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High-density lipoprotein cholesterol and left ventricular hypertrophy in essential hypertension

Schillaci, Giuseppea; Vaudo, Gaetanoa; Reboldi, Gianpaolob; Verdecchia, Paoloc; Lupattelli, Grazianaa; Pasqualini, Leonellaa; Porcellati, Carlod; Mannarino, Elmoa

Original papers: Heart

Objective  The proportion of left ventricular (LV) mass variability explained by blood pressure in essential hypertension is small, and several non-haemodynamic determinants of LV mass have been identified or hypothesized. This study examines the possible relation between blood lipids and LV mass in hypertension.

Design  Never-treated non-diabetic hypertensive patients.

Setting  Hospital hypertension outpatient clinics in Umbria, Italy.

Patients  We investigated the association between high-density lipoprotein (HDL)-cholesterol and echocardiographic LV mass in 1306 never-treated subjects with essential hypertension. Subjects with previous cardiovascular events, diabetes and current or previous antihypertensive or lipid-lowering therapy were excluded.

Results  HDL-cholesterol showed an inverse association with LV mass (r = −0.30, P < 0.001). No association was found between LV mass and total or low-density lipoprotein cholesterol. With multiple linear regression analysis we tested the independent contribution of several potential determinants of LV mass in women and in men. Average 24 h blood pressure (both pulse and mean), body mass index, height2.7, stroke volume, age (all P < 0.01) and low HDL-cholesterol (P < 0.0001 in women, P < 0.001 in men) were associated with a greater LV mass in both sexes. Triglycerides showed a weak univariate association with LV mass in women (r = 0.11, P < 0.02), which did not hold in a multivariate analysis.

Conclusions  Low HDL-cholesterol is an independent predictor of LV mass in untreated hypertensive subjects. Common hormonal and metabolic mechanisms, including insulin resistance, could explain this association, which may contribute to the adverse prognostic significance of low HDL-cholesterol levels.

aUnit of Internal Medicine, Angiology and Arteriosclerosis, bDepartment of Internal Medicine, cUnit of Cardiovascular Pathophysiology, University of Perugia, and dAzienda Ospedaliera di Perugia, Perugia, Italy.

Sponsorship: This study was supported in part by grant 806174392-007 from MURST, Rome, Italy.

Correspondence and request for reprints to Dr Giuseppe Schillaci, Unit of Internal Medicine, Angiology and Arteriosclerosis, Department of Clinical and Experimental Medicine, University of Perugia Medical School, via Brunamonti, 51, 06122 Perugia, Italy. Tel: +39 075 5783119; fax: +39 075 5736737; email:

Received 14 March 2001

Revised 21 June 2001

Accepted 6 August 2001

© 2001 Lippincott Williams & Wilkins, Inc.