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ACS

ACS. Rogers Kyle, MD 10/2/12. Learning Objectives. Define Acute Coronary Syndrome (ACS) Review the diagnostic approach to suspected ACS Review the rationale for risk stratification in ACS Outline initial management of ACS Examine antithrombotic options in ACS. Define ACS

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ACS

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  1. ACS Rogers Kyle, MD 10/2/12

  2. Learning Objectives • Define Acute Coronary Syndrome (ACS) • Review the diagnostic approach to suspected ACS • Review the rationale for risk stratification in ACS • Outline initial management of ACS • Examine antithrombotic options in ACS

  3. Define ACS • UA, NSTEMI, STEMI • Evaluation • Initial evaluation • CP characteristics, EKG, biomarkers

  4. Defining ACS • Chest pain - rest, new, increasing • 1/3 none (n/v, syncope, palps, dyspnea) • Old, female, DM • Less intervention, increased mort (JAMA 2000;284 (7):835)

  5. ECG • STEMI • Peaked T (localized inc K+) • J point elev with concave ST • ST elev, convex (no LVH, LBBB) • 2mm in men, 1.5mm women precordial • 1mm in other leads • ST-T merge • OR new LBBB • RV infarct, post-MI

  6. NSTEMI • Down-sloping ST ≥ 0.05 mV in 2 contig leads • And/or T wave inversion ≥ 0.1 mV in 2 contig leads with prominent R or R/S > 1 • Requires biomarker

  7. Non-Diagnostic • 45% (normal in 20%) • Repeat at 20-30 min interval with continued pain

  8. Biomarkers • Troponin • Increased sens/spec over CK-MB • Other causes: • Demand ischemia – O2 demand/supply mismatch • Demand – tachy, pre/after load, inc O2 consumption peripherally • Supply – tachy, hypotension, increased filling pressures, hypoxia • Ex - Critical illness, tachy, LVH, vasospasm, CVA/ICH • Direct injury • Defib shock, infiltrative disorders, chemoRx, inflam

  9. CHF • Strain 2/2 vol/pressure overload • Cell death 2/2 neurohumoral stim, cytokines • Pulmonary disease • PE, Pulm HTN • CKD • Burns • Other

  10. Management • UA/NSTEMI vs. STEMI • Complex, frequent updates

  11. Management ACS • Initial Evaluation • Pain relief • Assess hemodynamics – HTN/↓ BP, tachy/brady • Estimate risk (TIMI score) • Management strategy • STEMI – lytics vs. PCI • UA/NSTEMI – conservative vs. invasive strategy; if invasive, early vs. delayed • Antithrombotics (antiplt and anticoag) • Beta blocker (except when high risk for shock – age > 70, SBP < 120, HR > 110/<60) • IV vs. PO • CCB • Statin, ACE/ARB (AMI, EF < 40%, DM, HTN…?all), aldosterone antag (EF < 40%, CHF)

  12. STEMI • Focused update 2009 • Pain relief • Hemodynamic assessment • PCI vs. lytics • Early risk stratification (TIMI score) - ↑ age, ↓ BP, ↑ HR, CHF, AMI – the higher the risk the more beneficial PCI vs. lytics • Antithrombotic/antiplatelet therapy • β-blocker • 2007…2012 update on β-blocker – oral within first 24 hrs if no contraindications; IV only if hypertensive and no contraindications • Statin/ACE/aldosterone antag

  13. STEMI Lancet 2003; 361: 13

  14. STEMI • Factors determining reperfusion strategy – Thrombolysis vs. PCI • If early in presentation (< 3 hrs) AND If door to balloon time < 90 min → PCI • > 90 min from PCI → lytics • If PCI related delay < 60 min → PCI; if > 60 min → lytics • “high risk” STEMI → PCI • If between 3-12 hrs → PCI; lytics if PCI related delay ‘significantly greater than’ 120 min • Beyond 12 hrs– no lytics (F XIII) • If no response to lytics → transfer for PCI • If responds to lytics → transfer for PCI ASAP (Transfer-AMI, NEJM; 360:2705-18)

  15. TIMI Risk Score STEMI Circulation 2000; 102:2031

  16. TIMI Risk Score STEMI Circulation 2000; 102:2031

  17. STEMI • Factors determining reperfusion strategy – Thrombolysis vs. PCI • If early in presentation (< 3 hrs) AND If door to balloon time < 90 min → PCI • > 90 min from PCI → lytics • If PCI related delay < 60 min → PCI; if > 60 min → lytics • “high risk” STEMI → PCI • If between 3-12 hrs → PCI; lytics if PCI related delay ‘significantly greater than’ 120 min • Beyond 12 hrs– no lytics (F XIII) • If no response to lytics → transfer for PCI • If responds to lytics → transfer for PCI ASAP (Transfer-AMI, NEJM; 360:2705-18)

  18. STEMI • Initial therapy • O2, reperfusion strategy • Antiplatelet therapy • ASA 162-325mg (ISIS-2) + P2Y12 (clopidogrel, ticlopidine, prasugrel or ticagrelor) + PPI if GIB risk • Lytics – clopidogrel (others not studied) • For PCI - prasugrel favored over clopidogrel(NEJM 07) – but more bleeds…and ticagrelor too (NEJM 09) • IIb/IIIa inhibitors – depends…on antitcoag (bival vs. hep + IIb/IIIa) and use of P2Y12 (no) and IV vs. intracoronary and agent used (abciximab, eptifibitide, tirofiban); PCI only

  19. STEMI • Anticoagulants • PCI (typically d/c’d at end of procedure) • UFH – continue if already begun and add IIb/IIIa or switch to bivalrudin • Lovenox – continue; + IIb/IIIa • Fondaparinux – switch to bivalrudin • Bivalrudin – superior to UFH + IIb/IIIa (HORIZONS-AMI, NEJM 2008; 358:2218-30) • Lytics • UFH, Lovenox, fondaparinux

  20. UA/NTEMI • Focused update 2007…and 2011, 2012 • Risk stratification • Immediate high risk – shock, overt CHF, persistent angina, unstable vent. Arrhythmias • Early invasive strategy – 4-48 hrs – TIMI Risk Score (moderate to high risk = score ≥ 3)*

  21. Estimate Risk – TIMI Risk Score

  22. Anti-ischemic/analgesic therapy • O2 (Cochrane Review) • Nitrates – SL x 3, then IV if still with pain or htn, chf. (careful with ↑HR, ↓BP, RV infarct, AS/HOCM, viagra) (GISSI-3, ISIS-4); no mortality benefit • MSO4 – relieve pain, anxiety; don’t mask angina • Β-blockers – 40% mortality benefit; no ISA (metoprolol, atenolol); iv or po(avoid with active bronchospasm, brady, pulm edema, ↓BP, ±cocaine) • CCB – if ischemia despite max β –blockade or if contrainicated • Statin – atorvastatin 80mg prior to d/c; LDL < 70

  23. UA/NSTEMI – anti-thrombotic therapy

  24. UA/NSTEMI – anti-thrombotic therapy • Antiplatelet therapy • ASA 162 – 325 mg → 75 – 100 mg QD • Clopidogrel if ASA intol • P2Y12 receptor blockers • Add to ASA (CURE. NEJM 2001;345:494) • If conservative strategy – clopidogrel/ticagrelor ± IIb/IIIa (high risk patients) • Invasive strategy (TIMI ≥ 3) • Before PCI – clopidogrel/ticagrelor OR IIb/IIIa (unless on bivalrudin) • At PCI – clopidogrel/prasugrel/ticagrelorOR IIb/IIIa • If initial conservative becomes high risk and goes to angio - clopidogrel/ticagrelorOR IIb/IIIa • if no angio and on ASA/clopidogrel/ticagrelor – can add IIb/IIIa

  25. Prasugrel – • better than clopidogrel if going to PCI (TRITON TIMI-38. NEJM 2007;357:2001). • No worry with omeprazole (not CYP2C19) • Not for pts with prior TIA/CVA, ≥ 75 yrs, < 60 kg • Especially good in DM

  26. Ticagrelor • Better than clopidogrel - PLATO trial (NEJM 2009; 361:1045); + mortality benefit • All ACS, PCI or conservative • Very small excess bleeding • Reversible P2Y12 (vs. clopidogrel, prasugrel) – effects gone in couple of days. • ASA interferes so use < 100 mg/d

  27. UA/NSTEMI – anti-thrombotic therapy • Anticoagulation • UFH 60-70 U/kg (5000 max) → 12 U/kg/hr, PTT 50-75 • Enoxaparin – 1 mg/kg Q12 (vs. UFH - may be a little better in conservative strategy)(JAMA 2004; 292:45) • Fondaparinux – 2.5 mg (non-invasive strategy only) • Bivalrudin – 0.1mg/kg → 0.25mg/kg/hr (really only used during cath ≈ UFH + IIb/III) • No lytics in UA/NSTEMI

  28. References • Jneid H. et al. (2012) 2012 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction. J Am CollCardiol60: 646-681. • Kushner, FG, et al. (2009) 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction. Circulation 120: 2271-2306. • Antman, EM, et al. (2000) The TIMI Risk Score for Unstable Angina/Non-ST Elevation MI JAMA 284 (7): 835-842. • Morrow, DA, et al. (2000) TIMI Risk Score for ST-Elevation Myocardial Infarction. Circulation 102: 2031-2037. • Wiviott, SD, et al. (2007) Prasugrelversus Clopidogrel in Patients with Acute Coronary Syndromes (TRITON–TIMI 38 Investigators) N Engl J Med 357(20): 2001-2015. • Wallentin, L. (2009) Ticagrelorversus Clopidogrel in Patients with Acute Coronary Syndromes. N Engl J Med 361(11): 1045-1057.

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