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Reduced levels of N-terminal-proatrial natriuretic peptide in hypertensive patients with metabolic syndrome and their relationship with left ventricular mass

Rubattu, Speranzaa,b; Sciarretta, Sebastianoa; Ciavarella, Giuseppino Massimoa; Venturelli, Vanessaa; De Paolis, Paolac; Tocci, Giulianoa; De Biase, Lucianoa; Ferrucci, Andreaa; Volpe, Massimoa,b

doi: 10.1097/HJH.0b013e32803cae3c
Original papers: Metabolic syndrome

Objectives The metabolic syndrome (MS) is associated with left ventricular hypertrophy (LVH). Previous evidence has shown that LVH is favoured by low levels of atrial natriuretic peptide (ANP), independently from blood pressure (BP), in hypertension. Although levels of natriuretic peptides are known to be lower in obesity, plasma ANP levels have not yet been assessed in MS. We aimed to assess the ANP levels and their relationship with left ventricular mass (LVM) in patients affected by MS.

Methods One hundred and twenty-eight essential hypertensive patients were included in the study: 51 with MS and 77 without MS. Clinical, echocardiographical and biochemical parameters, and levels of both N-terminal (NT)-proANP and alphaANP were assessed.

Results Hypertensive patients affected by MS had higher LVM and increased frequency of LVH. NT-proANP levels were significantly lower in MS, independent of waist circumference (WC). Log(NT-proANP) levels were significantly inversely related to left ventricular mass index (LVMI) (β = −0.360, P < 0.001) and LVM/height2.7 (β = −0.370, P < 0.001) in the whole hypertensive population by multiple linear regression analysis. The relationship of log(NT-proANP) with LVM was more enhanced in patients with MS.

Conclusions The present study demonstrates that levels of NT-proANP are significantly reduced in hypertensive patients affected by MS, and they are significantly inversely related to the increased LVM observed in these patients. Our findings, while supporting previous experimental and clinical evidence of the antihypertrophic role of ANP in hypertension, may help to identify one of the possible mechanisms directly underlying LVH in MS.

aU.O. Cardiologia, IInd School of Medicine, University of Rome La Sapienza, S. Andrea Hospital, Rome, Italy

bIRCCS Neuromed, Polo Molisano University of Rome La Sapienza, Pozzilli (Is), Italy

cAfar, Centro di ricerche cardiovascolari, Fatebenefratelli S. Pietro Hospital, Rome, Italy

Received 7 October, 2006

Revised 22 November, 2006

Accepted 11 December, 2006

Correspondence and requests for reprints to Speranza Rubattu, MD, U.O. Cardiologia, IInd School of Medicine, University of Rome La Sapienza, Via di Grottarossa 1039, Rome, Italy Tel: +39 06 33775561; fax: +39 06 33775061; e-mail: rubattu.speranza@neuromed.it

© 2007 Lippincott Williams & Wilkins, Inc.