MI FAQs

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Definition of MI
Dual antiplatelet therapy in secondary prevention

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  • There is a lot of gray area that cannot be explained by the guidelines, but it is very important to know at least what the guidelines suggest to do.
  • Let’s go back to the basics
  • Traditional definition of MI / explain slide / the downside of this definition is, that we don’t know what happened or why this pt had MI even after making a final diagnosis.
  • That is one of the main reasons why ACC/AHA and ESC came up with a 3rd universal definition of MI consensus doc.
  • Historically, before the biomarker era,
  • Infarction / ischemia
  • However, in the real world, we see elevated (so called indeterminant) trop every single day. Should we call all of them MI? the answer is no.
  • MI FAQs

    1. 1. Myocardial Infarction FAQ : Based on Current Guidelines and Evidence Joonseok (“Joon”) Kim, M.D. MSU Internal Medicine PGY3 February 13, 2014
    2. 2. Contents • • • • Definition of MI Interpretation of Troponin Elevations MI in Critically Ill Patients Antiplatelet Therapy in Post MI
    3. 3. CASE • A 56-year-old man is admitted to the hospital with new-onset substernal chest pressure. Medical history is remarkable for hyperlipidemia. He is a cigarette smoker. His medications are aspirin and atorvastatin. • On physical examination, the patient is afebrile, blood pressure is 132/78 mm Hg, pulse rate is 82/min and regular, and respiration rate is 14/min. No jugular venous distention is noted, the lungs are clear to auscultation, no murmur or gallop is heard, and no peripheral edema is noted.
    4. 4. CASE • On admission, cardiac troponin I level was 1.2 ng/mL (1.2 µg/L); on hospital day 2 it peaks at 8.4 ng/mL (8.4 µg/L). An electrocardiogram on arrival to the emergency department demonstrated a nonspecific ST-T wave abnormality, but no ST-segment elevation or depression. He began receiving metoprolol, clopidogrel, and intravenous heparin. • Cardiac catheterization demonstrates overall preserved left ventricular systolic function with diffuse severe disease of the distal portion of all three major epicardial vessels. No catheter-based intervention is performed.
    5. 5. CASE • What do you want to do upon discharge? A. Continue aspirin only and stop clopidogrel B. Continue aspirin + clopidogrel therapy for 2 weeks C. Continue aspirin + clopidogrel therapy for 1 year D. Continue aspirin + clopidogrel therapy lifelong
    6. 6. In Reality…
    7. 7. Since 2011… • AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update • ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations • 2012 ACCF/AHA Focused Update of the Guideline for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction • 2012 Third Universal Definition of Myocardial Infarction • 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction
    8. 8. Let‟s Go Back to Basics What is MI?
    9. 9. Presentation Working Dx ECG Cardiac Biomarker Final Dx Ischemic Discomfort Acute Coronary Syndrome No ST Elevation Non-ST ACS UA NSTEMI ST Elevation Unstable Myocardial Infarction Angina NQMI Qw MI 10 Libby P. Circulation 2001;104:365, Hamm CW, Bertrand M, Braunwald E, Lancet 2001; 358:1533-1538; Davies MJ. Heart 2000; 83:361366. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 1. Reprinted with permission.
    10. 10. Causes of UA/NSTEMI • Thrombus or thromboembolism, usually arising on disrupted, or eroded plaque • Occlusive thrombus, usually with collateral vessels • Subtotal occlusive thrombus on pre-existing plaque • Distal microvascular thromboembolism from plaque-associated thrombus • Thromboembolism from plaque erosion • Non–plaque-associated coronary thromboembolism • Dynamic obstruction (coronary spasm or vasoconstriction) of epicardial and/or microvascular vessels • Progressive mechanical obstruction to coronary flow • Coronary arterial inflammation • Secondary UA • Coronary artery dissection DeWood MA, et al. N Engl J Med 1986;315:417–23; Braunwald E. et al. Circulation 1998;98:2219–22; Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157
    11. 11. ACC/AHA
    12. 12. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 1. Even though elevated troponin is a sensitive and specific indication of cardiac myonecrosis, by itself, it does not indicate a myocardial infarction (MI) (myonecrosis due to ischemia) or any specific etiology. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    13. 13. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 2. The ‘Third Universal Definition of Myocardial Infarction’ (2012) classifies 5 types of MI: Type 1 is termed spontaneous, related to ischemia due to a primary coronary event (e.g., plaque rupture); Type 2 is secondary to increased oxygen demand or decreased supply; Type 3 is associated with sudden unexpected cardiac death; Type 4a is associated with percutaneous coronary intervention (PCI); Type 4b is associated with stent thrombosis; and Type 5 is associated with coronary artery bypass grafting (CABG) surgery. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    14. 14. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 3. An elevated troponin level that is „smoldering‟ and relatively constant over an appropriate sampling interval is more likely to be caused by chronic diseases (e.g., heart failure) versus ischemia. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    15. 15. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 4. A 20% change at 3-6 hours from the baseline value may be suggestive of MI. That said, there is insufficient evidence to provide concrete guidelines on how to differentiate between acute coronary syndrome (ACS) and non-ACS ischemia-induced troponin elevations without accounting for the clinical circumstances. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    16. 16. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 5. It is imperative to incorporate troponin testing into global risk assessment. Those patients with an elevated troponin and a high pretest probability of ACS are most likely to derive benefit from a treatment strategy that targets coronary thrombosis. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    17. 17. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 9. Regardless of the etiology of troponin elevation (or associated disease state), troponin elevation offers incremental prognostic value. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    18. 18. Troponin I Levels to Predict the Risk of Mortality in Acute Coronary Syndromes Crude mortality rates at 42 days in patients with ACS 35 Antman EM, et al. N Engl J Med 1996;335:1342.
    19. 19. 10 Points to Remember from an Expert Consensus Document on Interpretation of Troponin Elevations • 10. Troponin may be a useful tool to detect chemotherapy-associated cardiac toxicity, and may have a role in informing the use of treatment in those patients who develop cardiac myonecrosis following high-dose chemotherapy. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. JACC 2012
    20. 20. Myocardial Infarction in the ICU • Elevations of troponin values are common in patients in the intensive care unit and are associated with adverse prognosis, regardless of the underlying disease state. Third Universal Definition of Myocardial Infarction, JACC 2012
    21. 21. Myocardial Infarction in the ICU • Some elevations may reflect MI type 2 due to underlying CAD and increased myocardial oxygen demand • Other patients may have elevated values of cardiac biomarkers, due to myocardial injury with necrosis induced by catecholamines or direct toxic effect from circulating toxins • Moreover, in some patients, MI type 1 may occur Third Universal Definition of Myocardial Infarction, JACC 2012
    22. 22. Myocardial Infarction in the ICU • It is often a challenge for the clinician, caring for a critically ill patient with severe single organ or multiorgan pathology, to decide on a plan of action when the patient has elevated cTn values. • If and when the patient recovers from the critical illness, clinical judgment should be employed to decide whether—and to what extent—further evaluation for CAD or structural heart disease is indicated. Third Universal Definition of Myocardial Infarction, JACC 2012
    23. 23. Antiplatelet Therapy
    24. 24. Applying Classification of Recommendations and Level of Evidence Class I Class IIa Class IIb Class III Benefit >>> Risk Benefit >> Risk Additional studies with focused objectives needed Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Risk ≥ Benefit No additional studies needed Procedure/ Treatment SHOULD be performed/ administered should is recommended is indicated is useful/effective/ beneficial IT IS REASONABLE to perform procedure/administer treatment is reasonable can be useful/effective/ beneficial is probably recommended or indicated Procedure/Treatment MAY BE CONSIDERED may/might be considered may/might be reasonable usefulness/effectiveness is unknown /unclear/uncertain or not well established Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL is not recommended is not indicated should not is not useful/effective/benefici al may be harmful ACC/AHA Recommendations
    25. 25. Applying Classification of Recommendations and Level of Evidence Class I Class IIa Class IIb Class III Benefit >>> Risk Benefit >> Risk Additional studies with focused objectives needed Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpful Risk ≥ Benefit No additional studies needed Procedure/ Treatment SHOULD be performed/ administered IT IS REASONABLE to perform procedure/administer treatment Procedure/Treatment MAY BE CONSIDERED Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluated Level C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated ACC/AHA Recommendations
    26. 26. Aspirin Evidence: Secondary Prevention Category Acute MI Acute CVA Prior MI Prior CVA/TIA Other high risk CVD (e.g. unstable angina, heart failure) PAD (e.g. intermittent claudication) High risk of embolism (e.g. Afib) Other (e.g. DM) All trials % Odds Reduction 0.0 0.5 Antiplatelet better 1.0 2.0 1.5 Control better Aspirin reduces the risk of adverse cardiovascular events *Aspirin was the predominant antiplatelet agent studied **Include MI, stroke, or death Antithrombotic Trialists’ Collaboration. BMJ 2002;324:71–86
    27. 27. Aspirin Recommendation: Secondary Prevention I IIaIIbIII Aspirin (75-162 mg daily) if known CAD† or NSTE-ACS‡ I IIaIIbIII Aspirin (81-325 mg daily) following PCI or fibrinolytic therapy for a STEMI* I IIaIIbIII Aspirin (preferentially at 81 mg daily) following PCI for a NSTE-ACS# or a STEMI* or fibrinolytic therapy for a STEMI* Smith SC Jr. et al. JACC 2011;58:2432-2446 Wright RS et al. JACC 2011;57:e215-367 O’Gara PT et al. JACC 2013;61:e78-e140
    28. 28. Aspirin Recommendation: Secondary Prevention I IIaIIbIII I IIaIIbIII Aspirin (162-325 mg daily) for at least 1 month after bare metal stent implantation (Class I, Level B), at least 3 months after sirolimus-eluting stent implantation (Class I, Level B), and at least 6 months after paclitaxel-eluting stent implantation (Class I, Level B) after which aspirin (75-162 mg daily) should be continued indefinitely (Class I, Level A for a bare metal stent and Class I, Level B for a drug eluting stent) I IIaIIbIII Aspirin (75-162 mg daily) as the initial dose after stent implantation in those at higher bleeding risk King SB 3rd et al. JACC 2008;51:172-209
    29. 29. Aspirin Recommendation: Secondary Prevention I IIaIIbIII Aspirin (100-325 mg daily) following CABG surgery Hillis LD et al. JACC 2011;58:e123-210
    30. 30. DAPT Recommendation: Secondary Prevention Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) Trial Rate of CV death, myocardial infarction, or stroke 12,562 patients with NSTE-ACS randomized to daily aspirin (75-325 mg) or clopidogrel (300 mg load, 75 mg thereafter) plus aspirin (75-325 mg) for 9 months Aspirin + Placebo Aspirin + Clopidogrel P<0.001 0 3 6 9 12 Months of Follow Up Dual antiplatelet therapy is more efficacious in NSTE-ACS CURE Trial Investigators. NEJM 2001;345:494-502
    31. 31. DAPT Recommendation: Secondary Prevention Clopidogrel for the Reduction of Events during Observation (CREDO) Trial Risk of MI, stroke, or death (%) 2,116 patients undergoing PCI randomized to 4 weeks of DAP* followed by aspirin (75-325 mg) monotherapy vs. persistent DAP* for 1 year 15 4 weeks of DAP* 10 1 year of DAP* 5 27% RRR, P=0.02 00 3 6 Months from Randomization 9 12 DAP therapy produces greater benefit when used for 1 year Steinhubl S et al. JAMA 2002;288:2411-2420
    32. 32. DAPT Recommendation: Secondary Prevention Clopidogrel and Metoprolol in Myocardial Infarction (COMMIT) Trial 45,852 patients presenting within 24 hours of STEMI treated medically and randomized to aspirin and clopidogrel (75 mg daily) vs. aspirin only Death, MI, or Stroke, % 9 8 7 6 5 4 9% relative risk reduction (P=.002) 3 0 (8.1%) (7.5%) 8 In-Hospital Mortality, % (10.1%) (9.2%) 10 7 6 5 4 3 2 7% relative risk reduction (P=.03) 1 0 0 7 14 21 28 Days Since Randomization (up to 28 days) 0 7 14 21 28 Days Since Randomization (up to 28 days) DAPT produces greater benefit in medically managed STEMI patients COMMIT Collaborative Group. Lancet 2005;366:1607-1621
    33. 33. DAPT Recommendation: Secondary Prevention I IIaIIbIII I IIaIIbIII I IIaIIbIII Clopidogrel (75 mg daily; Class I, Level B), prasugrel* (10 mg daily; Class I, Level C), or ticagrelor (90 mg twice daily; Class I, Level C) if aspirin intolerance or a true aspirin allergy following a NSTE-ACS Clopidogrel (75 mg daily) or ticagrelor (90 mg twice daily) in addition to aspirin for up to 1 year following a NSTE-ACS managed conservatively *In PCI treated patients Jneid H et al. JACC 2012;60:645-681
    34. 34. DAPT Recommendation: Secondary Prevention I IIaIIbIII Clopidogrel (75 mg daily), prasugrel (10 mg daily), or ticagrelor (90 mg twice daily) in addition to aspirin for 1 year following PCI for a NSTE-ACS or a STEMI I IIaIIbIII I IIaIIbIII Clopidogrel (75 mg daily) in addition to aspirin for a minimum of 14 days (Class I, Level A) and up to 1 year (Class I, Level C) following fibrinolytic therapy for a STEMI Jneid H et al. JACC 2012;60:645-681 O’Gara PT et al. JACC 2013;61:e78-e140
    35. 35. DAPT Recommendation: Secondary Prevention I IIaIIbIII If the risk of morbidity because of bleeding outweighs the anticipated benefit afforded by a P2Y12 receptor antagonist, earlier discontinuation should be considered I IIaIIbIII Continuation of a P2Y12 receptor antagonist beyond 1 year may be considered in patients undergoing drug eluting stent placement Kushner F et al. JACC 2009;54:2205-2241 Jneid H et al. JACC 2012;60:645-681 O’Gara PT et al. JACC 2013;61:e78-e140
    36. 36. CASE • A 56-year-old man is admitted to the hospital with new-onset substernal chest pressure. Medical history is remarkable for hyperlipidemia. He is a cigarette smoker. His medications are aspirin and atorvastatin. • On physical examination, the patient is afebrile, blood pressure is 132/78 mm Hg, pulse rate is 82/min and regular, and respiration rate is 14/min. No jugular venous distention is noted, the lungs are clear to auscultation, no murmur or gallop is heard, and no peripheral edema is noted.
    37. 37. CASE • On admission, cardiac troponin I level was 1.2 ng/mL (1.2 µg/L); on hospital day 2 it peaks at 8.4 ng/mL (8.4 µg/L). An electrocardiogram on arrival to the emergency department demonstrated a nonspecific ST-T wave abnormality, but no ST-segment elevation or depression. He began receiving metoprolol, clopidogrel, and intravenous heparin. • Cardiac catheterization demonstrates overall preserved left ventricular systolic function with diffuse severe disease of the distal portion of all three major epicardial vessels. No catheter-based intervention is performed.
    38. 38. Back to Initial Case… • What do you want to do upon discharge? A. Continue aspirin only and stop clopidogrel B. Continue aspirin + clopidogrel therapy for 2 weeks C. Continue aspirin + clopidogrel therapy for 1 year D. Continue aspirin + clopidogrel therapy lifelong
    39. 39. Q&A • Thank you for your attention

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