Idiopathic dilated cardiomyopathy. Elastic parallel element dysfunction as a physiopathological hypothesis for ventricular failure.

Abstract

BACKGROUND: Idiopathic dilated cardiomyopathy is a disease of unknown etiology, although the viral-immunologic pathogenesis has recently emerged as an important hypothesis. Its distinctive anatomopathologic features are: macroscopically, a great ventricular dilation with little hypertrophy, and microscopically marked diffuse interstitial fibrosis not observed in other pathologic entities with dilation. Hemodynamically, its main characteristic is a progressive loss of the systolic function, although the diastolic function is also impaired. To date it is accepted that in dilated states ventricular remodeling occurs due to sliding of fiber with a maximal sarcomere distention; it is also assumed that the ventricular dysfunction is due to a primary deficit in contractility caused by the injury and loss of myocites. HYPOTHESIS: The aggressive agent mainly attacks the interstitial tissue, thus damaging the elastic parallel element structures. This results in a loss of absorbing power during diastole, starting a progressive dilation which results in maximum sarcomere distention, and compromises the ventricular function. The organ response is to create a new parallel element, which results in an increased fibrosis which also compromises this function.