Sympathetic overdrive and cardiovascular risk in the metabolic syndrome.

Paper Abstract

Sympathetic neural factors are involved in energy balance as well as in blood pressure control. This represents the background for the hypothesis that an adrenergic overdrive may be implicated in the development and/or progression of the metabolic syndrome. Indirect and direct markers of sympathetic drive have confirmed this hypothesis, by showing the occurrence of an adrenergic activation both at the cardiac and peripheral vascular level. It is likely that this sympathetic dysfunction is triggered by reflex mechanisms (arterial baroreceptor impairment), metabolic factors (insulin resistance), and humoral agents (angiotensin II, leptin). The adrenergic overdrive exerts a number of adverse effects on the cardiovascular system, by favoring the genesis of cardiac hypertrophy, vascular hypertrophy, arterial remodeling and endothelial dysfunction and thereby aggravating the already elevated cardiovascular risk profile of the patient. This carries obvious clinical and therapeutic implications, including the suggestion that sympathetic inhibition should be included among the goals of both pharmacological and non-pharmacological interventions employed in the treatment of the metabolic syndrome.