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Acute Myocardial Infarction


Common Misconceptions

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    All patients suffering an acute myocardial infarction will complain of chest pain.

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    In evaluating a patient with a suspected acute coronary syndrome, it is important to note the severity of chest pain on a scale of 1 to 10.

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    The response of chest pain to nitroglycerin or antacids is useful in ruling in or ruling out an acute coronary syndrome as a cause of chest pain.

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    A normal electrocardiogram (ECG) rules out an acute myocardial infarction.

Pathogenesis of Acute Myocardial Infarction (MI)

Coronary Thrombosis and the Pathogenesis of Acute Myocardial Infarction

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    Although Herrick attributed fatal acute MI to a thrombotically occluded coronary artery in 1912, autopsy studies in the late 1970s did not demonstrate coronary thrombosis in patients who had died of an acute MI.

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    Thus, coronary thrombosis was considered a consequence, rather than the underlying cause, of acute MI.

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    In 1980, DeWood and colleagues reported the results of coronary angiography performed early after the onset of an acute transmural MI: within 4 hours of symptom onset, 87% of infarct-obstructed arteries were completely occluded. However, 12 to 24 hours after onset, the prevalence of coronary occlusion was only 65%.

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    When patients with subtotal occlusion of the obstructed artery were included, the prevalence of angiographically demonstrable coronary thrombosis in the first 4 hours was 98%.

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    Over the past decade, further understanding of the pathology underlying acute coronary occlusion has come from autopsy studies, angiography, and intracoronary imaging: underlying culprit soft lipid plaques, thin cap fibroatheromas, bulky plaques with characteristic erosion, and/or calcified nodules have all been found to predispose to plaque rupture and coronary occlusion ( Fig. 2.1 ).

    Fig. 2.1, The pathophysiology of acute ST elevation myocardial infarction requires thrombosis and occlusion of a coronary artery. Thrombosis is mediated by plaque rupture related to lipid pools, thin cap fibroatheroma, calcific nodules, and plaque erosion.

Diagnosis of Acute Myocardial Infarction

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    Myocardial infarction describes the process of myocardial cell death caused by ischemia or the imbalance between myocardial oxygen supply via the coronary arteries and demand.

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    In the United States each year, an estimated 1.1 million people experience an acute MI or die from coronary heart disease.

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    In 2016, it was estimated that approximately every 34 seconds one American would have a coronary event and about every 1 minute 24 seconds an individual would die from a coronary event.

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    According to the most recent World Health Organization report in 2015, coronary heart disease is the leading cause of death worldwide.

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    The early recognition and diagnosis of an acute MI are vital for the institution of therapy to limit myocardial damage, preserve cardiac function, and reduce mortality.

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    Patients can be grouped into two major categories of acute MI:

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      1. Patients with new ST segment elevation on the ECG that is diagnostic of acute ST segment elevation myocardial infarction (STEMI)

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      2. Patients with non–ST segment elevation myocardial infarction (NSTEMI) who have elevated cardiac biomarkers in an appropriate clinical setting, with or without ischemic ECG changes

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    Clinical trials have established the benefit of early reperfusion therapy in patients with STEMI and an early invasive strategy in patients with high-risk NSTEMI; thus a rapid and accurate assessment of patients with suspected acute MI is essential for optimal management.

Definition of Myocardial Infarction

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    MI is defined as myocardial necrosis caused by prolonged myocardial ischemia.

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    The diagnosis of an acute MI requires the rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value exceeding the 99th percentile of a normal reference population (the upper reference limit) and at least one of the following:

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      Symptoms of ischemia

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      ECG changes indicative of active ischemia (new ST segment–T wave changes or new left bundle branch block [LBBB]) or infarction (new pathologic Q waves)

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      3. Identification of an intracoronary thrombus by angiography or autopsy

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      4. Imaging evidence of a new regional wall motion abnormality, or new loss of viable myocardium

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    The type of acute MI can be classified further depending on the etiology of the infarct ( Table 2.1 ).

    Table 2.1
    Universal Classification of Myocardial Infarction (MI)
    Modified and adapted from Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol . 2012;60:1581–1598.
    Type Description
    1 Spontaneous MI resulting from an atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus
    2 MI associated with ischemia owing to an imbalance in myocardial oxygen supply and demand, such as in coronary endothelial dysfunction, coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension
    3 MI resulting in cardiac death, with symptoms suggestive of myocardial ischemia, accompanied by new ischemic electrocardiogram changes, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
    4a MI associated with percutaneous coronary intervention
    4b MI associated with stent thrombosis as documented by angiography or autopsy
    5 MI associated with coronary artery bypass graft surgery

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