Etiology and Pathogenesis

Several processes can result in an oxygen supply inadequate to meet myocardial demand, the hallmark of ACS. Most patients with an ACS share a common underlying pathophysiology: rupture of an atherosclerotic coronary artery plaque followed by the acute formation of a nonobstructive thrombus (Fig. 13-1). Plaque erosion, characterized by adherence of a thrombus to the plaque surface without an associated disruption of the plaque, is another mechanism of coronary thrombosis. Autopsy series have shown that the prevalence of plaque erosion—as opposed to plaque rupture—as the primary event in ACS is 25% to 40%. The frequency of plaque erosion is higher in women than in men.

Figure 13-1 Atherogenesis: unstable plaque formation.

Atherosclerotic lesions, composed primarily of a lipid-rich core and a fibrous cap, are extraordinarily common in adults and are present in most major arteries. Autopsy and intravascular ultrasound studies have confirmed the presence of coronary atherosclerotic lesions in most asymptomatic individuals older than 20 to 30 years of age. Why some plaques rupture and others do not is not entirely understood, although plaques prone to rupture do share certain characteristics. The presence of large, eccentric lipid cores and large numbers of inflammatory macrophages are common findings in fissured or ruptured plaques. The role of inflammatory cells and mediators that can effect the degradation and weakening of the protective fibrous cap is probably a critical component in ACS pathogenesis. The majority of lesions rupture at the site of greatest mechanical stress—shoulder regions where the fibrous cap is adjacent to normal intima—which are also often the site of greatest inflammatory activity. Importantly, neither the size of the plaque nor the degree of luminal obstruction caused by it correlates with the risk of rupture. In fact, nearly two thirds of plaques that subsequently rupture were lesions that resulted in stenoses at that site of less than 50%. In fact, the majority of atherosclerotic plaques that rupture are not flow-restricting, representing a stenosis of less than 70%. Thus, there is at most only partial overlap between the types of atherosclerotic lesions that would result in limiting angina (and be appropriate for surgical or percutaneous revascularization) and the less flow-limiting, more inflammatory atherosclerotic plaques that are most prone to rupture.

Other less common but important etiologies of ACS include intense focal spasm of epicardial coronary arteries (Prinzmetal angina) and conditions in which myocardial ischemia is secondary to a pathologic process extrinsic to the coronary arteries. Examples of the latter include an increase in myocardial oxygen demand secondary to tachycardia or fever or a decrease in myocardial oxygen supply due to systemic hypotension, severe anemia, or hypoxemia. These etiologies can result in a pattern of accelerating angina, particularly in individuals with significant underlying coronary atherosclerosis.

As illustrated in Figure 13-2, there are important differences in the pathophysiology of non–ST-elevation versus ST-elevation MI. The treatment of these two entities, and the long-term sequelae are also different.

Figure 13-2 Manifestations of myocardial infarction.

Clinical Presentation

Three principal presentations for ACS have been described: (1) angina that commences with a patient at rest, (2) new onset of severe angina (associated with minimal exertion), and (3) a distinct change in the frequency, duration, or threshold of a patient’s prior chronic angina pattern. However, the clinical presentation of ACS can vary considerably in different patients. Up to one third of patients subsequently proven to have an MI do not have chest pain at all, and an even larger number present with chest pain symptoms that are not clearly cardiac in description. The likelihood of an atypical presentation is increased in very young or old patients, in patients with diabetes, and in women.

Differential Diagnosis

The clinical manifestations of myocardial ischemia can be mimicked by many other processes (see also Chapter 1). Musculoskeletal disorders involving the cervical spine, shoulder, ribs, and sternum can result in nonspecific chest discomfort and even pain syndromes that are similar to angina pectoris. Symptoms from gastrointestinal causes, including esophageal reflux with associated spasm, peptic ulcer disease, and cholecystitis, are often indistinguishable from angina. Intrathoracic processes such as pneumonia, pleurisy, pneumothorax, aortic dissection, and pericarditis can produce chest discomfort. Finally, panic attacks and hyperventilation are neuropsychiatric syndromes that can be mistaken for ACS.

Diagnostic Approach

Electrocardiogram

The resting ECG is a key component for assessment of patients with suspected ACS. ST-segment and T-wave changes are the most reliable electrocardiographic indicators of myocardial ischemia (Fig. 13-2). Twelve-lead electrocardiography, performed when symptoms are present, is particularly valuable. Ideally, recordings should be obtained while symptoms are and are not present. When possible, the ECG tracing should be compared with a previous tracing, taken in the absence of chest discomfort. If transient ST-segment or T-wave changes are identified, the patient probably has acute myocardial ischemia.

It is important to note, however, that a normal ECG does not exclude ACS in a patient with symptoms of myocardial ischemia. Numerous studies suggest that 5% to 15% of patients with chest pain who are ultimately diagnosed with MI or unstable angina had a normal initial ECG.

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