Current concepts for the neurohormonal management of left ventricular dysfunction after myocardial infarction

Abstract

The importance of addressing neurohormonal activation in patients after a myocardial infarction is now well-appreciated. Inhibition of the renin-angiotensin-aldosterone axis and the sympathetic nervous system can result in improved cardiac function and survival. As we learn more about other systems, we should be able to realize further benefits. In particular, the roles of endothelin, matrix metalloproteinases, and cytokines in remodeling are being investigated, with the potential to result in better outcomes for patients.

Reinforcing a Continuum of Care: In-Hospital Initiation of Long-Term Secondary Prevention Following Acute Coronary Syndromes

“…β-blockers prevent myocyte apoptosis induced by intracellular calcium accumulation resulting from prolonged or heightened adrenergic activity [23]. In addition, these agents restore adrenergic sensitivity by reversing β-adrenergic receptor down-regulation, and have anti-inflammatory activity, mediated by a decrease in tumor necrosis factor-α and interleukin-1 levels.…”

“…Increased wall tension subjects the remaining viable myocardium to further stress, resulting in myocyte hypertrophy and apoptosis, progressive distortion of normal chamber geometry, and impaired systolic function. ACE inhibition improves cardiovascular outcomes following MI, in part, by inhibiting the maladaptive postinfarction remodeling process [23,27].…”