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ACS and Thrombosis in the Emergency Setting NSTEMI ACS Diagnosis Flow Chart ADMISSION CHEST PAIN WORKING DIAGNOSIS ACUTE CORONARY SYNDORME ECG persistent ST-elevation BIO-CHEMISTRY DIAGNOSIS STEMI ST/Tabnormalities normal or undetermined ECG troponin rise/fall troponin normal NSTEMI Unstable Angina European Heart Journal 2011; 32, 2999-3054 (ESC Guidelines for Management of ACS in patients without ST elevation) Q1: Do you routinely use and rely on an ischemic pain assessment protocol? a)Yes b) No Chest Pain 9% of all ER Visits (1) → 25-40% admitted → 13-23% have Acute Coronary Syndrome(1) → < 5% have STEMI (2) → < 25% Non STE ACS (3) → 75% “non-ACS chest pain” No gold standard for diagnosis Almost no follow-up data Many have atypical symptoms Missed MI rates (2-3%) (4) Missed MI associated with 2x higher mortality (4,) http://www.cdc.gov/nchs/data/databriefs/db43.pdf JAMA. 1993;270:1211–1216 Medicine 2009;88:307–313 N Engl J Med. 2000;342:1187–1195 Ann Intern Med. 1998; 129:845– 855 N Engl J Med 2000; 342:1163–1170 Am J Cardiol 1991; 68:171–17 Am J Cardiol 1987;60:219-24 Life Threatening Causes of Chest Pain Myocardial infarction Unstable angina Takotsubo Cardiomyopathy Thoracic aortic dissection Pulmonary embolus Tension pneumothorax Oesophageal rupture Assessment of Chest Pain: Asking the Right Questions Is the chest pain likely due to myocardial ischemia ? Has there been an acute coronary event ? Is there a precipitating cause ? ie Type 2 MI Recent onset AF Anemia / blood loss Sepsis Hypotension Are there high risk clinical features? Q2: If troponin I results upon this patient's admission were normal (0.02 ng/mL), what would be your next evaluation and treatment steps? a) Continue observing this patient and repeat troponin and ECG tests b) Consider additional diagnostic tests/biomarkers c) Initiate phone consult with a cardiologist if available Criteria for Acute Myocardial Infarction Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin) with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following: Ischaemic symptoms; ECG changes of new ischaemia (new ST-T changes or new LBBB); Development of pathologic Q waves in the ECG: Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality; Identification of an intracoronary thrombus by angiography or autopsy. www.escardio.org/guidelines European Heart Journal (2012) 33:2551-2567 doi: 10.1093/eurheartj/ehs 184. Applications of Troponin Testing Cardiac Troponin (cTn) Highly specific for myocardial injury Myocardial Injury NOT specific for Acute Coronary Syndromes with Ischemia induced injury Occurs in multiple other conditions Associated with worse prognosis ACS treatment not needed: May be harmful High Sensitivity Troponin (hs cTn) eg Roche Cobas cTnT, Siemens Stratus Ultra cTnI Increased sensitivity for detection of ACS Patients with negative standard Tn and symptoms of ACS 64% hs cTnI +ve Increased diagnostic accuracy especially for patients presenting early after symptom onset 84% positive at presentation with <3hrs symptoms vs 55% with previous Troponin T assay Potentially lower specificity for diagnosis of ACS Greater number of patients without ACS have elevated cTn Highlights importance of clinical evaluation Use of hs Troponin Use the 99th percentile of the ref population as cTn URL Diagnosis of AMI requires significant change of Tn with serial testing. Significant change > 20% if baseline markedly elevated If around URL 200% change needed Blood sampling at baseline and 3 hrs later. Repeat at 6hrs if 3hr value unchanged and clinical suspicion is high cTn marker of myocardial necrosis and not specific maker of AMI. Diagnosis of AMI only with significant change of cTn and clinical scenario (symptoms and or ECG) European Heart Journal 2011; 32, 2999-3054 (ESC Guidelines for Management of ACS in patients without ST elevation) Elevations of Cardiac Troponin Values Because of Myocardial Injury INJURY RELATED TO PRIMARY MYOCARDIAL ISCHAEMIA (TYPE 1 MI) INJURY NOT RELATED TO MYOCARDIAL ISCHAEMIA Plaque rupture. Cardiac contusion, surgery, ablation, pacing, or Intraluminal coronary artery thrombus defibrillator shocks. Rhabdomyolysis with cardiac involvement. Myocarditis. Cardiotoxic agents, e.g. anthracyclines, herceptin. formation. INJURY RELATED TO SUPPLY/DEMAND IMBALANCE OF MYOCARDIAL ISCHAEMIA (TYPE 2 MI) Tachy-/brady-arrhythmias. MULTIFACTORIAL OR INDETERMINATE MYOCARDIAL INJURY Aortic dissection or severe aortic valve disease. Heart failure. Hyperthrophic cardiomyopathy. Stress (Takotsubo) cardiomyopathy. Cardiogenic, hypovolaemic, or septic shock. Severe pulmonary embolism or pulmonary Severe respiratory failure. Severe anaemia. Hypertension with or without LVH. Coronary spasm. Coronary embolism or vasculitis. Coronary endothelial dysfunction without significant CAD. hypertension. Sepsis and critically ill patients. Renal failure. Severe acute neurological diseases, e.g. stroke, subarachnoid haemorrhage. Infiltrative diseases, e.g. amyloidosis, sarcoidosis. Strenuous exercise. www.escardio.org/guidelines European Heart Journal (2012) 33:2551-2567 doi: 10.1093/eurheartj/ehs 184. Q3: What is your risk-stratification scale/method of choice? a) TIMI b)GRACE Predicting Ischemic Outcomes Indicators of Increased Risk for Recurrent Ischemic Events ACS RISK BACKGROUND RISK Clinical Multiple episodes of chest pain Heart failure / hypotension Refractory ischemia Age ECG ST segment shift T wave inversion > 2mm VT Renal dysfunction Biomarkers Troponin > reference level LV function Diabetes Pre-existing CAD Early Risk Stratification in Acute Coronary Syndromes ED Clinical observations ECG on presentation Recurrent ischemia Bio-markers of myocyte injury Risk scores (TIMI or GRACE) LATER Myocardial perfusion LV function Coronary anatomy Risk Scores HISTORY TIMI Age Hypertension Diabetes Smoking ↑ Cholesterol Family history Documented CAD GRACE Age Severe angina Aspirin within 7 days Heart rate Systolic BP Elevated creatinine Heart failure Cardiac arrest Elevated markers ST-segment deviation Elevated markers ST-segment deviation PRESENTATION GRACE = Global Registry of Acute Coronary Events; TIMI = Thrombolysis in Myocardial Infarction. Antman EM, et al. JAMA 2000;284:835–42. Eagle KA, et al. JAMA 2004;291:2727–33. TIMI Risk Score for Prediction of Cardiac Events in ED Patients with Chest Pain 10 prospective cohort ED based studies with 17265 patients Linear relationship between TIMI risk score and cardiac outcome TIMI score 0 - 1.8% (20/1000) had cardiac event by 30 d TIMI risk score provides guidance but should not be used as sole means of determining patient disposition. Clinical assessment based on history, ECG and troponin should be fully evaluated before using TIMI risk score Hess et al: CMAJ 2010;182:1039 Bleeding Risk Assessment Bleeding risk factors similar to ischemia risk factors Identify patients at higher bleeding risk Prior bleeding history Age (> 75) Female gender Small body weight (<65kg) Renal dysfunction References: www.barnabashealth.org/services/cardiac/.../cohenwhitepaper09.pdf Q4:Which antiplatelet agent would you add to ASA and why? a) Clopidogrel b) Prasugrel c) Ticagrelor Q5:Which anticoagulant would you choose and why? a) Unfractionated heparin b) Low molecular weight heparin (enoxaparin) c) Fondaparinux Antiplatelet / Anticoagulant Therapy in ACS Available antiplatelet and anticoagulant therapies According to Invasive Strategy CLINICAL SCENARIO EARLY INVASIVE INITIAL CONSERVATIVE ASPIRIN ASPIRIN UPSTREAM ORAL ANTIPLATELET Ticagrelor Clopidogrel Clopidogrel Prasugrel Ticagrelor Fondaparinux Enoxaparin Unfractionated heparin ANTICOAGULANT PERIPROCEDURE Ticagrelor Clopidogrel Fondaparinux Enoxaparin Unfractionated heparin (Adapted from http://effectivehealthcare.ahrq.gov/index.cfm/search-for-guides-reviews-and-reports/?productid=954&pageaction=displayproduct) PLATO Study Design NSTEMI ACS (moderate-to-high risk) STEMI (if primary PCI) (N=18,624) Clopidogrel-treated or naive; randomized <24 hours of index event 1,261 patients underwent CABG on study drug for ≤7 days prior to surgery CLOPIDOGREL If pre-treated, no additional loading dose; if naive, standard 300 mg loading dose, then 75 mg qd maintenance; (additional 300 mg allowed pre-PCI) TICAGRELOR 180 mg loading dose, then 90 mg bid maintenance; (additional 90 mg pre-PCI) 6–12 months treatment Primary endpoint: CV death + MI + Stroke Primary safety endpoint: Total major bleeding Recommendations for patients undergoing CABG: Study drugs withheld prior to surgery – 5 days for clopidogrel and 24–72 hours fors ticagrelor. Study drug be restarted as soon as possible after surgery and prior to discharge Wallentin et al N Engl J Med 2009;361:1045-57 Comparison of Ticagrelor with Clopidogrel Primary Endpoint : Cardiovascular Death, MI or Stroke PLATO CUMULATIVE INCIDENCE (%) 13 12 11.7 Clopidogrel 11 10 9.8 9 Ticagrelor 8 7 6 5 4 16% 21% MI CV death 3 2 1 p=0.005 p=0.001 HR 0.84 (95% CI 0.77–0.92), p=0.0003 0 0 60 Wallentin et al N Engl J Med 2009;361:1045-57 120 180 240 300 360 DAYS Non-CABG and CABG-related Major Bleeding PLATO KAPLAN-MEIER ESTIMATED RATE (% PER YEAR) NS 9 7.9 8 Ticagrelor Clopidogrel 7.4 NS 7 6 5 4 5.8 p=0.026 5.3 4.5 3.8 p=0.025 2.8 3 2.2 2 1 362 vs. 306 221 vs. 177 619 vs. 654 446 vs. 476 NON-CABG PLATO MAJOR BLEEDING NON-CABG TIMI MAJOR BLEEDING CABG PLATO MAJOR BLEEDING CABG TIMI MAJOR BLEEDING 0 Wallentin et al N Engl J Med 2009;361:1045-57 Ticagrelor vs Clopidogrel Improved outcomes CV Death, MI, Stroke (NNT 54) CV death Benefit in STEMI, diabetes, reduced renal function Administered at first medical contact No harm with prior stroke (non hemorrhagic) Applicable in all ACS scenarios except fibrinolysis Off target adverse effects uncommon and mild Q6:This patient returns to the ER 5 days later complaining of the shortness of breath. How would you manage this patient upon ER readmission? a) Discontinue ticagrelor b) Assess for heart failure and advise continuation of ticagrelor c) Administer diuretic Q7: If the patient had bradycardia (HR=43bpm) and a history of sick sinus syndrome would this change your choice of antiplatelet therapy? a) Yes b) No Off Target Adverse Effects of Ticagrelor Dyspnea PLATO Ticagrelor 13.8% placebo 7.8%, 0.8% discontinued ONSET OFFSET Ticagrelor 38.6%, clopidogrel 9.3%, placebo 8.3% • Most mild, lasted < 24hrs, occurred within 1st week Evaluate for signs of heart failure, no need to stop ticagrelor Ventricular pauses Holter monitoring in 2866 PLATO patients 1st week: pauses >3 secs ticagrelor 5.8%, clopidogrel 3.6% Usually occurred during sleep, No clinical consequences After 1 month no pauses Brilinta® (ticagrelor) Product Monograph, Date of Preparation: March 07, 2013; Wallentin et al N Engl J Med 2009;361:1045-57 Initiating Ticagrelor from Clopidogrel in Nonresponders IPA (20μmol/L 100 Adp-induced Maximum 90 Aggregation) % 80 Clopidogrel Ticagrelor Ticagrelor Clopidogrel 70 60 50 40 30 20 10 0 0 .5 1 2 4 8 hr Day 1 PERIOD 1 Gurbel et al: Circulation 2010; 121:1188-1199 0 2 4 8 hr Day 14 CROSSOVER 0 .5 1 2 4 8 hr Day 15 PERIOD 2 0 2 4 8 hr Day 28 NSTE ACS Management Identify from history, ECG and cTn Initiate treatment with dual antiplatelet therapy with ASA + clopidogrel, or ASA + ticagrelor. Initiate anticoagulation with UFH, enoxaparin or fondaparinux Patients with high risk ACS will usually follow an early invasive management strategy