chest pain - pacemaker

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A 32-year-old woman is brought to the hospital with chest pain at rest after a party. She has had similar pain previously, primarily in the morning and rarely with exertion. The pain usually subsides spontaneously and occasionally is associated with diaphoresis but rarely dyspnea. She almost lost consciousness at work during the most recent episode. She smokes a half pack of cigarettes a week and has occasionally inhaled cocaine. She is otherwise healthy and takes no medications. She has no family history of coronary artery disease.

Her blood pressure is 128/70 mm Hg and pulse rate is 72/min. There is no neck vein distention or carotid bruits. The lungs are clear and cardiac examination reveals a normal S1 and S2 and a faint mid-systolic click but no murmur. Examination of the abdomen and extremities is normal. Electrocardiogram shows a 1-mV inferior ST-segment elevation; a subsequent electrocardiogram is normal. Serum troponin concentration is 1.5 times the upper limit of normal. Therapy with heparin, aspirin, metoprolol, and nitroglycerin is begun. The next morning, coronary angiography shows normal angiographic appearance of the arteries and normal left ventricular wall motion. The patient is prescribed a daily aspirin and encouraged to stop using cocaine.

What additional medical therapy should be prescribed at discharge?

A Angiotensin-converting enzyme inhibitor
B β-blocker
C Calcium-channel blocker
D Clopidogrel

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Key Point
Coronary artery disease vasospasm is treated with nitrates in the short term and calcium channel blockers in the long term.

This patient has a presumptive diagnosis of myocardial infarction due to vasospasm of the coronary artery. Factors favoring this diagnosis are the normal angiographic coronary arteries, use of cocaine, chest pain after a party, smoking, and the episodic ST-segment elevation with spontaneous resolution in the absence of fibrinolysis.

Other causes of myocardial ischemia or infarction in the absence of atherosclerotic coronary disease include vasculitis (scleroderma, connective tissue diseases), thromboembolism in the settings of endocarditis or paradoxical embolism, valvular disease, and hypertrophic cardiomyopathy. Spontaneous coronary artery dissection has been reported in pregnant women with or without hypertension. These conditions may produce ST-elevation myocardial infarction and should be considered in the differential diagnosis. A noncoronary cause of myonecrosis with normal coronary anatomy is atrial tachycardia. Heart rates of less than 150/min are rarely associated with limitation of coronary blood flow in young patients without significant atherosclerotic disease.

The best treatment for coronary artery vasospasm is nitrates in the short term and calcium-channel blockade over the long term. Angiotensin-converting enzyme inhibitors reduce mortality in patients with ST-segment elevation myocardial infarction and in patients with left ventricular ejection <40% following an acute myocardial infarction. This patient meets neither criteria and is unlikely to benefit from this therapy. β-blockade theoretically exacerbates coronary vasomotion by blocking the vasodilation β receptors, leaving α vasoconstrictor tone unopposed. Clopidogrel is prescribed for patients with significant atherosclerotic disease, patients after stent placement, and patients who have had a stroke related to vascular atherosclerosis.