Interplay Between Cardiac Function and Neurohumoral and Cytokine Systems
Myocardial injury, which may have any of a number of causes, might depress cardiac function, which in turn may cause activation of the sympathoadrenal system and the renin-angiotensin-aldosterone system and the elaboration of endothelin, arginine vasopressin, and cytokines such as tumor necrosis factor (TNF)-α. In acute heart failure (left), these are adaptive and tend to maintain arterial pressure and cardiac function. In chronic heart failure (right), they cause maladaptive hypertrophic remodeling and apoptosis, which cause further myocardial injury and impairment of cardiac function. The horizontal line on the right shows that chronic maladaptive influences can be inhibited by angiotensin-converting enzyme inhibitors, β-adrenergic blockers, angiotensin II type 1 receptor blockers, and/or aldosterone antagonists.
Reprinted with permission from Braunwald E. Normal and abnormal myocardial function, In Braunwald E et al. [eds]: Harrison’s Principles of Internal Medicine, 15th ed. New York: McGraw-Hill; 2001:1309–18.