Acute Myocardial Infarction

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Chapter 28 Acute Myocardial Infarction

Cameron Donaldson, MD , Harold L. Dauerman, MD

1 Who is at risk for acute myocardial infarction (AMI)?

image Nonmodifiable: older age, noncardiac atherosclerotic disease, first-degree relative with early atherosclerosis (male age < 55 years, female age < 65 years).

image Modifiable: diabetes mellitus; hypertension; smoking; elevated low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides; C-reactive protein; lipoprotein (a); low HDL; hypertriglyceridemia; metabolic syndrome; sedentary lifestyle; atherogenic diet.

image Unclear: In more than 10% of patients, no obvious risk factor is seen for coronary artery disease (CAD).

2 What causes an AMI?

Coronary arterial atherosclerotic plaque with a thin fibrous cap is the ideal substrate for myocardial infarction (MI). Shear stress created by turbulent flow through an irregular, diseased segment of coronary artery can result in sudden rupture of this thin-capped vulnerable plaque. Procoagulants from the plaque’s lipid core are extruded into the bloodstream, forming an occlusive thrombus at the site of insult. Plaque rupture accounts for roughly three quarters of fatal AMIs. The remaining 25% are due to erosion of the endothelial monolayer, uncovering a nidus for clot formation and extension into the arterial lumen.

3 How are patients typically seen initially with an AMI?

image Severe retrosternal pressure with radiation to arms, neck, or jaw. Usually ≥ 30 minutes in duration and associated with dyspnea, weakness, or diaphoresis. May be provoked by exertion, emotional stress, or extreme temperatures.

image Rales, diaphoresis, hypotension, bradycardia or tachycardia, and transient murmur of mitral regurgitation are potential physical findings, though the examination results are most often unremarkable.

image The key considerations in differential diagnosis are aortic dissection, pulmonary embolism, and pericarditis.

4 Which biomarkers diagnose AMI?

The recently adopted universal definition of AMI includes elevation in cardiac biomarkers above the 99th percentile of the upper reference limit. See Table 28-1.

Table 28-1 Biomarkers to Diagnose AMI

image

5 How do you diagnose an ST-elevation MI (STEMI)?

image New left bundle branch block or ≥ 1-mm ST elevations in two or more contiguous leads. Absence of these electrocardiogram (ECG) changes leads to the alternative diagnosis: non–ST-elevation MI (NSTEMI). Both types of MI demonstrate positive cardiac biomarkers.

image Formation of a fibrin-rich red clot, which adheres to activated platelets, causing total occlusion of the affected artery and probable transmural infarction.

image This syndrome was formerly termed Q-wave MI, but this terminology has been abandoned in favor of the more specific STEMI term.

6 In whom does cardiogenic shock develop?

image Shock complicating MI is most common among elderly patients.

image Criteria for cardiogenic shock include persistent hypotension with a systolic blood pressure < 90 mm Hg, cardiac index < 1.8 L/min1/m2, left ventricular end-diastolic pressure > 18 mm Hg, or need for pressors or hemodynamic support.

image Causes of cardiogenic shock include ventricular septal rupture, free wall or papillary muscle rupture, large MI, and nonischemic causes (myocarditis, takotsubo cardiomyopathy, valvular heart disease).

7 What is the prognosis of a patient with AMI and out-of-hospital cardiac arrest?

image The cause of cardiac arrest is AMI in ≥ 50% of patients. Other causes include nonischemic causes of arrhythmias (i.e., nonischemic cardiomyopathy).

image Approximately 40% of patients with cardiac arrest may survive to hospital discharge. Predictors of discharge from hospital include witnessed arrest, initial ventricular tachycardia or ventricular fibrillation, bystander cardiopulmonary resuscitation, cooling or hypothermia, younger age, male sex, acute myocardial ischemia or heart failure, early invasive management of CAD, and absence of comorbidities.

8 You diagnose a STEMI at a rural clinic without a catheterization laboratory; what do you do?

Reperfusion via percutaneous coronary intervention (primary PCI) is the preferred treatment for STEMI. A clear mortality benefit exists if this is done within 90 minutes of first contact with the medical system. In this case, door to balloon time is expected to exceed 120 minutes, and reperfusion should be achieved with fibrinolytics. In addition to fibrinolysis, adjunctive therapy with heparin, aspirin, and clopidogrel (600 mg) is warranted. Recent trials have demonstrated that a pharmacoinvasive approach leads to decreased risk of recurrent ischemia and infarction; thus all patients in the postlytic period should be transferred for cardiac catheterization and possible revascularization.

9 Which antithrombotic therapy should be administered to the patient in question 8?

After receiving fibrinolytics, choices of anticoagulant include weight-based dosing of unfractionated heparin, enoxaparin, or fondaparinux. The most common regimen in patients being referred for early catheterization is unfractionated heparin, along with aspirin and clopidogrel. If the patient is being transferred for primary PCI, bivalirudin is an alternative to heparin-based therapy.

10 Which antiplatelet therapies are indicated for the patient in question 8?

Aspirin (162-325 mg followed by 81 mg daily) and clopidogrel (600 mg loading dose followed by 75 mg daily) are the mainstays of antiplatelet therapy in STEMI and are indicated in our patient, who received full-dose fibrinolytic therapy. In the primary PCI population only, prasugrel (60 mg loading dose followed by 10 mg daily) reduces stent thrombosis compared with clopidogrel but is contraindicated in patients with prior stroke or transient ischemic attack. Addition of glycoprotein inhibition of platelets to unfractionated heparin or as bailout after bivalirudin (for slow flow in the culprit artery) is also possible.

11 Which patients with unstable angina or NSTEMI have the highest mortality?

Thrombolysis in Myocardial Infarction (TIMI), Global Registry of Acute Coronary Events (GRACE), and Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin (PURSUIT) are risk stratification schemes that aid in patient selection for early invasive versus conservative therapies. The TIMI risk score is composed of seven variables: age ≥ 65 years, three or more CAD risk factors, aspirin use within a week, two or more episodes of severe angina in the past day, elevated cardiac biomarkers, ST deviation ≥ 0.5 mm, and known ≥ 50% coronary stenosis. The presence of three variables indicates intermediate risk (13% chance of death, MI, or need for urgent revascularization within 14 days), and five or more predicts a doubling of this risk.

12 You are evaluating a patient with unstable angina. What patient characteristics would sway you to choose an early referral to the catheterization laboratory and possible invasive revascularization?

See Table 28-2.

Table 28-2 Risk Factors Associated with Referral for Invasive Management Strategy

image

13 What medications do you start in a patient initially seen with an NSTEMI?

Aspirin (162-325 mg) should be administered to every patient. Intermediate- or high-risk patients should receive clopidogrel (300 or 600 mg) plus weight-adjusted unfractionated heparin, renal function–adjusted enoxaparin, or bivalirudin. In patients with renal insufficiency or elevated bleeding risk, bivalirudin may be recommended instead of heparin-glycoprotein inhibitors. For the early invasive strategy, pretreatment with a statin may decrease periprocedural infarction. Prasugrel (60 mg) should be loaded after coronary angiography and may be given in place of clopidogrel as long as the patient is not at high risk for bleeding (defined as age ≥ 75 years, previous stroke, or weight ≤ 60 kg). Relief of chest pain may be achieved with nitrates and morphine but should alert the care team to a high-risk situation. Ongoing chest pain should warrant consideration for emergent catheterization because it may represent coronary occlusion and progression to STEMI.

14 Your AMI patient is ready to go home. What prescriptions do you consider at discharge?

Dual antiplatelet therapy should be continued in patients after MI, with clopidogrel (75 mg daily) 1 year after all acute coronary syndromes (STEMI, NSTEMI, or unstable angina) and aspirin (81 mg daily) indefinitely. More recently, 12 months of the new P2Y12 receptor antagonists (prasugrel) has been shown to decrease risk of recurrent ischemic events in patients with acute coronary syndrome, as compared with the older P2Y12 platelet receptor antagonist, clopidogrel, but with an increased risk of bleeding. β-Blockers, statins (goal LDL < 70 mg/dL), and angiotensin-converting enzyme (ACE) inhibitors (regardless of magnitude of blood pressure reduction) reduce cardiovascular morbidity and mortality and should be initiated in hospital. In addition, ACE inhibitors may reduce the risk of development of heart failure and mortality in select patients.

15 Your AMI patient has cardiogenic shock. What is the only thing that can improve mortality?

Early revascularization is recommended in all patients with AMI complicated by shock. The Should We Emergently Revascularize Occluded Arteries for Cardiogenic Shock (SHOCK) trial randomly assigned patients with cardiogenic shock due to acute MI and left ventricular failure to early revascularization with PCI and coronary artery bypass grafting (CABG) or initial medical stabilization and balloon pump placement. The 30-day mortality rate was lower in the early revascularization group (47% vs. 56%), with significantly better mortality and quality of life up to 6 years after MI. Of note, patients surviving their shock hospitalization were remarkably healthy at 1-year follow-up; 87% were class I or II New York Heart Association heart failure (none or minimal limitation of activity due to heart failure symptoms).

16 Name the most appropriate first and second choice of vasopressor in cardiogenic shock

After PCI or early revascularization with CABG, pressors may be required for a period of time to allow hemodynamic stabilization. Dopamine and norepinephrine are the medications most often used for hypotension in cardiogenic shock. Both agents have α- and β-adrenergic properties, though to different degrees, resulting in disparate effects on renal and splanchnic perfusion. A recent multicenter randomized trial established norepinephrine as the first-line vasopressor in cardiogenic shock, with dopamine resulting in more arrhythmic events and a lower survival at 28 days. In patients with refractory hemodynamic instability, referral for left ventricular assist support devices and cardiac transplantation may be warranted.

17 What are the indications for cooling or hypothermia after AMI and cardiac arrest?

image Adult successfully resuscitated from a witnessed out-of-hospital or in-hospital cardiac arrest and now hemodynamically stable

image Patient with a presenting rhythm of ventricular fibrillation or nonperfusing ventricular tachycardia who remains comatose after restoration of spontaneous circulation

After cooling, patients should be monitored for electrolyte abnormalities, coagulation disturbances, pancreatitis, and leukopenia or thrombocytopenia. Contraindications to cooling include admission temperature < 30° C and patients who are pregnant, are terminally ill, have an inherited coagulopathy, or were comatose before arrest.

Key Points Treatment of Acute Myocardial Infarctionimage

1. Distinguish between unstable angina [UA]–NSTEMI and STEMI: STEMI is an occluded artery and requires immediate reperfusion with PCI or fibrinolysis; UA-NSTEMI requires medical therapy and invasive approach (within 4-48 hours of presentation) for all patients at increased risk.

2. Oral antiplatelet therapy should be initiated including aspirin and clopidogrel, prasugrel, or ticagrelor.

3. Antithrombotics (heparin, enoxaparin, fondaparinux, or bivalirudin) should be administered with weight- and glomerular filtration rate–adjusted dosing to avoid bleeding risks.

4. Statin, β-blocker, and ACE inhibitors should be considered in all patients with AMI regardless of baseline LDL level, blood pressure, and heart rate.

5. Revascularization (PCI, CABG) is warranted immediately (STEMI–primary PCI) or urgently (STEMI-postlytic, pharmacoinvasive approach) or within 4 to 48 hours of presentation (high-risk UA-NSTEMI).

Bibliography

1 Antman E.M., Cohen M., Bernink P.J., et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA. 2000;284:835–842.

2 Dauerman H.L. Challenges in oral antiplatelet therapy: ST-segment elevation myocardial infarction. Am J Cardiol. 2009;104(5 Suppl):39C–43C.

3 Dauerman H.L., Sobel B.E. Synergistic treatment of ST-segment elevation myocardial infarction with pharmacoinvasive recanalization. J Am Coll Cardiol. 2003;42:646–651.

4 De Backer D., Biston P., Devriendt J., et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362:779–789.

5 Holzer M. Targeted temperature management for comatose survivors of cardiac arrest. N Engl J Med. 2010;363:1256–1264.

6 Redpath C., Sambell C., Stiell I., et al. In-hospital mortality in 13,263 survivors of out-of-hospital cardiac arrest in Canada. Am Heart J. 2010;159:577–583. e1

7 Reynolds H.R., Hochman J.S. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117:686–697.

8 Sleeper L.A., Ramanathan K., Picard M.H., et al. Functional status and quality of life after emergency revascularization for cardiogenic shock complicating acute myocardial infarction. J Am Coll Cardiol. 2005;46:266–273.

9 Stone G.W., Maehara A., Lansky A.J., et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011;364:226–235.

10 Thygesen K., Alpert J.S., White H.D., et al. Universal definition of myocardial infarction. J Am Coll Cardiol. 2007;50:2173–2195.

11 White H.D., Chew D.P. Acute myocardial infarction. Lancet. 2008;372:570–584.

12 Wiviott S.D., Braunwald E., McCabe C.H., et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357:2001–2015.

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