A nurse is reinforcing teaching to a client who has restrictive cardiomyopathy (RCM). Which of the following statements should the nurse include in the client teaching to explain the cause of RCM?

Restrictive cardiomyopathy is a structural myocardial disorder characterized by rigid, non-compliant ventricular walls that severely impair diastolic filling. The rigid myocardium restricts ventricular relaxation, raising intracardiac diastolic pressures and causing backward venous congestion. While systolic function remains largely preserved early on, the stiffened ventricles cannot accommodate normal venous return volumes. A. "Your heart condition is caused by thickening of the ventricular walls and septum.": Pronounced, asymmetric muscular thickening of the left ventricular wall and interventricular septum defines hypertrophic cardiomyopathy. That condition involves cellular disarray and outflow tract obstruction, which is distinct from restrictive pathology. Hypertrophy is not the primary mechanism of restriction. B. "Your heart condition is caused by excessive stretching of the ventricles.": Pathological dilation and stretching of the ventricular chambers describe dilated cardiomyopathy, which causes severe systolic contractile failure. Restrictive cardiomyopathy features normal or reduced chamber dimensions with rigid, non-stretched walls. Ventricular stretching represents an entirely different structural disease. C. "Your heart condition is caused when the ventricular tissue becomes fibrous and fatty.": Myocardial replacement by fibrous and adipose tissue is the specific pathognomonic feature of arrhythmogenic right ventricular cardiomyopathy. Restrictive disease involves interstitial infiltration by substances like amyloid, or endomyocardial fibrosis, rather than fatty transmutation. This describes a separate genetic dystrophy. D. "Your heart condition is caused from stiffening of the walls of the ventricles.": Idiopathic fibrosis or infiltrative protein deposition decreases the elasticity of the heart muscle, making the ventricular walls exceptionally stiff. This stiffness impedes normal diastolic relaxation and filling, driving the clinical manifestations of restrictive disease. It accurately explains the core pathology.