Published online before print August 16, 2004, doi: 10.1161/01.CIR.0000140973.60992.9A
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(Circulation. 2004;110:1263-1268.)
© 2004 American Heart Association, Inc.
Original Articles |
Increased Collagen Type I Synthesis in Patients With Heart Failure of Hypertensive Origin
Relation to Myocardial Fibrosis
From the Division of Cardiology (R.Q., E.S.), Donostia University Hospital, San Sebastián; the Area of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine (B.L., A.G., J.D.), and Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona; and the Division of Hemodynamics (M.L., J.L.M.U.), Guipuzcoa Polyclinics, San Sebastián, Spain.
Correspondence to Javier Díez, MD, PhD, Area de Fisiopatología Cardiovascular, Facultad de Medicina, C/ Irunlarrea 1, 31080 Pamplona, Spain. E-mail jadimar{at}unav.es
Received January 5, 2004; de novo received March 3, 2004; revision received April 29, 2004; accepted April 30, 2004.
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).
Methods and 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.
Key Words: collagen • heart failure • hypertension • myocardium • peptides
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