Heart rate, sympathetic cardiovascular influences, and the metabolic syndrome

Prog Cardiovasc Dis. 2009 Jul-Aug;52(1):31-7. doi: 10.1016/j.pcad.2009.05.007.

Abstract

Alterations in glucose and lipid metabolism frequently cluster with overweight, obesity as well as hypertension in the clinical condition known as metabolic syndrome. The "cardiometabolic clustering" is characterized by well-known alterations that increase cardiovascular risk profile such as insulin-resistance, endothelial dysfunction, arterial stiffening, cardiac hypertrophy, and sympathetic activation. The present article will review the evidence collected throughout by years that an increase in the different markers of adrenergic drive, such as plasma norepinephrine and muscle sympathetic nerve traffic, characterizes this condition. Frequently, the increase also involves heart rate, as documented by the results of different epidemiological studies, such as the Pressioni Arteriose Monitorate E Loro Associazioni, in which an increase in heart rate has been shown in patients with metabolic syndrome, in which this hemodynamic parameter has been assessed in the doctor's office, at home, or during the 24-hour period. Finally, current findings suggest that in metabolic syndrome heart rate displays a significant correlation with other indirect and direct adrenergic markers. Taken together, these findings reinforce the concept that drugs used in the metabolic syndrome should exert sympathoinhibitory effects.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Antihypertensive Agents / pharmacology
  • Antihypertensive Agents / therapeutic use
  • Catecholamines / blood
  • Endothelium / physiopathology
  • Heart Rate / drug effects
  • Heart Rate / physiology*
  • Humans
  • Hypertension / drug therapy
  • Hypertension / physiopathology*
  • Metabolic Syndrome / physiopathology*
  • Norepinephrine / blood
  • Sympathetic Nervous System / physiopathology*

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Antihypertensive Agents
  • Catecholamines
  • Norepinephrine