Markers of inflammation and fibrosis are related to cardiovascular damage in hypertensive patients with metabolic syndrome.
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.
Sciarretta
Sebastiano
S
Cardiology Department, II School of Medicine, University of Rome La Sapienza, S. Andrea Hospital, Rome, Italy.
Ferrucci
Andrea
A
Ciavarella
Giuseppino Massimo
GM
De Paolis
Paola
P
Venturelli
Vanessa
V
Tocci
Giuliano
G
De Biase
Luciano
L
Rubattu
Speranza
S
Volpe
Massimo
M
D000419:Albuminuria / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood / Q000378:metabolism / Q000652:urine; D001794:Blood Pressure / Q000502:physiology*; D002097:C-Reactive Protein / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000503:physiopathology; D016022:Case-Control Studies; D003971:Diastole / Q000502:physiology; D005260:Female; D005355:Fibrosis / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology*; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D013599:Systole / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; C042813:procollagen type I carboxy terminal peptide; D002097:C-Reactive Protein