Literature DB >> 17317538

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

Mesut Demir1, Esmeray Acartürk, Tamer Inal, Gülen Attila, Yurdaer Dönmez, Mahir Avkaroğullari, Murat Cayli.   

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 microg/L, P<.001). The cutoff values of PIP to predict left ventricular hypertrophy and DD were 155.0 microg/L (sensitivity, 84%; specificity, 73%) and 150.2 microg/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.

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Year:  2007        PMID: 17317538     DOI: 10.1016/j.carpath.2006.09.010

Source DB:  PubMed          Journal:  Cardiovasc Pathol        ISSN: 1054-8807            Impact factor:   2.185


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