disease (resulting in myocardial infarction), promotingarterial stiffening (which may increase left ventricular afterload) and affecting the myocardium (resulting in hypertrophy and otherchanges). It is therefore important to treat hypertension effectively, in order to reduce the risk of HF development. 24-h ambulatoryblood pressure (BP) monitoring appears to be a better predictor of organ damage from hypertension than clinic BP recordings, sodrugs that effectively lower BP over 24h without increasing its variability might be predicted to have an advantage in preventing organdamage and reducing the risk of HF. It is unclear whether any particular class of antihypertensive drug is more effective in preventingHF development, but once HF is established, hypertension guidelines such as those from the European Society of Hypertension(ESH) and European Society of Cardiology (ESC) recommend treatment with thiazide diuretics, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs).1 Thedoses of these treatments should be gradually increased up to the target dose or the maximum tolerated dose.

If left ventricular hypertrophy is present, ACE inhibitors (or ARBs if ACE inhibitors are not tolerated), some calcium channel blockersor some beta-blockers may be preferred. There are also studies, such as the Valsartan Antihypertensive Long-term Use Evaluation(VALUE) trial 2 and the Losartan Intervention For Endpoint reduction (LIFE) study, 3 showing that higher levels of heart rate, either atbaseline or during the course of treatment with antihypertensive drugs, may predict adverse outcomes including HF development.Whether treatment specifically aimed at reducing elevated heart rate with drugs such as beta-blockers would improve outcomeshas not been tested in prospective trials,. However, the Study Assessing the Morbidity-Mortality Benefits of the If Inhibitor Ivabradinein Patients with Coronary Artery Disease (SIGNIFY) showed no improvement in outcome from heart rate lowering with ivabradine inpatients with stable coronary artery disease without clinical heart failure, many of whom had hypertension.4 Whether reduction ofheart rate in patients with hypertension should be considered a treatment goal remains uncertain but elevated resting heart ratedoes appear to predict increased risk of developing HF.

Brian TomlinsonDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China

References:1 - Mancia G, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the

European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2013; 34: 2159-219.2 - Julius S, et al. Usefulness of heart rate to predict cardiac events in treated patients with high-risk systemic hypertension. Am J Cardiol 2012; 109: 685-92.3 - Okin PM, et al. Effect of changing heart rate during treatment of hypertension on incidence of heart failure. Am J Cardiol 2012; 109: 699-704.4 - Fox K, et al. Ivabradine in stable coronary artery disease without clinical heart failure. N Engl J Med 2014; 371: 1091-9.

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L5. Diabetes as a promoter of heart failure

Diabetes is a chronic progressive disease and is a well-recognized risk factor for heart failure (HF), independent of coronary arterydisease (CAD). The association between diabetes and HF could be equivalent to that of CAD and HF, and greater thanelectrocardiogram (ECG)-demonstrated left-ventricular hypertrophy and renal dysfunction. Nearly 25 years ago the Framinghamstudy demonstrated the increased risk of HF in patients with diabetes. A 1% rise in glycated haemoglobin (HbA1C) increases the riskof HF by 25%. However, it is not certain that improving glycaemic control reduces the risk of HF; this was also the finding of theUnited Kingdom Prospective Diabetes Study (UKPDS). Epidemiological studies show that HF is twice as common in men and fivetimes more common in women with diabetes; in addition, diabetes leads to a two-fold increased risk of HF, hospitalization and death.The incidence of diabetes in patients with HF may be as high as 25%.

It is postulated that diabetes can have direct effect on left ventricular systolic and diastolic dysfunction. The mechanisms involvedcould be vascular stiffness, mitochondrial dysfunction caused by reduction in ATP production and increased reactive oxygen-mediated mitochondrial uncoupling. Insulin resistance and hyperglycemia may directly contribute to cardiac dysfunction byincreasing the production of advanced glycation end products, increased myocardial fibrosis, oxidative stress and local activation ofthe renin–angiotensin–aldosterone system. Comorbid conditions such as hypertension, CAD, hyperlipidaemia and renal dysfunctionwill also promote HF development.

The modalities suitable for diagnosing HF in people with diabetes are echocardiography, cardiac magnetic resonance imaging,radioisotope studies and biochemical markers such as brain natriuretic peptide (BNP) and N-terminal of the prohormone BNP (NT-proBNP).

The management principle would be same as treating HF of any other cause, although special attention has to be made in initiatingdiabetic medications in view of recent findings from the SAVOR TIMI studies, and concern about usage of metformin in people withHF.

In the end we need well powered prospective randomized controlled trials to look at the mortality and morbidity benefits associatedwith various HF medications in subjects with diabetes. In addition we should more comprehensively evaluate the effects of diabetictreatments on various CV risk factors.

Saifuddin M. BandukwalaLilavati Hospital and Research Centre Bandra West, Mumbai, India

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L6. Heart failure and co-morbidities

The clinical management of co-morbidities is challenging in patients with heart failure (HF). Although people with five or morecomorbidities comprise only 39% of the HF population, they account for 81% of total hospital days. Among the several conditionsthat are associated with cardiac insufficiency, the most frequently encountered are chronic renal failure, anaemia and chronicobstructive pulmonary disease (COPD).

The simultaneous presence of renal failure and HF is common. This specific relationship is known as cardiorenal syndrome, whichis defined as disorders of the heart and kidneys where acute or chronic dysfunction in one organ may induce acute or chronicdysfunction in the other. In nearly 60% of patients with chronic HF, renal function is also reduced, and often the clinical scenariomakes it impossible to establish which disease came first. It is interesting to observe that several classes of drug treatment(including renin–angiotensin system [RAS]-blockers, loop diuretics and aldosterone antagonists) are effective in both situations.

It is important to underline that, in clinical practice, treatment is not always optimal in patients with HF and renal failure. Thus, inpatients with HF who also have severe reductions in glomerular filtration rate, many physicians reduce or withdraw treatment withRAS-blockers. This is surprising, as it is well documented that some RAS-blockers (especially angiotensin-converting enzymeinhibitors) exert protective cardiovascular effects in patients with advanced renal failure.

Anaemia is also often present in patients with HF. Haemoglobin levels <12 g/dL are observed in between three and 20% ofambulatory patients with chronic HF. In these patients, the cause of anaemia is often related to concomitant chronic kidney diseaseor inflammation. In addition, in patients with chronic HF, haemoglobin values <12 g/dL are associated with increased risk ofhospitalization or death from any cause. However, the correction of anaemia has been shown to reduce symptoms of HF, andimprove exercise tolerance and health-related quality-of-life.

Finally, the prevalence of COPD is greater in patients with HF than in the general population. Between 11 and 52% of people in inUS cohorts, and between nine and 41% of people in European cohorts, have been reported to have both conditions concomitantly.Severe COPD (which is defined as GOLD stages III and IV) is associated with a worse prognosis in patients with HF, together withhigh rates of mortality and long durations of in-patient treatment.

Although severe COPD and HF are often coexisting conditions, it is common for only one of the conditions to be diagnosed, whichresults in undertreatment of the other condition, and unsatisfactory overall response. It is important to observe that COPD mayproduce – or obscure –every symptom and sign of HF, thus masking a HF diagnosis. Monitoring brain natriuretic peptide (BNP)levels is useful in the acute setting for excluding HF in patients with acute dyspnoea. However, in those with chronic illness, thediagnostic accuracy of the BNP level in patients with concurrent COPD is less certain, since levels may also be elevated in primarypulmonary hypertension or right-HF secondary to COPD.

One important therapeutic aspect is that clinicians may be hesitant to administer beta-blockers in the presence of COPD, for fearof acute bronchospasm occurring during noncardioselective beta-blocker use. In contrast, the majority of patients with HF andCOPD can safely tolerate beta-blocker therapy. Initiation at a low dose and gradual up-titration is recommended. Mild deteriorationin pulmonary function and symptoms should not lead to prompt discontinuation of beta-blocker therapy. If symptoms worsen, areduction in dosage or withdrawal may be necessary. Selective beta-blockade is obviously the preferable option, and among thebeta-blockers proven to be efficacious in patients with HF, bisoprolol is the compound with the highest level of beta-1 selectivity.

Stefano Taddei Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy

19

L7. International guidelines for the management of diabetes:evidence based medicine vs personalized medicine

There is extensive evidence on the optimal management of diabetes, offering the opportunity of improving health-related quality-of-life in people with diabetes. However, such optimal management is not reaching the many diabetics who would benefit from it.Reasons include complexity of evidence base, complexity of diabetes care and diversity of clinical practice standards. Hence,guidelines are being developed to address those issues and guide health care practitioners to provide cost-effective, evidence-basedcare in settings where resources vary widely.

The International Diabetes Federation Global Guideline for Type 2 Diabetes 2012 recommended three levels of care to cater forvarying availability of resources:

• Recommended Care – evidence-based care, cost-effective in most nations with a well-developed service base

• Limited Care – care that seeks to achieve the major objectives of diabetes management, but is provided in healthcare settingswith very limited resources

• Comprehensive Care – care with some evidence–based approaches, provided in health-care settings with considerableresources.

The American Diabetes Association Standards of Medical Care in Diabetes 2015 grades its clinical practice recommendations basedon levels of evidence:

• Grade A – clear or supportive evidence from adequately powered well-conducted, generalizable, randomized controlled trials

• Grade B – supportive evidence from well-conducted cohort studies or case-control studies

• Grade C – supportive evidence from poorly controlled or uncontrolled studies, or conflicting evidence with the weight ofevidence supporting the recommendation

• Grade E – expert consensus or clinical experience.

However, evidence is not available in certain patient conditions, hence guidelines may not be applicable in specific situations (suchas elderly patients or those with advanced complications). The ADA guidelines advise health care practitioners to adopt patient-centeredness (personalized medicine), tailoring treatment to individual patients’ preferences, prognoses and co-morbidities.

In conclusion, treatment guidelines are developed based on evidence and cost effectiveness. In daily practice, the approach shouldbe patient-centered; in other words, based on evidence but tailored to individual characteristics.

Mafauzy MohamedHealth Campus, University Sains Malaysia, Kelantan, Malaysia

20

L8. Thyroid nodules in clinical practice: from medicaltherapy to ultrasonically-guide intervention

XXXX xxxxxxxxxxxxxxxxx


1. Adapting the ovarian stimulation protocol according to the patient’s individual profile and the experience from her previousstimulation cycles.

2. Reducing FSH and compensating with LH in the stimulation protocol to selectively stimulate the greatest follicles andprevent the growth of smaller ones.

Learning ObjectivesBy the end of the programme participants should appreciate: • International Variation in Assisted Reproduction Practice• Need to collect data to reflect practice• Value of e-Learning to facilitate best practice

IntroductionXxx xxx

MethodsXxx xxx

ResultsXxx xxx

ConclusionsXxx xxx

Abstract not in hand at the time of printing.

Nemecio A. NicodemusUniversity of the Philippines, College of Medicine, Ateneo School of Medicine & Public Health,Endocrinology, Diabetes & Metabolism, Manila, Philippines

References:1 - Chappel SC, Howles C 1991 Reevaluation of the roles of luteinizing hormone and follicle-stimulating hormone in the ovulatory process. Human Reproduction

6 1206-1212. 2 - Filicori M, Cognigni GE, Pocognoli P et al. 2003 Current concepts and novel applications of LH activity in ovarian stimulation. Trends in Endocrinology and

Metabolism 14, 267-273.

21

D1. Management of pre-diabetes: lifestyle vs drug therapy

1 - Diabetes Action Centre, Mumbai, India;2 - Department of Medicine, Our Lady of Lourdes Hospital, Manila, Philippines.

LifestyleSanjiv Shah

Xxx xxxxxxxxxxxxxxxxxxx

Drug therapyPatricia Gatbonton

Pre-diabetes is defined by the American Diabetes Association (ADA) as a “state of abnormal glucose homeostasis characterized by• Impaired fasting glucose IFG (100–125 mg/dl) [5.6–6.9 mmol/l] or• Impaired glucose tolerance (IGT) (2-h postglucose load, 140–199 mg/dl [7.8–11 mmol/l]) • or both.”

The World Health Organization terms the condition “intermediate hyperglycaemia,” while the ADA prefers “high risk state fordeveloping diabetes.” Regardless of the nomenclature, prediabetes confers increased risk not only for type 2 diabetes, but also fordevelopment of the metabolic syndrome.

Obesity is the most important risk factor for progression to full diabetes. Lifestyle modifications (which focus on improving dietaryquality, with a reduction in total calories by 500–1000 kcal/day, and undertaking physical activity of 150 min per week that results ina sustained 5–10% weight loss) are the foundations of pre-diabetes treatment. When successful, this approach can reduceprogression to full diabetes by 50–60%. However, 40–50% of people with IGT still develop diabetes, despite successful weight loss.This implies that lifestyle intervention is not enough to prevent diabetes from developing in a large percentage of patients, and thatweight loss does not have a legacy effect on diabetes prevention.

In randomized trials - including the Da Qing Study, the Diabetes Prevention Program (DPP), the Finnish Diabetes PreventionProgram (FDPP) and the Indian Diabetes Prevention Program (IDPP) - therapeutic efficacy has been shown conclusively for theselifestyle changes, with a range varying between 26 and 58%, in terms of reduction in progression to prediabetes compared withpharmacotherapy, for up to 10 years.

To prevent one case of diabetes during a 3-year period, 6.9 persons would have to participate in the lifestyle intervention programme.In addition, data suggest that the difference in direct and indirect costs for caring for a patient with prediabetes versus a patient withdiabetes may be as much as $7000 per year.

However, an ADA statement on diabetes prevention acknowledges the difficulty in replicating the lifestyle interventions from theDiabetes Prevention Program and Finnish Diabetes Prevention Study, which require considerable effort, resources and funding.

Pharmacologic management of prediabetes is indicated in patients whose lifestyle interventions are unsuccessful, or in those withobesity and additional cardiometabolic risk factors.

Sanjiv Shah, India 1

Patricia Gatbonton, Philippines 2

22

In addition to metformin (which has been shown to reduce the progression of type 2 diabetes in the aforementioned trials), acarbose,pioglitazone and orlistat have also been proven to decrease progression to diabetes. Other agents such as GLP-1 analogues,bromocriptine, and the weight-loss agents phentermine, topiramate and lorcaserin have also been shown to be effective, in small-scale studies.

Some argue that we should wait until diabetes is diagnosed before we initiate pharmacotherapy. However, in the UK ProspectiveDiabetes Study, interventions in newly diagnosed type 2 diabetes mellitus reduced, but did not prevent, microvascular complications:10–15% of people with prediabetes already have complications at diagnosis.

De Fronzo and colleagues argue that since “prediabetic individuals already manifest all of the pathophysiological abnormalitiespresent in overt [type 2 diabetes mellitus], it seems reasonable to institute pharmacological (plus lifestyle) therapy at the prediabeticstage, especially in high-risk individuals, rather than wait for the diagnosis of diabetes, which is arbitrary and based on the glucoselevel and not on pathophysiology, loss of b-cell mass, or presence of microvascular complications.”

References:- Garvey WT, Ryan DH, Henry R et al. Prevention of Type 2 Diabetes in Subjects With Prediabetes and Metabolic Syndrome Treated With Phentermine andTopiramate Extended Release. Diabetes Care 2014;37:912–21.

- McLellan KPC, Wyne K, Villagomez ET et al. Therapeutic Interventions to reduce the risk of progression of prediabetes to type 2 diabetes mellitus. Therapeuticsand Clinical Risk Management 2014;10:173–88.

- Tuso P. Prediabetes and Lifestyle Modification: Time to Prevent a Preventable Disease. Perm J 2014;18: 88–93. - Daniele G, Abdul-Ghani M. DeFronzo RA. What are the pharmacotherapy options for treating prediabetes? Expert Opin Pharmacother 2014;15: 2003–18.

23




D2. Subclinical hypothyroidism: to treat or not to treat?

1 - St. Luke’s Medical Center, Section of Endocrinology, Diabetes and Metabolism, Quezon City, Philippines2 - Hinduja Hospital & Research Centre, Mumbai, India

To treat Roberto Mirasol


Not to treatManoji Chadha


Roberto Mirasol, Philippines 1

Manoji Chadha, India 2

24

L9. Diabetes in pregnancy

The role of hyperglycaemia in driving the chronic complications of diabetes is well established but needs lifelong vigilance,monitoring and titration. The adverse impact of hyperglycaemia in pregnancy offers opportunities for patients to make substantiallifestyle changes with similar efforts, over a much shorter period.

Caring for a pregnant woman who has previously been diagnosed with diabetes presents management challenges. However, in thistime of the type 2 diabetes epidemic, it is also increasingly common to encounter women who have become pregnant without everhaving been diagnosed as diabetic. In addition, the number of women who develop diabetes during pregnancy appears to be on theincrease. Glucose tolerance testing in pregnant women has moved from its original intent of being a future predictor of diabeteswithout any bearing on fetal outcome, to the present stage where the cut-offs are solely based on fetal outcome. Most currentguidelines diagnose diabetes during pregnancy when any one of the following values is exceeded in a 75g glucose tolerance test:fasting blood glucose (FBG) level >92mg/dl; 1h blood glucose, >180mg/dl; 2h blood glucose, > 153mg/dl.

Glycaemic targets in pregnancy are FBG <90 mg/dl and postprandial blood glucose <140 mg/dl at 1h and <120 mg/dl at 2h. Insulinhas been and remains the cornerstone of treatment for diabetes in pregnancy, if and when lifestyle modifications do not permit theachievement of targets, though oral agents (most notably metformin and glibenclamide) have been considered as alternatives toinsulin. However, the safety of these oral therapies is not clearly established. Pre-term labour, hyperbilirubinaemia (with metformin)and neonatal hypoglycaemia, respiratory distress and greater need for neonatal intensive care stay (with glibenclamide) have beenreported.

The management of diabetes in pregnancy requires a multidisciplinary approach that focuses on early diagnosis, aggressivemanagement and intense monitoring – not just during pregnancy but also at postnatal follow up. As of now, however, diabetes inpregnancy is a stark example of lost opportunities in terms of the diagnosis, management and prevention (or postponement) ofeventual type 2 diabetes mellitus development in women.

Bipin SethiDepartment of Endocrinology, CARE HospitalsHyderabad, India

25

L10. Hypothyroidism and hyperthyroidism in pregnancy

In pregnancy the thyroid gland increases in size; production of T3 andT4 increases by 50% and daily iodine requirement alsoincreases by 50%. However thyroid stimulating hormone (TSH) levels decrease during pregnancy, due to the impact of humanchorionic gonadotropin (hCG). Adverse outcomes associated with hypothyroidism include increased risk of premature birth, fetaldeath, low birth weight or miscarriage, impaired fetal neurocognitive development and gestational hypertension. Treatment ofhypothyroidism in pregnancy is L-T4, the aim being to normalize TSH values within trimester-specific ranges. L-T4 requires doseadjustment, however, as there is increased demand as pregnancy progresses. For patients who are hypothyroid before pregnancy,the dose of L-T4 should be adjusted to optimize TSH at <2.5mIU/L during the preconception phase. During pregnancy, there is a 25–30% increase in L-T4 dose requirement.

The obstetric and medical complications of hyperthyroidism in pregnancy include heightened risk of miscarriage, pregnancy-induced hypertension, prematurity, low birth weight, intrauterine growth restriction, stillbirth, thyroid storm and maternal congestiveheart failure.

Fetal risks for women with Graves’ hyperthyroidism include fetal hyperthyroidism, neonatal hyperthyroidism, fetal hypothyroidism,neonatal hypothyroidism and central hypothyroidism. High titres of serum thyrotropin receptor antibody (TRAb) is a risk factor forfetal or neonatal hyperthyroidism. Serum TRAb titres may remain elevated following thyroid ablation therapy, hence indications forordering TRAb tests in patients with Graves’ disease include those with active hyperthyroidism, previous history of treatment withradioiodine, previous history of delivering an infant with hyperthyroidism and thyroidectomy for treatment of hyperthyroidism inpregnancy.

Treatment is anti-thyroid drugs (ATD), with the initial dose depending on severity of symptoms and degree of hyperthyroxinaemia.Propylthiouracil (PTU) is the preferred treatment in the first trimester of pregnancy, but for the second (and possibly third) trimester,physicians should consider switching the patient to methimazole (MMI). The primary therapeutic goal is to attain a serum FT4 at (ormoderately above) the normal reference range. Discontinuation of ATD is feasible in 20-30% of patients in the third trimester ofpregnancy, but women with high levels of TRAb should continue ATD until delivery. Thyroidectomy is indicated in the followingsituations: allergies/contraindications to ATD; a requirement for high-dose ATD; non-compliance with drug therapy. The optimaltime for surgery is during the second trimester.

In conclusion, both hypothyroidism and hyperthyroidism are associated with adverse maternal and fetal outcomes, although optimaltreatment results in improved outcomes for both mother and child.

Mafauzy MohamedHealth Campus, University Sains Malaysia, Kelantan, Malaysia

26

L11. Hypertension in pregnancy

Hypertensive disorders of pregnancy are the most common medical complications of pregnancy, and are important causes ofmaternal and perinatal morbidity and mortality.

An estimated 1.5% of pregnancies are complicated by pre-existing hypertension, 5–6% by gestational hypertension withoutproteinuria and 1–2% by pre-eclampsia. These rates will increase as the obstetric population becomes older and more obese infuture.In most cases, hypertension is usually mild, occurs in later stages of pregnancy, has no renal or other systemic involvement and usuallyresolves 12 weeks postpartum. Hypertension is more common in the woman’s first pregnancy and with mothers who are < 18 years ofage, > 35 years of age, or expecting twins.

The exact mechanisms of hypertensive disorders of pregnancy are unknown, but possibilities include:

• Immunologic factors

• Genetic factors

• Placental ischaemia

• Endothelial cell dysfunction

• Vasospasm

• Hyper-responsive response to vasoactive hormones (e.g. angiotensin II & epinephrine)

In treating hypertensive disorders of pregnancy one must remember the following issues:

• Pregnancy ,and the associated hypertension,is limited to short duration of time

• Two individuals are involved: mother and fetus; treatment is essential to avoid complications to both

• Choosing drugs safe for both mother and fetus is of utmost importance

• Lifestyle modifications, such as fluid and salt restrictions, are of limited value

Compared with women who have had normotensive pregnancies, those who are hypertensive during pregnancy are at greater riskof cardiovascular and cerebrovascular events, and also have a less favourable risk profile for cardiovascular disease, years after theaffected pregnancies.

Treatment must be initiated in all pregnant or postpartum patients with systolic BP ≥ 150 mm Hg or diastolic BP ≥ 100 mm Hg thatpersists over two readings 15 minutes apart using the same arm. Overzealous treatment of maternal hypertension must be avoidedto reduce the risk of intrauterine growth restriction and low birth weight in the fetus (poor fetal growth is probably due to reducedutero–placental perfusion caused by excessive BP reduction).

The CHIPS TRIAL , performed on women at a mean of 14 weeks gestation and who had nonproteinuric preexisting or gestationalhypertension, showed no significant differences in the risk of pregnancy loss, high-level neonatal care, or overall maternalcomplications. The findings suggested it was safe to aim for tight BP control for the baby; however, less-tight BP control wasassociated with a significantly higher frequency of severe maternal hypertension.

The treatments most commonly used to treat hypertensive disorders of pregnancy are nifedipine, hydralazine and labetalol. ACEIand ARBs must be avoided. Diuretics may reduce milk volume/suppress lactation. No short-term adverse effects have beenreported with methyldopa, or hydralazine or beta-blockers

Future preventive measures for the mother are important.

Pre-eclampsia in pregnancy is associated with an increased risk of cardiovascular disease (the increase is between two and eighttimes that for other people). Treatment with daily low-dose aspirin (75 mg), beginning in first trimester, initiated before 16 weeksgestation is advised for those who have had:

• Early onset of hypertension in a prior pregnancy

• Persistent hypertension beyond 5 weeks postpartum

• High baseline BP early in pregnancy

Jamshed J. DalalCentre for Cardiac Sciences, Mumbai, India

27

L12. Thyroid cancer guidelines



1. Adapting the ovarian stimulation protocol according to the patient’s individual profile and the experience from her previousstimulation cycles.

2. Reducing FSH and compensating with LH in the stimulation protocol to selectively stimulate the greatest follicles andprevent the growth of smaller ones.

Learning ObjectivesBy the end of the programme participants should appreciate: • International Variation in Assisted Reproduction Practice• Need to collect data to reflect practice• Value of e-Learning to facilitate best practice

IntroductionXxx xxx

MethodsXxx xxx

ResultsXxx xxx

ConclusionsXxx xxx

Abstract not in hand at the time of printing.

Shashank JoshiJoshi Clinic, Lilavati & Bhatia Hospital, Grant Medical College & Sir JJ Group of Hospitals, Mumbai, India




NOTES

NOTES

NOTES

NOTES

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2015 Asia Pacific conference on cardiometabolic diseases management · 2015-10-26 · 2015 Asia Pacific conference on cardiometabolic diseases management EXCEMED live educational