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A 38-year-old woman arrived at the emergency department by private car complaining of substernal chest pain and nausea. Symptoms were relieved after administration of 2 sublingual nitroglycerin tablets. Electrocardiogram (ECG) demonstrated nonspecific T-wave changes, and initial troponin level was normal. Physical examination and chest x-ray were unremarkable. She was admitted for observation. Her second troponin level was elevated, and an echocardiogram showed anterior wall hypokinesis consistent with non–ST-segment elevation myocardial infarction (NSTEMI). She does not have diabetes, hypertension, or hyperlipidemia and has no family history of premature myocardial infarction. Coronary angiography showed narrowing in the left anterior descending coronary artery (Figure 19-1). Intravascular optical coherence tomography (OCT) confirmed intramural hematoma consistent with spontaneous coronary artery dissection (SCAD) (Figure 19-2). SCAD is nonatherosclerotic disruption and/or intramural hematoma of the coronary artery wall that can obstruct coronary blood flow and cause myocardial ischemia and/or infarct. Since the patient was pain free and hemodynamically stable, no intervention was performed. She was treated with baby aspirin, β-blockade, and low-dose nitrates. She had an uncomplicated hospital course and was dismissed after monitoring for 5 days.
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Previously considered rare, SCAD is increasingly recognized as an important cause of acute coronary syndrome (ACS) and sudden cardiac death.
SCAD primarily occurs in younger people with few or no risk factors for coronary heart disease, in contrast to atherosclerotic myocardial infarction (MI).
It most commonly affects women (74%-92%) at mean age of 42 to 52 years.1-4
It is the etiology of 10% to 20% of MIs in women <55 years old.2,5,6
It is the most common cause of pregnancy-associated MI.7
As much as 18% of SCAD occurs during the peripartum period.1
SCAD patients are commonly (25%-86%) found to have a systemic arteriopathy, most often fibromuscular dysplasia (FMD).4,8-10
Survival is generally high among patients who survive to hospital admission.1
Recurrent SCAD or MI is relatively common, and no secondary preventive measures have been identified.1
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ETIOLOGY AND PATHOPHYSIOLOGY
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The underlying causes and mechanisms of SCAD are uncertain. The female predominance suggests a sex-based or hormonal influence. It is likely that there is no single etiology for SCAD, and instead, the coronary arterial tear and/or intramural hematoma is a result of a combination of both a vulnerable patient and vulnerable coronary artery. Hypotheses for underlying mechanism include the following:
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