title: Effect of sympathetic overactivity on cardiovascular prognosis in hypertension.
abstract: Increased sympathetic tone is found in about 30% of patients with hypertension. This abnormality is closely associated with the metabolic syndrome of dyslipidaemia and hyperinsulinaemia. In this short review we discuss the mechanisms by which sympathetic over-activity could cause the metabolic syndrome. Sympathetic stimulation enhances cardiac and vascular hypertrophy. Left ventricular hypertrophy is a strong predictor of poor cardiovascular outcomes. Hypertrophy of resistance vessels accelerates hypertension, whereas hypertrophy of smaller coronary vessels limits coronary reserve and increases tendency for coronary spasms. Epidemiologically, high haematocrit is associated with hypertension and is recognized as an independent coronary risk factor. Sympathetic stimulation increases haematocrit through an increase of post-capillary vascular resistance. Sympathetic over-activity is also associated with platelet activation which may further add to the risk of coronary thrombosis in neurogenic hypertension. Tachycardia, which is due to increased sympathetic and deceased parasympathetic tone, is a hallmark of neurogenic hypertension. Fast heart rate is a strong predictor of coronary events and sudden death. The mechanisms by which tachycardia increases the cardiovascular risk are outlined.
authors.affiliation: Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0356, USA.
authors.forename: S
authors.initials: S
authors.lastname: Julius
mesh_terms: D001143:Arousal / Q000502:physiology; D002319:Cardiovascular System / Q000294:innervation*; D003327:Coronary Disease / Q000175:diagnosis / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D011379:Prognosis; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology