Cardiac rupture complicating myocardial infarction

Abstract

Rupture of the ventricular free wall is a leading cause of death in patients with acute myocardial infarction (MI). There are a number of risk indicators that are associated with cardiac rupture, such as female gender, old age, hypertension, and first MI. Typical symptoms of cardiac rupture are recurrent or persistent chest pain, syncope, and distension of jugular veins. Electrocardiographic signs may include sinus tachycardia, new Q-waves in 2 or more leads, persistent or recurrent ST segment elevation, deviation of expected evolutionary T-wave pattern, and electromechanical dissociation in end-stage cases. Once patients at risk have been identified using clinical symptoms and electrocardiographic signs, a fast and sensitive diagnostic test to confirm cardiac rupture is transthoracic echocardiography (TTE). New insights in the etiology of subacute myocardial rupture suggests that defective cardiac remodeling may predispose the heart for rupture. The matrix metalloproteinase (MMP) system has been shown to play an important role in cardiac extracellular matrix (ECM) remodeling and cardiac rupture. Current therapy of cardiac rupture consists mainly of surgery, and conservative management with hemodynamic monitoring, prolonged bed rest, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors in selected cases.