CVD.ramadan and Announcement 2

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______ CVD News in Yemen a national quarterly cardiovascular newsletter ______October – December1999 1 A NATIONAL CARDIOVASCULAR NEWSLETTER October – December 1999 Volume 3, Number 2 ______ CVD News in Yemen a national quarterly cardiovascular newsletter ______October – December1999 2 Editorial board: Editors in chief: Dr. A-Kader Abbas Dr. Ahmed Daifalla Members: (Alphabitically) Dr. A-Hamid S. Fath Dr. Abdulla Abdu Ismail Dr. Abdulla Al-Shibani Dr. Abdulla Bin Mazroa Dr. Ahmed Al-Motta
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  CVD News in Yemen a national quarterly cardiovascular newsletter   ______  October – December1999  ______   A NATIONAL CARDIOVASCULAR NEWSLETTER October – December 1999 Volume 3, Number 2 1  CVD News in Yemen a national quarterly cardiovascular newsletter   ______  October – December1999  ______  Editorial: Cardiology in Yemen, realities and hopes We can say that the last 10 years have seen un- precedented quantitative and qualitative progress incardiology. 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 inconsideration the big herited health burden that washandicapping, 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 datemedical information, 2 nd  announcement for the 3 rd  YemeniCardiac Meeting which will be held in Aden (6-9, march2000), and other practical medical problems. 2 Editorial board:Editors in chief:Dr. A-Kader AbbasDr. Ahmed DaifallaMembers:(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-HadadAdvisory board:Prof. Abu-Baker Al-QirbiDr. J. Veerman Contents: ♦  New and oldantiplatelet drugs incardiovascular diseases ♦ Endocarditisdiagnosis (updateinformation) ♦ Summary of  preoperative andintraoperativecardiovascular factors thatcorrelate with perioperative morbidity(for noncardiac urgery) ♦ Sedentary Life-Styleand Coronary HeartDisease Risk  ♦ ECG quiz  CVD News in Yemen a national quarterly cardiovascular newsletter   ______  October – December1999  ______  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 theinternational and national cardiologist to deliver this issue isof crucial importance toward realizing serious and worthfull dream. Dr.Ahmed Daifalla, M.D. State of the Art Lecture NEW AND OLD ANTIPLATELET DRUGS INCARDIOVASCULAR DISEASES  Dr Jean-Louis GEORGES, MD,Cardiac Intensive Care Unit and  Interventional Cardiology Departments,Centre Hospitalier de Versailles, France.General Secretary of the Yemeni-Frenchmedical Association (AMFY) The importance of thrombosis in the pathogenesisof cardiovascular syndromes is now wellestablished. These syndromes include acutecoronary syndromes (unstable angina, non-Q-wave myocardial infarction, (acute ST-elevation)myocardial infarction, and abrupt closure after coronary intervention), ischemic stroke in part, andacute complications of arteritis. All share acommon pathophysiology of atherosclerotic plaquerupture, activation of coagulation cascade, andadhesion, activation, and aggregation of platelets. Mechanism of action There are at least nine pathways for plateletactivation, and only few of them are targets of current antiplatelet drugs (figure 1). Antiplatelet agents :mechanisms of action GPIIb IIIa PlateletFibrinogenTX A2ThrombinADP TiclopidineClopidogrelAspirinAbciximabFibans -Aspirin acetylates prostaglandin H-syntheses, andirreversibly inhibits the cyclooxygenese activityand the thromboxane A2 production in theactivated platelet, decreasing the further stimulation of inactivated platelet. Its action is notreversible.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 plateletsfunction normally.-Dypiridamole inhibits phosphodiestrase and blocks the platelet uptake of adenosine. Its precisemechanism of action remains unclear.-Teclopidine (TICLID®) and clopidogrel(PLAVEX®) selectively inhibit adenosinediphosphate (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, incontrast to other antiplatelet drugs, inhibit the finalcommon pathway of platelet aggregation.Glycoprotein IIb/IIIa is a binding site of fibrinogenand Von Willebrand factor to the platelet, and plays a key role in final process of plateletsaggregation, regardless of the initial stimulus. Theinhibitors of GPIIb/IIIa include monoclonalantibodies (abciximab-REOPRO®), peptidesderives from snake venom (Integrelin), peptidomimetic agents for IV use (Tirofibran-AGGRASTAT®, Lamifiban), and oral use(Sibrafiban, Xemilofiban and others…). Clinical Aspects Ticlopidine Ticlopidine is commercially available since the last70s for the prevention of cardiovascular events in patients suffering from minor stroke and peripheralvascular 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 hasreduced enthusiasm for this therapy as analternative 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 3  CVD News in Yemen a national quarterly cardiovascular newsletter   ______  October – December1999  ______  reduced deeply the acute stent thrombosis (<2% atone month versus 4 to 6% with warfarin), withoutexcess of bleeding complications. These resultswere confirmed by randomized studies (STARS,ISAR, MATTIS, and FANTASTIC). Ticlopidinecombined to aspirin during at least 2 weeks after  procedure is, until now, the reference treatmentafter coronary stent placement. Clopidogrel  Clopidogrel is structurally related to ticlopidinewith some putative advantages: a quicker activity(the inhibition of platelet aggregation is detectableat 2h after oral dosing of 400 mg), and no excess of neutropenia or other hematological disorders.Clinical effectiveness and tolerance of Clopidogrel75mg 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 atincreased risk of recurrent ischemic events(patients with recent stroke, recent myocardialinfarction, and symptomatic peripheral arterydisease). Overall the CAPRIE showed modestdifferences in effectiveness; the annual event ratecalculated for aspirin was 5.83% compared with5.32% for Clopidogrel (relative risk reduction8.7%, p<0.043).Moreover the effectiveness of Clopidogrel waslimited to patients who entered the trial because of  peripheral artery disease (risk reduction of 3.7%after MI and 7.3% after stroke). Clopidogrel wasalso compared to ticlopidine after coronarystenting.Recent US registers and the randomized studyCLASSICS shown a comparable effectiveness of  both treatment and a better tolerance withclopidogrel (Table 1). Table 1. Comparison between Ticlopidine and Clopidogrel after coronary stenting: Results of the randomized CLASSICS study. TICLOPIDINECLOPIDOGREL75mg / d300/75 mg / dTotaln = 340n = 335n = 345n = 680Adverseevents31(9.1%)21(6.3%)10(2.9%)31(4.6%) *Cardiacevents3(0.9%)5(1.5%)4(1.2%)9(1.3%)* p < 0.05  Abciximab (REOPRO ®  ) Abciximab is the first antagonist of GPIIb/IIIareceptors available for clinical use. It is a chimericmonoclonal anti GPIIb/IIIa antibody, and is activevery quickly (20 mn) after IV bolus injection (0.25mg/kg). This treatment, completed by a 12hours IVinfusion (0.10 μg/kg), reduced significantly the rateof complications after complex coronaryangioplasty (EPIC, EPILOG studies). Its efficacyfor preventing death, MI recurrence, or need of emergency revascularization after angioplasty wasof similar magnitude to that of stent placement, andthe two treatment had additive effects (EPISTENTstudy). Abciximab also appears to be an effectivetreatment in refractory unstable angina (CAPTUREtrial) and in acute myocardial infarction, combinedwith 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 itscost (approximately 1.000 US $ for one patient!) Other GP IIb/IIIa receptors antagonists Eptifibatide (Integrilin) is a synthetic cyclicheptapetide, derived from the snake venomdisintegrin. Tirofiban (AGGRASTAT®) andlimifiban are nonpeptide compounds thatselectively inhibit the GPIIb/IIIa receptor. All thesetreatments are intravenously administered. Four completed trials (PRISM, PRISM plus,PARAGON, PURSUIT) have examined theefficacy and safety of these treatments inapproximately 18.000 patients with unstable anginaor non-Q-wave MI, randomized to receive antiGPIIb/IIIa antagonist or placebo, in addition toconventional antithrombotic therapy (that is, IVheparin and aspirin)(Table 2). This studydemonstrated 10 to 27% relative risk reduction inMI or death at 30 days, but an increased risk of  bleeding complications.These treatments have also been evaluated after  percutaneous coronary interventions, withmoderate superiority as compared to placebo(IMPACT II, RESTORE trials). Whereas the USfood and Drug administration have approved mostof these treatments, clinical results are overalldisappointing.Orally active non-peptide GPIIb/IIIa inhibitorshave been developed and have the potential to begiven long term. Xemilofiban, however, did not 4
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