CVD.ramadan and Announcement 2

CVD News in Yemen a national quarterly cardiovascular newsletter ______October – December1999 ______

A NATIONAL CARDIOVASCULAR NEWSLETTER

October – December 1999 Volume 3, Number 2

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Editorial:Cardiology in Yemen, realities and hopesWe can say that the last 10 years have seen un-

precedented quantitative and qualitative progress in cardiology. There has been an increasing number of qualified specialists and improving performance regarding the cardiac problems through the encouragement of governmental and private cardiac sectors.

The global health status is promising, taking in consideration the big herited health burden that was

handicapping, in addition to the demographic, educational, geographic, and economic difficulties.

In this issue you will find some of modest efforts that can be done by Yemeni cardiologist through up to date medical information, 2nd announcement for the 3rd Yemeni Cardiac Meeting which will be held in Aden (6-9, march 2000), and other practical medical problems.

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Editorial board:

Editors in chief:Dr. A-Kader AbbasDr. Ahmed Daifalla

Members:(Alphabitically)Dr. A-Hamid S. FathDr. Abdulla Abdu IsmailDr. Abdulla Al-ShibaniDr. Abdulla Bin MazroaDr. Ahmed Al-MottarebDr. Badae AlmekhlafiDr. Dhaifullah GayedDr. Ghalib AlhaifiDr. Moh. Al-NoamiDr. Omar BaselmDr. Sultan Al-DobaiDr. Yahia Al-Hadad

Advisory board:Prof. Abu-Baker Al-QirbiDr. J. Veerman

Contents: New and old

antiplatelet drugs in cardiovascular diseases

Endocarditis diagnosis (update information)

Summary of preoperative and intraoperative cardiovascular factors that correlate with perioperative morbidity(for noncardiac urgery)

Sedentary Life-Style and Coronary Heart Disease Risk

ECG quiz


This is one of our continuous initiatives to expand medical knowledge, updating our cardiologists and mediating the Cardiology facts, and perspectives. Scientific objectives and sincere participation of the international and national cardiologist to deliver this issue is of crucial importance toward realizing serious and worthfull dream.

Dr.Ahmed Daifalla, M.D.

State of the Art Lecture

NEW AND OLD ANTIPLATELET DRUGS IN CARDIOVASCULAR DISEASES

Dr Jean-Louis GEORGES, MD, Cardiac Intensive Care Unit and Interventional Cardiology Departments, Centre Hospitalier de Versailles, France.General Secretary of the Yemeni-French medical Association (AMFY)

The importance of thrombosis in the pathogenesis of cardiovascular syndromes is now well established. These syndromes include acute coronary syndromes (unstable angina, non-Q- wave myocardial infarction, (acute ST-elevation) myocardial infarction, and abrupt closure after coronary intervention), ischemic stroke in part, and acute complications of arteritis. All share a common pathophysiology of atherosclerotic plaque rupture, activation of coagulation cascade, and adhesion, activation, and aggregation of platelets.

Mechanism of actionThere are at least nine pathways for platelet activation, and only few of them are targets of current antiplatelet drugs (figure 1).

-Aspirin acetylates prostaglandin H-syntheses, and irreversibly inhibits the cyclooxygenese activity and the thromboxane A2 production in the activated platelet, decreasing the further stimulation of inactivated platelet. Its action is not reversible.The mean life span of human platelets is ten days. Therefore, approximately 10% of circulating platelets are replaced every 24h, and 7-8 days after aspirin withdrawal, approximately 80% of platelets function normally.-Dypiridamole inhibits phosphodiestrase and blocks the platelet uptake of adenosine. Its precise mechanism of action remains unclear.-Teclopidine (TICLID®) and clopidogrel (PLAVEX®) selectively inhibit adenosine diphosphate (ADP)-induced platelet aggregation. Both are clinically active after 2-4 days of treatment, and their activity lasts 7 days after withdrawal.-New glycoprotein IIb/IIIa receptor antagonists, in contrast to other antiplatelet drugs, inhibit the final common pathway of platelet aggregation. Glycoprotein IIb/IIIa is a binding site of fibrinogen and Von Willebrand factor to the platelet, and plays a key role in final process of platelets aggregation, regardless of the initial stimulus. The inhibitors of GPIIb/IIIa include monoclonal antibodies (abciximab-REOPRO®), peptides derives from snake venom (Integrelin), peptidomimetic agents for IV use (Tirofibran- AGGRASTAT®, Lamifiban), and oral use (Sibrafiban, Xemilofiban and others…).

Clinical AspectsTiclopidineTiclopidine is commercially available since the last 70s for the prevention of cardiovascular events in patients suffering from minor stroke and peripheral vascular disease. It is also more effective than placebo in reducing acute occlusion of coronary bypass grafts. However, the association of ticlopidine therapy with severe neutropenia (WBC< 1200/ml in 2.4% of the cases, and < 450/ml in 0.8%) and its comparative expense has reduced enthusiasm for this therapy as an alternative to aspirin in most situations. Interest for ticlopidine has regained in France since 1995, after multicenter register had shown that ticlopidine (500 mg daily) combined to low doses of aspirin

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reduced deeply the acute stent thrombosis (<2% at one month versus 4 to 6% with warfarin), without excess of bleeding complications. These results were confirmed by randomized studies (STARS, ISAR, MATTIS, and FANTASTIC). Ticlopidine combined to aspirin during at least 2 weeks after procedure is, until now, the reference treatment after coronary stent placement.ClopidogrelClopidogrel is structurally related to ticlopidine with some putative advantages: a quicker activity (the inhibition of platelet aggregation is detectable at 2h after oral dosing of 400 mg), and no excess of neutropenia or other hematological disorders. Clinical effectiveness and tolerance of Clopidogrel 75mg daily to aspirin 325mg daily in >18.000 patients. CAPRIE is unique compared to other studies in that it incorporated three groups of patients, all of whom are recognized to be at increased risk of recurrent ischemic events (patients with recent stroke, recent myocardial infarction, and symptomatic peripheral artery disease). Overall the CAPRIE showed modest differences in effectiveness; the annual event rate calculated for aspirin was 5.83% compared with 5.32% for Clopidogrel (relative risk reduction 8.7%, p<0.043).Moreover the effectiveness of Clopidogrel was limited to patients who entered the trial because of peripheral artery disease (risk reduction of 3.7% after MI and 7.3% after stroke). Clopidogrel was also compared to ticlopidine after coronary stenting.Recent US registers and the randomized study CLASSICS shown a comparable effectiveness of both treatment and a better tolerance with clopidogrel (Table 1).

Table 1. Comparison between Ticlopidine and Clopidogrel after coronary stenting:Results of the randomized CLASSICS study.

TICLOPIDINE CLOPIDOGREL75mg / d 300/75 mg / d Total

n = 340 n = 335 n = 345 n = 680Adverse events

31(9.1%) 21(6.3%) 10(2.9%) 31(4.6%) *

Cardiac events

3(0.9%) 5(1.5%) 4(1.2%) 9(1.3%)

* p < 0.05

Abciximab (REOPRO®) Abciximab is the first antagonist of GPIIb/IIIa receptors available for clinical use. It is a chimeric monoclonal anti GPIIb/IIIa antibody, and is active very quickly (20 mn) after IV bolus injection (0.25 mg/kg). This treatment, completed by a 12hours IV infusion (0.10 μg/kg), reduced significantly the rate of complications after complex coronary angioplasty (EPIC, EPILOG studies). Its efficacy for preventing death, MI recurrence, or need of emergency revascularization after angioplasty was of similar magnitude to that of stent placement, and the two treatment had additive effects (EPISTENT study). Abciximab also appears to be an effective treatment in refractory unstable angina (CAPTURE trial) and in acute myocardial infarction, combined with angioplasty and stent (PAMI stent, ADMIRAL trials). Main side effects are bleedings (4%) and thrombocytopenia (1%). Unfortunately, the clinical use of abciximab is still limited by its cost (approximately 1.000 US $ for one patient!)

Other GP IIb/IIIa receptors antagonistsEptifibatide (Integrilin) is a synthetic cyclic heptapetide, derived from the snake venom disintegrin. Tirofiban (AGGRASTAT®) and limifiban are nonpeptide compounds that selectively inhibit the GPIIb/IIIa receptor. All these treatments are intravenously administered. Four completed trials (PRISM, PRISM plus, PARAGON, PURSUIT) have examined the efficacy and safety of these treatments in approximately 18.000 patients with unstable angina or non-Q-wave MI, randomized to receive anti GPIIb/IIIa antagonist or placebo, in addition to conventional antithrombotic therapy (that is, IV heparin and aspirin)(Table 2). This study demonstrated 10 to 27% relative risk reduction in MI or death at 30 days, but an increased risk of bleeding complications.These treatments have also been evaluated after percutaneous coronary interventions, with moderate superiority as compared to placebo (IMPACT II, RESTORE trials). Whereas the US food and Drug administration have approved most of these treatments, clinical results are overall disappointing. Orally active non-peptide GPIIb/IIIa inhibitors have been developed and have the potential to be given long term. Xemilofiban, however, did not

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reduced death or MI or emergency revascularization after percutaneous coronary intervention in the EXCITE trial, and Orbofiban was not superior to placebo in patients with acute coronary syndromes in the OPUS-TIMI 16 trial. Ongoing trials with other oral fibans (SYMPHONY 1 and 2 with the Sibrafiban) will precise what we can expect from these promising new treatments.

Table 2. GPIIb/IIIa antagonists in unstable angina and non-Q-wave MI _____________________________________________________Trial N° Compound Placebo GP IIb/IIIa RRR% p % antagonist %_______________________________________________________ PRISM 3.232 Tirofiban 7.1 5.8 18.3 NS PRISM-Plus1.570 Tirofiban 11.9 8.7 26.9 0.03PARAGON 2.282 Lamifiban 11.7 10.3 12.0 NSPURSUIT 10.948 Eptifibatide 15.7 14.2 9.6 0.04______________________________________________________________Rates of death or MI at 30 days are shown for each trial. RRR= relative risk reduction; NS = non significant

Is there still a place for aspirin?Aspirin has been tested in patients demonstration the whole spectrum of atherosclerosis, from apparently low-risk individuals presenting with an acute MI or an acute ischemic stroke. Overall, aspirin has been found to prevent vascular death by approximately 15% and nonfatal vascular events by about 30% in a Meta analysis of > secondary prevention trials (BMJ 1994). In the ISIS 2 trial (1986), a single tablet of aspirin 162.5 mg started within 24 h of MI produced highly significant reduction in the risk of vascular mortality (by 23%), non fatal reinfarction (by 49%) and nonfatal stroke (by 46%), without increase in hemorrhage stroke or gastrointestinal bleeding. Aspirin 160 to 325 mg should be administered routinely to virtually all patients with suspected acute MI.For secondary prevention in patients with hypertension, stable or unstable angina, transient ischemic attack, and acute ischemic stroke, a lower dose of 75mg was shown to be the minimum effective dose for antithrombic efficacy, with reduced gastrointestinal side effects. In prevention of stent thrombosis, aspirin should be systematically associated with an ADP-inhibitor, ticlopidine, or clopidogrel. No recent trial could demonstrate a benefit of other antiplatelet agents,

such as oral GPIIb/IIIa inhibitors, as compared to this association.

In conclusion, despite an extensive basic and clinical research for novel antiplatelet agent, aspirin, the cheapest and the most widely used of the antiplatelet drugs, remains the gold standard of the antithrombotic treatment of cardiovascular diseases. The minimal effective dose, adjusted to each clinical situation, improves the tolerance. New antiplatelet agents (clopidogrel, intravenous GPIIb/IIIa inhibitors), when indicated, act essentially as adjunctive treatment in special situations (stent placement, refractory unstable angina, complex coronary interventions). Preliminary results obtained with new oral GPIIb/IIIa inhibitors are disappointing, with regard to their theoretical advantages.______________________________________

CRITERIA FOR DIAGNOSIS OF INFECTIVE ENDOCARDITIS

(DOKE UNIVERSITY ENDOCARDITIS SERVICE)

1-Definitive Diagnosis…One. Pathology, Microbiology of vegitation

obtained at surgery or outopsyTwo. B. Tow major criteriaThree. One major & three minorFour. Five minor criteria

2-Possible diagnosis…Finding consistent with but fall-short of definitive diagnosis of infective endocarditis

3-No endocarditis…No pathology at surgery or outopsy or clinical resolution within 3 days of antimicrobial therapy: firm alternate diagnosis

Major criteria1-Blood culturea-Two separate blood culture positive for: 1.Veridants Streptococci, S-bovis, HACEK 2.Community acquired S.aureus or enterococci in absence of primary focusb-Positive blood culture>12hrs apartc-Positive blood culture 3of 3 or majority of >4 within first & last > one hr. apart

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2-EchocardiographyOscillating intracardiac mass on valve or supporting structure or in the path of jet stream, valve ring abscess, new dehiscence of prosthetic valve, or new valvular regurgitation

Minor criteria1-Predisposing heart condition or intravenous drug users2-Fever >38C°3-Systemic or pulmonary emboli, mycotic aneurysm4-Immunological phenomena: glomerulonephritis, Roth's spot, and Osler's node. Janeway lesion, Rheumatoid factor5-Echocardiography finding consistent but not definitive of endocarditis

Updated information selectionMolecular diagnosis of endocarditis

Dukes criterion*

Infective endocarditis is associted with a high degree of morbidity and mortality.Dukes criteria is now recognized as the most accurate diagnosis and classification of this disease.Current study using blood calure material from patients with suspected infective endocarditis for usual culture and novel molecular technique.The molecular approach of (pcr) amplification of genes specific for bacteria and fungi/ yeast and sequencing was used to identify the possible microbial agents responsible for the infection.The findings obtained from the molecular approach indicate that it may aid in the diagnosis of endocaritis and should therefor be included as an additional criterion in the Dukes classification scheme.In conclusion,molecular identification of the aetiological agent responsible for endocarditis directly from blood culture material will enable specific treatment directed at this agents to be commenced at an earlier stage of the disease and hence reduce the need for valve replacement.*Topic selected by; Dr.K.Alaghbari.MD

Molecular diagnosis of endocarditis - a new Duke's criterion?

B.C. Millar, J.E. Moore, P. Mallon, M.J. Crowe, R.B.

McClurg, M.D. Curran1, J.A.P. Earle2, B. Rima2, P.G. Murphy

Bacteriology Dept., Belfast City Hospital, Belfast; 1 Immunogenetics and Histocompatability, Belfast City

Hospital, Belfast; 2 Genetic Engineering Dept., The Queen's University of Belfast, Belfast, United Kingdom

Infective endocarditis is associated with a high degree of morbidity and mortality. Duke's criteria is now recognized as the most accurate diagnosis and classification of this disease. The aim of this current study was to examine blood culture material from such patients both by cultural and novel molecular techniques. The molecular approach of PCR amplification of genes specific for bacteria (16S rRNA) and fungi/yeast (28S rRNA) and sequencing was used to identify the possible microbial agent(s) responsible for the infection. Blood culture material from six patients were positive by both culture (Staphylococcus aureus, coagulase negative staphylococci [CNS], Streptococcus mitis (2), MRSA, Haemophilus influenzae) and PCR (S. aureus, S. epidermidis, S. gordonni, S. mitis/pneumoniae, MRSA, H. influenzae/aegyptus), respectively. Blood culture material from four patients were negative by culture except for isolated cultures which were classified as environmental contaminants namely Corynebacterium spp., Micrococcus spp., CNS and Propionibacterium spp, which were also identified by PCR. However, blood culture material from one patient revealed the presence of DNA from Propionibacterium acnes in three sets of blood cultures, indicating that it may have been the causative agent. Seven patients' blood culture were culture-negative but PCR-positive for Acinetobacter spp. (1), Nocardiodies spp. (2), Nocardiodes albus (1), Candida-like spp. (1). Bacterial DNA was identified in three other patients but the sequence data was mixed and could not confirm the identity of the organism detected. These findings were analysed along with the patients' clinical background in light of the Duke's criteria.

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These results demonstrated that (i) all patients who were classified as definite or possible endocarditis cases by Duke's criteria were positive by PCR, (ii) all patients who were rejected as having endocarditis according to this criteria were negative by PCR except for one patient who had bacteraemia originating from a different source. These findings indicate that a molecular approach may aid in the diagnosis of endocarditis and should therefore be included as an additional criterion in the Duke's classification scheme. In conclusion, molecular identification of the aetiological agents responsible for endocarditis directly from blood culture material will enable specific treatment directed at this agent to be commenced at an earlier stage of the disease and hence reduce the need for valve replacement.

Citation: European Heart Journal Vol 20, Abstr. Suppl. August/September 1999, page 362

Value of new diagnostic criteria in prosthetic valve endocarditis

G. Habib, J.F. Avierinos, G. Derumeaux, C. Médail, J.P. Casalta, F. Biou, M. Garcia, P. Ambrosi, D. Raoult, R. Luccioni

Cardiologie B, La Timone Hospital, Marseille, France

Background. Duke criteria (DC) have been shown to be sensitive in diagnosing native valve infective endocarditis (IE), but their accuracy in pts with prosthetic valve endocarditis (PVE) are not known. We recently proposed modified Duke criteria (MDC) in which serologic diagnosis of Q fever was accepted as a major criterion and IE was considered as "definite" even when only 1 major and 2 minor criteria were present in pts with prior antibiotic therapy and typical echocardiographic findings.Objectives: To assess the value of DC and MDC in pts with PVE.Methods. DC and MDC were applied in 131 consecutive pts with proved IE (with pathological confirmation in 93 cases). Blood cultures (BC), serology of Q fever, transthoracic and transoesophageal echocardiography (TOE) were performed in all. Fourty-two pts with PVE (group 1) (16 bioprosthetic, 23 mechanical, 3 homografts)

were compared with 89 pts with native IE (group 2).Results. Using DC, the sensitivity for diagnosis of IE was lower in group 1 than in group 2 (64 vs 84%, p < 0.01), 15 (36%) of 42 pts with proved PVE being misclassified as "possible IE" using DC. The causes for misclassification were negative BC in 8 pts (resulting from prior antibiotic therapy in 6), Q fever IE in 3 pts, and a negative TEE in 3 pts. Application of MDC resulted in a better diagnosis of PVE, with sensitivities of 81 and 92% in groups 1 and 2, respectively.Conclusion.

1) clinical diagnosis of IE is more difficult in pts with prosthetic than in pts with native IE.2) DC have a relatively low sensitivity in these pts.3) Use of MDC allows improvement in the clinical diagnosis of PVE

Citation: European Heart Journal Vol 20, Abstr. Suppl. August/September 1999, page 361

SUMMARY OF PREOPERATIVE AND INTRAOPERATIVE

CARDIOVASCULAR FACTORS THAT CORRELATE WITH

PERIOPERATIVE MORBIDITY (for noncardiac surgery)

Michael F. Roizen, MDProfessor and Chairman, Department of Anesthesia and Critical Care; Professor, Department of Medicine, University of Chicago, Division of the Biological Sciences, Pritzker School of Medicine, Chicago, Illinois

To summarize a large number of studies preoperative findings that correlate with perioperative morbidity and that can be corrected prior to operation are as follows:(1) recent MI (within 6 months)(2) severe CHF (i.e., sufficiently severe to produce

rules, an S3 gallop, or distention of the jugular vein

(3) severe angina(4) heart rhythm other than sinus(5) premature atrial contractions(6) more than five premature ventricular

contractions per minute

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(7)blood urea nitrogen levels higher than 50 mg% or potassium levels lower than 3 mEq/L.84Preoperative factors that correlate with perioperative risk but cannot be altered include: (1) old age (perioperative risk increases with age)(2) significant aortic stenosis(3) emergency operation(4) cardiomegaly(5) history of CHF(6) angina (or history of angina) or ischemia on

ECG(7) abnormal ST-segment or inverted or flat T

waves on ECG or an abnormal QRS complex on ECG

(8) significant mitral regurgitant murmur

Significant intraoperative factors that correlate with perioperative risk and can be avoided or altered are as follows: (1) unnecessary use of vasopressors(2) unintentional hypotension (this point is

controversial, however, as some investigators have found that unintentional hypotension does not correlate with perioperative morbidity)

(3) high rate-pressure product (i.e., if the product of heart rate times systolic blood pressure exceeds 11,000)

(4) long operations.

Significant intraoperative factors that correlate with perioperative morbidity and probably cannot be avoided are (1) emergency surgery (2) thoracic or intraperitoneal surgery or above-

the-knee amputations

Although the evidence for the above statements is fairly substantial, virtually none of the data derive from prospective randomized studies indicating that treatment of these conditions reduces perioperative risk to patients with ischemic heart disease. Nevertheless, logic dictates that such treatment does reduce risk. Thus, the goal in giving anesthesia to patients with ischemic heart disease is to have the patient in the best preoperative condition obtainable by treating those conditions that correlate with perioperative risk. Then the anesthesiologist usually monitors intraoperatively for conditions that correlate with perioperative risk and, by that monitoring and attentiveness to detail,

avoids those circumstances leading to perioperative risk. Although local anesthesia may reduce perioperative risky epidemiologic studies do not reveal significant differences in perioperative morbidity for patients with ischemic heart disease who are given local anesthesia as opposed to general anesthesia.

DETERMINING AND REDUCING PERIOPERATIVE RISK BEFORE SURGERYPreoperative evaluation and a consultant's note about the patient with ischemic heart disease should include a review of the clinical course of any previous MIs and a review of studies made subsequent to those events. Because the patients most likely to benefit are those with severe coronary artery disease (i.e., multivessel left main stem coronary artery disease) and ejection fractions of 21% to 50%, some strategies have been devised to limit routine exercise testing, dipyridamole-thallium scanning, Holter monitoring, and angiographic testing to only such patients. Each group of internists, cardiologists, surgeons, and anesthesiologists could agree on their choice of strategy.The strategy I use is based on studies showing that history is better at predicting cardiovascular risk than laboratory tests given to populations unselected by history.Thus, if the patient does not have (1st) a history of MI(2nd) recurrent angina (or equivalent)(3rd) CHF or equivalent(4th) diabetes requiring treatment(5th) Q waves on ECGI recommend proceeding directly with noncardiac surgery without special monitoring or special precautions for postoperative management. This patient has minimal-to-no risk of severe CAD or perioperative cardiac events. If three or more of the above findings exist, I recommend proceeding directly with cardiac catheterization of the patient. If one or two of the above findings exist, I recommend 24 hours of Holter monitoring and subsequent evaluation, based on the amount and degree of ischemia on that test. I then plan perioperative monitoring, care site, and selection of analgesia.

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The preoperative evaluation and consultation note should include a review of

exercise studies, Holter monitoring results, dipyridamole-thallium scans, and coronary angiogram in order to determine which ECG lead to monitor for ischemia. Although, in theory, the ECG lead that first reveals ischemia or best represents the stenosed artery on exercise should be the first to reveal ischemia in the operating room, no study has confirmed this assumption. If no exercise or coronary angiographic study has been performed, precordial lead V5 is preferred.

Currently, the only known way to increase oxygen supply to the myocardium of patients with coronary artery stenosis is to maintain diastolic blood pressure, hemoglobin concentration, and oxygen saturation. Therefore, the main goal of anesthesia practice for such patients has been to decrease the determinants of myocardial oxygen demand: heart rate, ventricular wall tension, and contractile performance. Thus, medical management to accomplish the goal of preserving all viable myocardial tissue may include:(1) administration of -adrenergic receptor

blocking drugs (propranolol, esmolol, or metoprolol) to decrease contractility and heart rate

(2) vasodilation with nitroglycerin (or its "long-acting" analogues), nitroprusside, hydralazine, or prazosin to decrease ventricular wall tension.

The goal of anesthesia management should be the same, although no prospective controlled studies have documented a decrease in perioperative morbidity by reducing preload or afterload or by decreasing heart rate. However, the goals of keeping cardiovascular variables within an acceptable range and the rate-pressure product below the threshold for angina appear appropriate. In addition, I believe— and what little data we

have support the plan—that drugs given chronically (e.g., antihypertensive medications) should be continued through the morning of surgery.

Finally, the assumption that a patient with subendocardial MI is at less perioperative risk than a patient with transmural MI is now being questioned. Thus, I believe that patients with subendocardial MI should be treated no differently than those with transmural MI.

The Third Yemeni Cardiac Meeting, 6 – 9 March, 2000, Aden

Final announcement

The Third Yemeni Cardiac Meeting will handle the Cardio-Vascular Diseases (CVD), it is organized by the Yemeni Heart Patients’ Friends Association, in co-operation with the Yemeni Cardiac Society. This meeting is the third gathering for the Yemeni cardiologist. The echoes of the two previous meetings (1995 & 1997) were well known for the health professionals in Yemen and in the region, a main recommendation of both, was the establishment of a cardiac surgery program in the country. Nowadays the cardiac surgery program is in its early phase and it will be emerged during The Third Yemeni Cardiac Meeting.The aims of this meeting will include: sharing the experience of the local doctors with the invited guests speakers; getting together to discuss the common cardiovascular problems in the different Yemeni towns; discussing the early experience of invasive cardiology and closed cardiac surgery in Yemen; keeping-in touch with the recent advances in cardiovascular diseases and establishment of a solid program for prevention and control in this field. The scientific activity of the meeting will extend over four days, and a social program will be included.

This meeting will be attended by a large number of eminent cardiologists, physicians, cardiac surgeons from the Arab world and Europe.

Special emphasis will be put on common cardiac problems in Yemen. There will be a Scientific Program: main sessions and symposia, workshops, etc..

Main Topics will be: *Rheumatic Heart Disease *Cardiac Surge

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ECG quizECG quizWhat kind of arrhythmia shows the following ECG?


*Interventional cardiology *Hypertension*Ischaemic Heart Disease *Vascular Diseases *Congenital Heart Disease *Cardiac Imaging *Arrhythmia *Miscellaneous.

Target audience: cardiologists, cardiac surgeons, internists, general practitioners, medical students, nurses and technicians. Registration:Registration fee:

*6000 Y.R. including accommodation in shared room, breakfast and lunch

*10000 Y.R. including accommodation in single

room, breakfast and lunch*3000 Y.R. including lunch (no accommodation)*1000 Y.R. For student (only workshops)Congress informationDate: March 6-9, 2000Venue: Al Aroosa Tourism Complex, AdenOfficial Language: Arabic, EnglishFor more information please contact:

Dr. Abdul-Kader Abbas

Sana’aRepublic of YemenP. O. Box: 8831Tel.: +967 1 263 105Fax: +967 1 246 971E-Mail: Yemcard.hotmail.com

THIS ISSUE WAS GRATEFULLY SPONSERD BY

Mohdar Corporation – Tel : 274691- Fax : 272215 Sana’a Yemen

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CVD.ramadan and Announcement 2