Increased collagen type I synthesis in patients with heart failure of hypertensive origin: relation to myocardial fibrosis.
BACKGROUND
We investigated whether increased collagen type I synthesis and deposition contribute to enhancement of myocardial fibrosis and deterioration of cardiac function in patients with hypertensive heart disease (HHD).


RESULTS
We studied 65 hypertensives with left ventricular hypertrophy subdivided into 2 groups: 34 patients without heart failure (HF) and 31 patients with HF. Transvenous endomyocardial biopsies of the interventricular septum were performed to quantify the amount of fibrotic tissue and the extent of collagen type I deposition. The carboxy-terminal propeptide of procollagen type I (PIP), an index of collagen type I synthesis, was measured by radioimmunoassay in serum samples from the coronary sinus and the antecubital vein. Compared with normotensives, the amount of collagen tissue, the extent of collagen type I deposition, and coronary and peripheral PIP were increased (P<0.01) in the 2 groups of hypertensives. These parameters were also increased (P<0.01) in HF hypertensives compared with non-HF hypertensives. Coronary PIP was higher (P<0.01) than peripheral PIP in hypertensives but not in normotensives. The amount of collagen tissue was inversely correlated with the ejection fraction and directly correlated with both coronary and peripheral PIP in all hypertensives.


CONCLUSIONS
These findings suggest that an excess of cardiac collagen type I synthesis and deposition may be involved in the enhancement of myocardial fibrosis that accompanies the development of HF in HHD. In addition, our data show that the heart secretes PIP via the coronary sinus into the peripheral circulation in patients with HHD. Thus, PIP determined in peripheral blood can be a useful marker of myocardial fibrosis in these patients.
Division of Cardiology, Donostia University Hospital, San Sebastián, Spain.
Ramón
R
Querejeta
Begoña
B
López
Arantxa
A
González
Eloy
E
Sánchez
Mariano
M
Larman
José L
JL
Martínez Ubago
Javier
J
Díez
D015415:Biomarkers; D001706:Biopsy; D024042:Collagen Type I / Q000096:biosynthesis*; D004719:Endomyocardial Fibrosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood / Q000378:metabolism; D011347:Procollagen / Q000097:blood / Q000378:metabolism; D014463:Ultrasonography
D015415:Biomarkers; D024042:Collagen Type I; D010446:Peptide Fragments; D011347:Procollagen; C042813:procollagen type I carboxy terminal peptide