Acute myocardial infarction with normal coronary arteries: Role of coronary artery spasm and arrhythmic complications

Abstract

Myocardial infarction (MI) with normal coronary arteries is likely a multifactorial syndrome the exact cause of which remains often undetermined in individual patients. Possible mechanisms include hypercoagulable states, coronary embolism, intense sympathetic stimulation, transient coronary thrombosis and coronary artery spasm (CAS). Specifically, epicardial CAS is the unique mechanism of variant angina (VA), but it has been shown to play also an important role in the pathogenesis of other acute forms of ischemic heart disease, including unstable angina, MI and sudden death [1–3]. Although several pathogenetic hypotheses have been formulated, the predisposing factors and the mechanisms responsible for CAS remain still largely unknown. The final common pathway in these patients is thought to be a coronary hyperreactivity of coronary smooth muscle cells to various vasoconstrictor agents [4]. The importance of CAS as a cause of MI with normal coronary arteries is supported by the not negligible occurrence of MI, in patients with variant angina without any obstructive coronary artery stenosis at angiography [5,6]. Prolonged CAS and thrombotic complications at its site may variably contribute to cause acute MI in these patients. Accordingly, several studies have also shown an increased prevalence of CAS induction by provocative vasoconstrictor stimuli among patients presenting with an acute coronary syndrome different from variant angina. In large studies on unselected populations of patients undergo-