Markers of inflammation and fibrosis are related to cardiovascular damage in hypertensive patients with metabolic syndrome

被引:92
作者
Sciarretta, Sebastiano
Ferrucci, Andrea
Ciavarella, Giuseppino Massimo
De Paolis, Paola
Venturelli, Vanessa
Tocci, Giuliano
De Biase, Luciano
Rubattu, Speranza
Volpe, Massimo
机构
[1] Univ Roma La Sapienza, S Andrea Hosp, Sch Med 2, Dept Cardiol, Rome, Italy
[2] Polo Molisano Univ Rome La Sapienza, IRCCS Neuromed, Pozzilli, Italy
[3] S Pietro Hosp, Res Ctr, AFaR, Rome, Italy
关键词
inflammation; essential hypertension; metabolic syndrome; cardiovascular damage;
D O I
10.1016/j.amjhyper.2007.01.023
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Background: Previous studies have shown that metabolic syndrome (MS) is associated with an increased susceptibility to develop cardiovascular damage (CD). Experimental evidence indicates that inflammation and fibrosis could play a critical role in the development of CD in hypertension. This issue has not been clarified yet in patients with MS. The aim of our study was to investigate the relationship between markers of inflammation and fibrosis with CD in hypertensive patients with and without MS. Methods: One hundred twenty-eight essential hypertensive patients were included in the study: 51 with MS and 77 without MS. Clinical, biochemical parameters, 24-h urinary albumin excretion rate (UAER), levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), and procolla-alpha Oren type I carboxy-terminal propeptide (PICP) were measured. All patients underwent an echocardiographic examination with transmitral Doppler and tissue Doppler imaging (TDI). Results: Left ventricular mass indexed by height(2.7) (LVM/h(2.7)) (p < .001), early diastolic peak flow velocity/early myocardial diastolic velocity ratio (E/Em ratio), a TDI index of diastolic function (P < .001), and 24-h UAER (P < .05) were significantly higher in the group with MS, whereas peak myocardial systolic velocity (Sm), a TDI index of systolic function (P < .001), was lower. Serum levels of CRP (P < .001), TNF-alpha (P < .05), TGF-beta (P < .01), and PICP (P < .001) were significantly increased in MS. These markers were significantly related to higher LVMI2.7, higher E/Em ratio, and increased 24-h UAER and a lower Sm in the whole population, with a further significant enhancement in MS. Conclusions: Cardiovascular damage is more frequent in hypertensives with MS than in hypertensives without MS, and this is significantly related to the increased levels of inflammation and fibrosis found in hypertensives with MS. Am J Hypertens 2007;20:784-791 (c) 2007 American Journal of Hypertension, Ltd.
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页码:784 / 791
页数:8
相关论文
共 33 条
[1]   Endothelial dysfunction in chronic myocardial infarction despite increased vascular endothelial nitric oxide synthase and soluble guanylate cyclase expression -: Role of enhanced vascular superoxide production [J].
Bauersachs, J ;
Bouloumié, A ;
Fraccarollo, D ;
Hu, K ;
Busse, R ;
Ertl, G .
CIRCULATION, 1999, 100 (03) :292-298
[2]   Metabolic syndrome and target organ damage in untreated essential hypertensives [J].
Cuspidi, C ;
Meani, S ;
Fusi, V ;
Severgnini, B ;
Valerio, C ;
Catini, E ;
Leonetti, G ;
Magrini, F ;
Zanchetti, A .
JOURNAL OF HYPERTENSION, 2004, 22 (10) :1991-1998
[3]   LEFT-VENTRICULAR MASS AND BODY SIZE IN NORMOTENSIVE CHILDREN AND ADULTS - ASSESSMENT OF ALLOMETRIC RELATIONS AND IMPACT OF OVERWEIGHT [J].
DESIMONE, G ;
DANIELS, SR ;
DEVEREUX, RB ;
MEYER, RA ;
ROMAN, MJ ;
DEDIVITIIS, O ;
ALDERMAN, MH .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1992, 20 (05) :1251-1260
[4]   ECHOCARDIOGRAPHIC DETERMINATION OF LEFT-VENTRICULAR MASS IN MAN - ANATOMIC VALIDATION OF METHOD [J].
DEVEREUX, RB ;
REICHEK, N .
CIRCULATION, 1977, 55 (04) :613-618
[5]   Losartan-dependent regression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients [J].
Díez, J ;
Querejeta, R ;
López, B ;
González, A ;
Larman, M ;
Ubago, JLM .
CIRCULATION, 2002, 105 (21) :2512-2517
[6]   Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) Final Report [J].
Grundy, SM ;
Becker, D ;
Clark, LT ;
Cooper, RS ;
Denke, MA ;
Howard, WJ ;
Hunninghake, DB ;
Illingworth, R ;
Luepker, RV ;
McBride, P ;
McKenney, JM ;
Pasternak, RC ;
Stone, NJ ;
Van Horn, L ;
Brewer, HB ;
Cleeman, JI ;
Ernst, ND ;
Gordon, D ;
Levy, D ;
Rifkind, B ;
Rossouw, JE ;
Savage, P ;
Haffner, SM ;
Orloff, DG ;
Proschan, MA ;
Schwartz, JS ;
Sempos, CT ;
Shero, ST ;
Murray, EZ ;
Keller, SA ;
Jehle, AJ .
CIRCULATION, 2002, 106 (25) :3143-3421
[7]   Definition of metabolic syndrome - Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition [J].
Grundy, SM ;
Brewer, HB ;
Cleeman, JI ;
Smith, SC ;
Lenfant, C .
CIRCULATION, 2004, 109 (03) :433-438
[8]  
HernandezPresa M, 1997, CIRCULATION, V95, P1532
[9]   Monocyte chemoattractant protein-1 and macrophage infiltration in hypertensive kidney injury [J].
Hilgers, KF ;
Hartner, A ;
Porst, M ;
Mai, M ;
Wittmann, M ;
Hugo, C ;
Ganten, D ;
Geiger, H ;
Veelken, R ;
Mann, JFE .
KIDNEY INTERNATIONAL, 2000, 58 (06) :2408-2419
[10]   TNF-α induces protein synthesis through PI3-kinase-Akt/PKB pathway in cardiac myocytes [J].
Hiraoka, E ;
Kawashima, S ;
Takahashi, T ;
Rikitake, Y ;
Kitamura, T ;
Ogawa, W ;
Yokoyama, M .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 280 (04) :H1861-H1868