Microvascular and epicardial endothelial dysfunction are highlighted as key pathophysiological mechanisms in patients presenting with angina or myocardial infarction despite normal coronary angiograms.
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May inform endothelial assessment in angina/MI with normal coronaries; leaves open targeted therapy trials.
Chest pain with normal coronary angiograms is a relatively common syndrome. The mode of presentation of this syndrome includes patients with syndrome X and patients with an acute myocardial infarction and angiographically normal coronary arteries. Different mechanisms have been proposed to elucidate the exact cause and to explain the various clinical presentations in these patients. Abnormalities of pain perception and the presence of oesophageal dysmotility have all been reported in patients with syndrome X. In situ thrombosis or embolization with subsequent clot lysis and recanalization, coronary artery spasm, cocaine abuse, and viral myocarditis have been described as potential mechanisms responsible for an acute myocardial infarction in patients with angiographically normal coronary arteries. Recent data suggest that both microvascular and epicardial endothelial dysfunction may play an important role in the pathophysiological mechanism of the syndrome of stable angina or acute myocardial infarction with normal coronary arteries.
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Sztajzel et al. (2000) studied this question.
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