Why the study?
Does metabolic syndrome amplify hypertension-related target organ damage in nondiabetic essential hypertensive patients?
Does metabolic syndrome amplify hypertension-related target organ damage in nondiabetic essential hypertensive patients?
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Metabolic syndrome amplifies hypertension-related preclinical cardiac, renal, and retinal damage independently of its individual components in nondiabetic hypertensive patients, potentially explaining the enhanced cardiovascular risk associated with the syndrome.
The aim of our study was to analyze, in a wide group of young and middle-aged essential hypertensive patients without diabetes mellitus, the influence of metabolic syndrome (MS), defined according to the NCEP-ATPIII criteria, on markers of preclinical cardiac, renal and retinal damage. Three hundred fifty three nondiabetic hypertensive subjects (mean age 46±10 years), free from cardiovascular and renal diseases (37% of which had MS), underwent echocardiographic examination, microalbuminuria determination and non-mydriatic retinography. Hypertensive patients with MS exhibited higher left ventricular (LV) mass [either normalized by body surface area or by height elevated by a power of 2.7 (LVMH2.7)], myocardial relative wall thickness (RWT), albumin excretion rate (AER) and greater prevalences of LV hypertrophy (LVH), of microalbuminuria and of grade I and grade II hypertensive retinopathy (simplified Keith-Wagener classification) than subjects without MS (see table 1). These results held even after correction for age, duration of hypertension, previous antihypertensive therapy, and gender distribution. The relationships between MS and LV mass and between MS and AER were confirmed in multivariate regression models including MS together with its individual components, as independent variables. MS amplifies hypertension-related cardiac and renal changes, over and above the potential contribution of each single component of this syndrome. Since these markers of target organ damage are well-known predictors of cardiovascular events, our results may partly explain the enhanced cardiovascular risk associated with MS.
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Mulè et al. (2005) studied this question.
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