Procollagen type I carboxy-terminal peptide shows left ventricular hypertrophy and diastolic dysfunction in hypertensive patients

• Published in: Cardiovascular pathology Vol. 16; no. 2; pp. 69 - 74
• Main Authors: Demir, Mesut, Acartürk, Esmeray, İnal, Tamer, Attila, Gülen, Dönmez, Yurdaer, Avkaroğulları, Mahir, Çaylı, Murat
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.03.2007
• Subjects: Adult; Biomarkers - metabolism; Diastole; Diastolic dysfunction; Echocardiography, Doppler - methods; Female; Humans; Hypertension; Hypertension - complications; Hypertension - metabolism; Hypertension - physiopathology; Hypertrophy, Left Ventricular - blood; Hypertrophy, Left Ventricular - etiology; Hypertrophy, Left Ventricular - physiopathology; Male; Middle Aged; Pathology; Peptide Fragments - blood; Procollagen - blood; Procollagen type I carboxy-terminal peptide; Ventricular Dysfunction, Left - blood; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - physiopathology; Hypertension; Procollagen type I carboxy-terminal peptide; Diastolic dysfunction
• ISSN: 1054-8807; 1879-1336
• DOI: 10.1016/j.carpath.2006.09.010

Abstract Background An excess of myocardial collagens in hypertension is a result of increased collagen synthesis and unchanged or decreased collagen degradation. Increased collagen content, which is shown by the procollagen type I carboxy-terminal peptide (PIP), promotes cardiac remodeling and function abnormalities. Objectives The objectives of this study were to assess PIP levels as a marker of myocardial collagen synthesis and to investigate the relationship between PIP levels and left ventricular mass index (LVMI) as well as diastolic function in patients with mild-to-moderate essential hypertension. Methods The study subjects were divided into three groups: healthy subjects (Group I, n =30); hypertensive patients without left ventricular hypertrophy (Group II, n =30); and patients with left ventricular hypertrophy (Group III, n =30). Left ventricular diastolic function was assessed by standard echocardiography and tissue Doppler imaging. Serum PIP was measured by radioimmunoassay. Results The serum concentration of PIP was higher in Group III than in Groups I and II ( P <.001). A positive correlation was found between serum PIP and LVMI in hypertensive patients ( r =.57, P <.001). Patients with diastolic dysfunction (DD) had significantly higher PIP levels as compared with patients without DD (177.3±52.25 vs. 138.8±38.0 μg/L, P <.001). The cutoff values of PIP to predict left ventricular hypertrophy and DD were 155.0 μg/L (sensitivity, 84%; specificity, 73%) and 150.2 μg/L (sensitivity, 71%; specificity, 70%), respectively. Conclusion An elevated serum concentration of PIP shows left ventricular hypertrophy and DD in the course of hypertension and may be used to follow up on the efficacy of the antihypertensive treatment used.