An “event,” regardless of the cause, produces an initial damage and reduction of cardiomyocyte contractility in HF. The initial injury results in a reduction in cardiac output resulting in the activation of the sympathetic nervous system (SNS) which increases heart rate, cardiac contractility, and vasoconstriction (increasing norepinephrine levels). These mechanisms provide helpful support for the heart as a transitory compensation when the myocardium starts to fail. The release of renin leads to the production of angiotensin II, which, in turn, causes vasoconstriction of renal afferent arterioles, as well as the release of aldosterone, which causes an increase in sodium reabsorption.

Prolonged activation of SNS increases afterload due to sustained vasoconstriction and renin release. Unfortunately, the deleterious effects predominate over the long-term, leading to pathologic myocardial remodeling, and more rapid progression of myocardial dysfunction: VICIOUS CIRCLE OF HF