No abstract

Cardiac injury, specifically valvular rupture, must be considered after blunt chest trauma even in previously healthy patients. Isolated mitral regurgitation (MR) and tricuspid regurgitation (TR) due to blunt chest trauma are rare phenomena. More unique is simultaneous complete papillary muscle rupture of the mitral valve (MV) and tricuspid valve (TV) with only four patients being previously reported in the literature. This case describes a patient with complete transection of the posteromedial papillary muscle of the MV with severe MR and a concomitant flail TV with severe TR following a motor vehicular accident. The importance of transthoracic and transesophageal echocardiography in the early evaluation of patients following blunt chest trauma is also highlighted by this case.

Our findings establish an important link between inflammatory cytokine gene expression, interstitial fibrosis and myocardial electrical activation delays during premature excitation and provide insight into the mechanisms by which mineralocorticoid receptor antagonism may prevent development of an arrhythmogenic ventricular substrate in systolic heart failure.

MR antagonism regresses rapid pacing-induced electrical delays, inflammatory cytokine gene activation, and fibrosis in heart failure. Ventricular arrhythmia vulnerability in heart failure is correlated with extent of fibrosis and electrical activation delays during premature excitation.