Right Ventricular Infarction: Pathogenesis of Low Output

Abstract

Right ventricular myocardial infarction (RVMI) is being recognized with increasing frequency because of better understanding of the hemodynamic consequences of RV dysfunction and of the availability of the improved techniques of diagnosis. Isolated RVMI in the absence of left ventricular myocardial infarction is rare, and the incidence is only 3–4% in the autopsy studies [1]. However, the frequency of RVMI in association with left ventricular infarction is more frequent and the incidence in the postmortem hearts of patients dying of acute myocardial infarction ranged from 14 to 44% [2–5]. The clinical incidence of RVMI is high and in patients with inferior wall myocardial infarction, involvement of the free wall of the right ventricle can be documented in up to 40% of patients [6]. Although a proximal right coronary artery occlusion is invariably present, RV necrosis occurs uncommonly in the absence of stenosis of the left anterior descending coronary artery, suggesting that the left to right collaterals play a role in the genesis and extent of RVMI. Preexisting RV hypertrophy and RV systolic hypertension may be associated with a greater extent of RV myocardial necrosis with acute right coronary artery occlusion. Thus, several anatomic and pathophysiologic factors may contribute to the extent of RVMI and the severity of hemodynamic compromise.