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Hypertension. 2001;38:1222-1226
doi: 10.1161/hy1101.098549
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(Hypertension. 2001;38:1222.)
© 2001 American Heart Association, Inc.


Fourth International Seminar on Cardiovascular Biology
and Medicine: Part I

Biochemical Assessment of Myocardial Fibrosis in Hypertensive Heart Disease

Begoña López; Arantxa González; Nerea Varo; Concepción Laviades; Ramón Querejeta; Javier Díez

From the Division of Cardiovascular Pathophysiology, School of Medicine (B.L., A.G., J.D.), Department of Clinical Chemistry, University Clinic (N.V.), and Department of Cardiology and Cardiovascular Surgery, University Clinic (J.D.), University of Navarra, Pamplona, Spain; and Division of Nephrology, San Jorge General Hospital (C.L.), Huesca, Spain; and Division of Cardiology, Na Sa de Aránzazu Hospital (R.Q.), San Sebastián, Spain.

Correspondence to Dr Javier Díez, Division of Fisiopatologia Cardiovascular, Facultad de Medicina, C/Irunlarrea s/n, 31008 Pamplona, Spain. E-mail jadimar{at}unav.es

Abstract

Abstract— Fibrous tissue accumulation is an integral feature of the adverse structural remodeling of cardiac tissue seen with hypertensive heart disease. Given the importance of fibrous tissue in leading to myocardial dysfunction and failure, noninvasive monitoring of myocardial fibrosis by use of serological markers of collagen turnover could prove a clinically useful tool, particularly given the potential for cardioprotective and cardioreparative pharmacological strategies. An emerging experimental and clinical experience holds promise for the use of radioimmunoassays of various serological markers of fibrillar collagen type I and type III turnover in arterial hypertension. More specifically, the measurement of serum concentrations of procollagen type I C-terminal propeptide (a peptide that is cleaved from procollagen type I during the synthesis of fibril-forming collagen type I) may provide indirect diagnostic information on both the extent of myocardial fibrosis and the ability of antihypertensive treatment to diminish collagen type I synthesis and reduce myocardial fibrosis. This approach represents an exciting and innovative strategy, and available data set the stage for larger trials, in which noninvasive measures of fibrosis in hypertensive heart disease could prove useful.


Key Words: collagen • hypertension, essential • myocardium • remodeling • renin-angiotensin system




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