Model of a normal heart (left); and a weakened heart, with over-stretched muscle and dilation of left ventricle (right); both during diastole Heart failure is caused by any condition that reduces the efficiency of the heart muscle, through damage or overloading. Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin–angiotensin system, lead to fibrosis, dilation, and structural changes in the shape of the left ventricle from elliptical to spherical. The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a normal heart, increased filling of the ventricle results in increased contraction force by the Frank–Starling law of the heart, and thus a rise in cardiac output. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.
complications of Fabry disease
complications of Xeroderma pigmentosum
complications of Myotonic dystrophy
symptom of Glycogen storage disease type III
complications of Lesch–Nyhan syndrome
complications of Friedreich's ataxia
complications of Cat-scratch disease
complications of Okamoto syndrome