Relation of circulating markers of fibrosis and progression of left and right ventricular dysfunction in hypertensive patients with heart failure.
OBJECTIVE
To study the association of circulating markers of fibrosis: procollagen type III amino-terminal propeptide (PIIINP), procollagen type I carboxy-terminal propeptide (PIP) and collagen type I carboxy-terminal telopeptide (CITP): with left (LV) and right ventricular (RV) longitudinal and LV radial systolic function in patients with heart failure in the course of essential hypertension.


METHODS
The study population consisted of 81 patients with hypertension divided into four groups according to NYHA classification and 20 healthy controls. Cardiac function was estimated by myocardial deformation indices assessed by tissue Doppler imaging. Serum PIIINP, PIP and CITP levels were quantified by radioimmunoassay.


RESULTS
Progressive LV longitudinal function impairment was demonstrated in all hypertension groups as indicated by reduced peak systolic strain and strain rate and increased postsystolic strain index. The respective indicators of LV radial function were deteriorated only in NYHA classes III-IV. Concurrently, RV longitudinal function was found abnormal in NYHA classes II-IV. PIIINP concentration was higher in NYHA class III and IV, whereas CITP level was increased and PIP/CITP ratio was decreased in the NYHA IV individuals. PIIINP was an independent correlate of LV and RV longitudinal strain (R = 0.52, beta = -0.34, P < 0.001; R = 0.25, beta = -0.27, P < 0.01, respectively). PIP/CITP ratio independently determined LV radial strain in patients with LV ejection fraction less than 50% (R = 0.44, beta = 0.52, P < 0.008).


CONCLUSIONS
In hypertensive patients, the progressive decline in cardiac longitudinal function is related to increased collagen III synthesis, whereas the changes in collagen I turnover favoring its increased degradation might contribute to LV radial and global systolic dysfunction seen in the advanced hypertensive heart disease.
Plaksej
Rafal
R
Department of Cardiology, Wroclaw Medical University, Wroclaw, Poland.
Kosmala
Wojciech
W
Frantz
Stefan
S
Herrmann
Sebastian
S
Niemann
Markus
M
Störk
Stefan
S
Wachter
Rolf
R
Angermann
Christiane E
CE
Ertl
Georg
G
Bijnens
Bart
B
Weidemann
Frank
F
D000368:Aged; D015415:Biomarkers / Q000097:blood; D018450:Disease Progression; D015150:Echocardiography, Doppler / Q000379:methods; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood*; D018487:Ventricular Dysfunction, Left / Q000097:blood* / Q000503:physiopathology; D018497:Ventricular Dysfunction, Right / Q000097:blood* / Q000503:physiopathology
D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; C093212:procollagen type II carboxy-terminal peptide