Document Detail


Markers of inflammation and fibrosis are related to cardiovascular damage in hypertensive patients with metabolic syndrome.
MedLine Citation:
PMID:  17586414     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 procollagen type 1 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 LVMI(2.7), 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.
Authors:
Sebastiano Sciarretta; Andrea Ferrucci; Giuseppino Massimo Ciavarella; Paola De Paolis; Vanessa Venturelli; Giuliano Tocci; Luciano De Biase; Speranza Rubattu; Massimo Volpe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of hypertension     Volume:  20     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-06-25     Completed Date:  2007-11-01     Revised Date:  2009-02-24    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  784-91     Citation Subset:  IM    
Affiliation:
Cardiology Department, II School of Medicine, University of Rome La Sapienza, S. Andrea Hospital, Rome, Italy.
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MeSH Terms
Descriptor/Qualifier:
Albuminuria / physiopathology*
Biological Markers / blood,  metabolism,  urine
Blood Pressure / physiology*
C-Reactive Protein / metabolism
Cardiovascular Diseases / physiopathology
Case-Control Studies
Diastole / physiology
Female
Fibrosis / physiopathology
Humans
Hypertension / complications,  physiopathology*
Hypertrophy, Left Ventricular / physiopathology*
Inflammation / physiopathology
Male
Metabolic Syndrome X / physiopathology*
Middle Aged
Peptide Fragments / blood
Procollagen / blood
Systole / physiology
Transforming Growth Factor beta / blood
Tumor Necrosis Factor-alpha / blood
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Peptide Fragments; 0/Procollagen; 0/Transforming Growth Factor beta; 0/Tumor Necrosis Factor-alpha; 0/procollagen type I carboxy terminal peptide; 9007-41-4/C-Reactive Protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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