Acute Myocardial Infarction

Published on 07/03/2015 by admin

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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)?

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

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.

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?

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.

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

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

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

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.

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

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?

Shock complicating MI is most common among elderly patients.

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.

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?

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

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