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Vasc Health Risk Manag. 2010 Jun 1;6:387-97.

Heart rate control with adrenergic blockade: clinical outcomes in cardiovascular medicine.

Author information

  • 1Heart Failure/Transplant and VAD Programs, Minneapolis Heart Institute, Minneapolis, Minnesota 55407, USA. dfeldman@mplsheart.com

Abstract

The sympathetic nervous system is involved in regulating various cardiovascular parameters including heart rate (HR) and HR variability. Aberrant sympathetic nervous system expression may result in elevated HR or decreased HR variability, and both are independent risk factors for development of cardiovascular disease, including heart failure, myocardial infarction, and hypertension. Epidemiologic studies have established that impaired HR control is linked to increased cardiovascular morbidity and mortality. One successful way of decreasing HR and cardiovascular mortality has been by utilizing beta-blockers, because their ability to alter cell signaling at the receptor level has been shown to mitigate the pathogenic effects of sympathetic nervous system hyperactivation. Numerous clinical studies have demonstrated that beta-blocker-mediated HR control improvements are associated with decreased mortality in postinfarct and heart failure patients. Although improved HR control benefits have yet to be established in hypertension, both traditional and vasodilating beta-blockers exert positive HR control effects in this patient population. However, differences exist between traditional and vasodilating beta-blockers; the latter reduce peripheral vascular resistance and exert neutral or positive effects on important metabolic parameters. Clinical evidence suggests that attainment of HR control is an important treatment objective for patients with cardiovascular conditions, and vasodilating beta-blocker efficacy may aid in accomplishing improved outcomes.

KEYWORDS:

adrenergic beta-antagonists; heart failure; hypertension; myocardial infarction

PMID:
20539841
PMCID:
PMC2882891
[PubMed - indexed for MEDLINE]
Free PMC Article
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