Pathophysiology of Chronic Heart Failure

Heart failure is a progressive disorder that is initiated after an event either damages the heart muscle, with resultant loss of functioning cardiac myocytes, or disrupts the ability of the myocardium to contract normally. This event may have an abrupt onset, as in the case of a myocardial infarction; a gradual onset, as in the case of hemodynamic pressure or volume overloading; or it may be hereditary.1

The neurohormonal imbalance associated with chronic heart failure is a contributing factor to the progression of the disease. Overactivation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS), as well as other systems, contributes to cardiac remodeling and decline in heart function; the normal counterregulatory beneficial effects of the natriuretic peptide system (NPS)—one of the most important counterregulatory neurohormonal systems—are diminished in heart failure.1-4

In addition, emerging research suggests that inflammation may play a role in the progression of structural heart failure and cardiac remodeling. Circulating levels of proinflammatory cytokines including TNF and IL-6 are increased in patients with heart failure and correlate with adverse patient outcomes.1

Are chronic heart failure patients "stable" or silently progressing?

*Other compensatory mediators include adrenomedullin, prostaglandin E, bradykinin, etc.1


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