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Dr. Doni Firman , SpJP (K)

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Translating Evidence into Clinical Practice : Role of More Potent Antiplatelet in Acute Coronary Syndrome. Dr. Doni Firman , SpJP (K). CASE 1. Usia : 63 tahun - PowerPoint PPT Presentation

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Translating Evidence into Clinical Practice : Role of More Potent Antiplatelet in Acute Coronary Syndrome

Dr. Doni Firman, SpJP(K)CASE 1 Usia : 63 tahunPasien masuk dengan keluhan nyeri dada sejak 2 jam SMRS, terus menerus seperti ditekan benda berat, tidak menjalar, muntah (-)keringat dingin (+) hingga basah kuyup. Keluhan timbul saat sedang menunggu di bandara ,sesak (-), jantung berdebar (-)Pasien baru pertama kali mengalami hal ini, riwayat mudah lelah saat aktivitas

Faktor risiko HipertensiKolesterol tinggiMerokok (-)DM (-)FH (-)Proprietary and Confidential. AstraZeneca 2011. Document intended for internal discussion purposes.Pasien pria usia 66 tahun masuk UGD dengan nyeri dada yang hebat berlangsung selama 30 menit , pasien juga obesitas ditunjukkan dengna BMI 31

Pasien tidak mempunyai riwayat stroke atau TIA bukan perokok dan belum pernah mengalami MI namun menderita hiperlipidemia. Physical Examination and ECGKU nyeri dadaTD 134/78 mmHgNadi 90 x / menitRR 16 x / menit


Hb 13.6 mg/dlLekosit 11.450Hs Trop T 32GDS 1733

Proprietary and Confidential. AstraZeneca 2011. Document intended for internal discussion purposes.Case 2Laki-laki 73 tahunDikirim dari sejawat dengan riwayat NSTEMI, DM ,CKD CABG 1996EF 63 %Diagnostik Angio RCA distal CTO stent patent, LM stenosis 95%, LAD CTO, LCx CTO. LIMA Patent, SVG-RCA total oklusi, SVG-LCx total oklusi, LIMA patentProprietary and Confidential. AstraZeneca 2011. Document intended for internal discussion purposes.Atherothrombosis: A Generalized and Progressive Disease

Unstable angina MI Ischemic stroke/TIACritical leg ischemiaIntermittentclaudicationCV deathACSAtherosclerosisStable angina/Intermittent claudicationAtherothrombosisAdapted from Libby P. Circulation 2001; 104: 365372Smooth muscleand collagenFrom first decadeFrom third decadeFrom fourth decadeGrowth mainly by lipid accumulationThrombosis,haematoma5Atherosclerosis is an ongoing process affecting mainly large- and medium-sized arteries; it can begin in childhood and progresses throughout a persons lifetime.1Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected.Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms.2A large rupture typically results in the formation of a large thrombus that completely occludes the vessel, resulting in an acute vascular event. A smaller rupture may result in a mural thrombus that partially or transiently occludes the artery, causing acute ischemia and, in the long term, contributing to progression of atherothrombosis.

ReferencesJager A, Stehouwer CDA. Early detection of diabetic and non-diabetic subjects with increased cardiovascular risk: new risk indicators. Heart and Metabolism. Available at: www.heartandmetabolism.org/HMScardiac_metabolism.htm. (Last accessed 3 March, 2003).Rauch U et al. Ann Intern Med. 2001; 134: 224238.Activated platelets are central to thrombus formation in ACSPlatelets do 3 things that promote thrombus formation :Adhesion Activation Aggregation

Plaque rupture leads to platelet adhesion to the exposed subendotheliumAdherent platelet become activatedActivated platelets aggregate and assemble a critical mass of activated, pro-thrombotic platelet membrane at the site of injury213Vorchheimer DA, et al. Mayo Clin Proc. 2006;81:59-68; Davies MJ. Heart. 2000;83:361-366.

Platelets play a key role in the development of thrombus, which happens via a 3-step process: adhesion, activation, and aggregation[Vorchheimer 2006:A,B,C] Thrombosis involves interactions among the endothelium, the plaque, and the blood platelets[Brogan 2002:A] When the endothelium over a plaque becomes eroded or the plaque ruptures, the subendothelium, which is highly thrombogenic, is exposed to arterial blood flow[Brogan 2002:A]In the case of plaque rupture, the lipid core of the plaque also has thrombotic properties; a thrombus forms over the plaque when activated platelets adhere to the exposed subendothelium[Brogan 2002:A]

Vorchheimer DA, et al. Mayo Clin Proc. 2006;81:59-68.Brogan GX. Acad Emerg Med. 2002;9:1029-1044.

ACS with persistent ST segment elevationACS without persistent ST segment elevationTroponin Elevated Troponin Elevated or not Rupture plaque or erosionDifferent degrees of superimposed thrombosisDistal embolizationMyocardial underperfusion


ACS with persistent ST segment elevationACS without persistent ST segment elevationManagement :Primary PCIFibrinolytic Management :Risk StratificationOptimal DAPTEarly invasiveRupture plaque or erosionDifferent degrees of superimposed thrombosisDistal embolizationMyocardial underperfusion

8GRACE RISK SCORENon-ST elevation acute coronary syndrome PredictorScoreAge, years< 40040 - 491850 - 593660 - 695570 - 79738091PredictorScoreHeart Rate , beats/min< 70070-89790-10913110 - 14923150 - 19936> 20046PredictorScoreSystolic Blood Pressure (mmHg)< 806380 9958100 - 11947120 - 13937140 - 15926160 - 19911> 2000PredictorScoreCreatinine (mol/L)0 - 34235 70571 1058106 14011141 17614177 35323 35431PredictorScoreKillip classI0II21III43IV64PredictorScoreCardiac arrest at admission 43Elevated cardiac markers15ST Segment deviation30Khalill R et al. Exp Clin Cardiol.2009; 14(2): e25 e30GRACE RISK SCORE

Khalill R et al. Exp Clin Cardiol.2009; 14(2): e25 e30Importance of Primary Care Physician role in ACS managementPlay a major role in the early care of acute myocardial infarctionOften the first to be contacted by patientsWhat GP should do Can perform and interpret the ECGAlert EMSAdminister opioids and antithrombotic drugs (including fibrinolytic)Undertake defibrillation if neededSteg PG, et al. European Heart Journal. 2012;33:2569-2619 EARLY DIAGNOSIS AND TREATMENT10-questions strategy in selecting oral antiplatelet in ACSFirst Medical ContactCath LaboratoryICU and Long TermQ#1:ACS Diagnosis doubtfulQ#1:Definite ACSAdmit to ICCUContinue diagnostic testsNo antiplatelet therapyQ#2 : STEMI ?Q#4 : Invasive strategy for NSTE-ACS ?Q#3 : Reperfusion ?Aspirin : oral 150-300 or IV 80-150 mgNo ReperfusionReperfusionClopidogrel 75 mgAge 75 : Clopidogrel 300 mgAge > 75 : Clopidogrel 75 mgTicagrelor 180 mg Or Clopidogrel 600 mg if high bleeding riskThrombolysisPrimary PCIProbable non InvasiveDefinite InvasiveTicagrelor 180 mgOr clopidogrel 75 mg if high bleeding riskTicagrelor 180 mgOr Clopidogrel 600 mg if high bleeding riskConfirmed non invasiveSwitch to invasiveQ#5 : Large thrombus burden?Yes : ThrombectomyLow Bleeding Risk ?If yes, then GPIIb/IIIa inhibitor according to renal functionIf yes, continue Ticagrelor 90 mg/12h if ongoing OR switch from clopidogrel to ticagrelor 90 mg/12h.If no, Clopidogrel 75 mg/d if ongoing OR discuss switch from Prasugrel to ClopidogrelConfirmed ACS ?If not, stop DAPTQ#8 : normal coronary arteries?Q#7 : Adequate antiplatelet Rx for PCI ?Q#6 : Surgery ?Q#10 : Stent Thombosis Risk ?Q#9 : Low Bleeding Risk ?Clopidogrel pre RxNo ClopidogrelClopidogrel or switch to Ticagrelor Discuss Tirofiban or EptifibatideTicagrelor or ClopidogrelDiscuss Tirofiban or EptifibatideStop P2Y12 :Clopidogrel or ticagrelor 5 days before. Resume DAPT after CABGFrancois Schiele and Nicolas Meneveau. European Heart Journal: Acute Cardiovascular Care 1(2) 170176Dual Antiplatelet Therapy is the STANDARD for ACSHamm CW et al. Eur Heart J 2011;32:2999 3054Recommendation Class & levelAspirin should be given to all patients without contraindications at an initial loading dose of 150300 mg, and at a maintenance dose of 75100 mg daily long-term regardless of treatment strategy.1 AA P2Y12 inhibitor should be added to aspirin as soon as possible and maintained over 12 months, unless there are contraindications such as excessive risk of bleeding.1 ADaysCumulative Hazard0. 0.96 (0.85-1.08)P = 0.489ASA 81-100 mgASA 300-325 mg

Mehta SR et al. N Engl J Med. 2010;10:930-42ESC STEMI GUIDELINES : P2Y12 InhibitorP2Y12 inhibitor is recommended in addition to aspirin : TicagrelorKelasLevel1BKelasLevel1CSteg GS et al. doi:10.1093/eurheartj/ehs215Aspirin oral or iv (if unable to swallow) is recommendedKelasLevel1BClopidogrel, preferably when prasugrel or ticagrelor are either not available or contraindicatedNSTEMI ACS Guidelines : P2Y12 InhibitorClopidogrel (300-mg loading dose, 75-mg daily dose) is recommended for patients who cannot receive ticagrelor orprasugrel.A 600-mg loading dose of clopidogrel (or a supplementary 300-mg dose at PCI following an initial 300-mg loadingdose) is recommended for patients scheduled for an invasive strategy when ticagrelor or prasugrel is not an option.KelasLevel1AKelasLevel1BHamm CW, et al. European Heart Journal (2011) 32, 29993054Ticagrelor (180-mg loading dose, 90 mg twice daily) is recommended for all patients at moderate-to-high risk of ischaemic events (e.g. elevated troponins) , regardless of initial treatment strategy and including those pre-treated with clopidogrel (which should be discontinued when ticagrelor is commenced).KelasLevel1BLimitation of clopidogrelDual antiplatelet therapy (DAPT) with aspirin & clopidogrel is the current standard treatment in patients with ACS1With or without ST segment elevation1Poor platelet inhibition response to clopidogrel is seen in approximately 15% - 40% of patients2Contribute to residual high risk of recurrent resultsClopidogrel has slow onset of action1Prodrug that requires conversion to active metabolite1Variable metabolism results in interindividual variability in inhibition of platelet agregation1

1. Bassand JP . European Heart Journal Supplements (2008