Papillary Muscle Rupture

Excerpt

Papillary muscle rupture is a rare and potentially fatal complication often following a myocardial infarction or secondary to infective endocarditis. Acute rupture frequently results in severe mitral valve regurgitation and subsequent acute life-threatening cardiogenic shock and pulmonary edema.

There are 5 papillary muscles in the heart originating from the ventricular walls. These muscles attach to the tricuspid and mitral valve leaflets via the chordae tendineae and functionally prevent regurgitation of ventricular blood via tensile strength by preventing prolapse or inversion of the valves during systole. Three of these papillary muscle and chordae tendineae complexes are attached to the tricuspid valve (anterior, posterior, septal), and 2 are attached to the mitral valve (anterolateral and posteromedial). Papillary muscle dysfunction leads to regurgitation of blood through the valves causing backflow of blood that can lead to left or right-sided heart failure.

Literature first identified papillary muscle rupture as early as 1948. Visualization via 2-dimensional echocardiography was first reported in 1981. Transesophageal echocardiography was first used in 1985 in identifying the condition.

The classic scenario is that of a patient with an MI involving the posterior descending coronary artery who develops sudden decompensated heart failure on days 2-7 after the infarction. The competence of the mitral valve is maintained by the actions of the anterolateral and posteromedial papillary muscles. The anterolateral muscle has a dual blood supply, whereas the posteromedial muscle has blood supply only from the posterior descending coronary; thus in most patients, it is the posteromedial papillary muscle that will rupture following an MI.

Without surgical treatment, mortality is very high.