MI FAQs

Myocardial Infarction FAQ: Based on Current Guidelines and Evidence

Joonseok (“Joon”) Kim, M.D.MSU Internal Medicine PGY3

February 13, 2014

Contents

• Definition of MI• Interpretation of Troponin Elevations• MI in Critically Ill Patients• Antiplatelet Therapy in Post MI

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.

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.

CASE

• What do you want to do upon discharge?

A. Continue aspirin only and stop clopidogrelB. Continue aspirin + clopidogrel therapy for 2 weeksC. Continue aspirin + clopidogrel therapy for 1 yearD. Continue aspirin + clopidogrel therapy lifelong

In Reality…

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

Let’s Go Back to Basics

What is MI?

NSTEMI

Presentation

Working Dx

ECG

CardiacBiomarker

Final DxNQMI Qw MI

UA

UnstableAngina

Ischemic Discomfort

Acute Coronary Syndrome

Myocardial Infarction

ST Elevation

No ST Elevation

Non-ST ACS

Libby P. Circulation 2001;104:365, Hamm CW, Bertrand M, Braunwald E, Lancet 2001; 358:1533-1538; Davies MJ. Heart 2000; 83:361-366. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 1. Reprinted with permission.

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

ACC/AHA

• 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

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.



• 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.



• 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.



• 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.



• 9. Regardless of the etiology of troponin elevation (or associated disease state), troponin elevation offers incremental prognostic value.



Troponin I Levels to Predict the Riskof Mortality in Acute Coronary Syndromes

35Antman EM, et al. N Engl J Med 1996;335:1342.

Crude mortality rates at 42 days in patients with ACS

• 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.



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


• 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



• It is often a challenge for the clinician, caring for a critically ill patient with severe single organ or multi-organ 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.


Antiplatelet Therapy

Class I Benefit >>> Risk

Procedure/ Treatment SHOULD be performed/ administered

Class IIa Benefit >> RiskAdditional studies with focused objectives needed

IT IS REASONABLE to perform procedure/administer treatment

Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful

Procedure/Treatment MAY BE CONSIDERED

Class III Risk ≥ BenefitNo additional studies needed

Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL

shouldis recommendedis indicatedis useful/effective/

beneficial

is reasonable

can be useful/effective/ beneficial

is probably recommended or indicated

may/might be consideredmay/might be reasonableusefulness/effectiveness

is unknown /unclear/uncertain or not well established

is not recommendedis not indicatedshould notis not

useful/effective/beneficial

may be harmful

Applying Classification of Recommendations and Level of Evidence

ACC/AHA Recommendations

Class I Benefit >>> Risk

Procedure/ Treatment SHOULD be performed/ administered

Class IIa Benefit >> RiskAdditional studies with focused objectives needed

IT IS REASONABLE to perform procedure/administer treatment

Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful

Procedure/Treatment MAY BE CONSIDERED

Class III Risk ≥ BenefitNo additional studies needed

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

Applying Classification of Recommendations and Level of Evidence

ACC/AHA Recommendations

Antithrombotic Trialists’ Collaboration. BMJ 2002;324:71–86

Category % Odds ReductionAcute MIAcute CVA Prior MIPrior CVA/TIAOther 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

1.00.50.0 1.5 2.0 Control better Antiplatelet better

*Aspirin was the predominant antiplatelet agent studied**Include MI, stroke, or death

Aspirin reduces the risk of adverse cardiovascular events

Aspirin Evidence: Secondary Prevention

Aspirin (75-162 mg daily) if known CAD† or NSTE-ACS‡

Aspirin (81-325 mg daily) following PCI or fibrinolytic therapy for a STEMI*

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;58:2432-2446Wright RS et al. JACC 2011;57:e215-367

O’Gara PT et al. JACC 2013;61:e78-e140Jneid H et al. JACC 2012;60:645-681

I IIaIIbIII

I IIaIIbIII

I IIaIIbIII

Aspirin Recommendation: Secondary Prevention

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)

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

I IIaIIbIII

I IIaIIbIII

I IIaIIbIII


Aspirin (100-325 mg daily) following CABG surgery

Hillis LD et al. JACC 2011;58:e123-210

I IIaIIbIII


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

Dual antiplatelet therapy is more efficacious in NSTE-ACS

3 6 90 12

Rat

e of

CV

dea

th,

myo

card

ial i

nfar

ctio

n,

or s

trok

e

P<0.001

Months of Follow Up

CURE Trial Investigators. NEJM 2001;345:494-502

Aspirin + Placebo

Aspirin + Clopidogrel

Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) Trial

DAPT Recommendation: Secondary Prevention

2,116 patients undergoing PCI randomized to 4 weeks of DAP* followed by aspirin (75-325 mg) monotherapy vs. persistent DAP* for 1 year

DAP therapy produces greater benefit when used for 1 year

Steinhubl S et al. JAMA 2002;288:2411-2420

0 123 6 90

Ris

k of

MI,

stro

ke,

or d

eath

(%

)

27% RRR, P=0.02

10

5

15 4 weeks of DAP*

Months from Randomization

1 year of DAP*

Clopidogrel for the Reduction of Events during Observation (CREDO) Trial


COMMIT Collaborative Group. Lancet 2005;366:1607-1621

9% relative risk reduction (P=.002)

(10.1%)(9.2%)

Days Since Randomization (up to 28 days)

Dea

th,

MI,

or

Str

oke,

%

10

9

8

7

6

5

4

3

0

0

In-H

ospi

tal M

orta

lity,

%

Days Since Randomization (up to 28 days)

(8.1%)(7.5%)

7% relative risk reduction (P=.03)

7 14 21 28 7 14 21 280

8

7

6

5

4

3

2

1

0

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

DAPT produces greater benefit in medically managed STEMI patients


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

Jneid H et al. JACC 2012;60:645-681

I IIaIIbIII

I IIaIIbIII

I IIaIIbIII

*In PCI treated patients


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

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;60:645-681O’Gara PT et al. JACC 2013;61:e78-e140

I IIaIIbIII

I IIaIIbIII

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

Continuation of a P2Y12 receptor antagonist beyond 1 year may be considered in patients undergoing drug eluting stent placement

I IIaIIbIII

I IIaIIbIII

Kushner F et al. JACC 2009;54:2205-2241Jneid H et al. JACC 2012;60:645-681

O’Gara PT et al. JACC 2013;61:e78-e140


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.

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.

• What do you want to do upon discharge?

A. Continue aspirin only and stop clopidogrelB. Continue aspirin + clopidogrel therapy for 2 weeksC. Continue aspirin + clopidogrel therapy for 1

yearD. Continue aspirin + clopidogrel therapy lifelong

Back to Initial Case…

Q & A

• Thank you for your attention

MI FAQs

Education

Transcript of MI FAQs