Heart Failure Research

Heart failure, also known as congestive heart failure or CHF, is an inability of the heart to pump sufficient blood around the body.Heart failure typically occurs secondary to an existing pathology that alters cardiac function. Examples of syndromes that can precede heart failure include myocardial infarction, arrhythmia or infection. These can also cause dilated cardiomyopathy, a condition which accounts for approximately one third of all cases of heart failure. The pathogenesis of heart failure is cyclical and progressive; endogenous mechanisms, which are activated during heart failure in an attempt to counteract the symptoms, actually worsen cardiac function. Cardiac dysfunction, either systolic or diastolic, triggers a decrease in stroke volume and a resultant increase in cardiac output. In healthy individuals the body responds to decreases in cardiac output by initiating the renin-angiotensin-aldosterone system (RAAS) to promote fluid retention, and also by activating the sympathetic nervous system to cause peripheral vasoconstriction. Under normal circumstances this counteracts the imbalance in stroke volume, restoring cardiac output to normal levels. In patients with heart failure the increase in blood volume, together with the heightened peripheral resistance and elevated levels of circulating catecholamines, causes an increased load on the already weakened ventricles with each contraction, and the stroke volume does not return to normal levels. Repeated cycles of this process further weaken the ventricle walls, prompting ventricular hypertrophy and a decreased force of contraction.