Serum carboxyl-terminal propeptide of procollagen type I in exercise-induced left ventricular hypertrophy.
نویسندگان
چکیده
BACKGROUND Left ventricular hypertrophy (LVH) induced by exercise is considered to be a physiologic adaptive mechanism without fibrogenic hyperactivity, as occurs in pathologic hypertrophy. HYPOTHESIS This study investigated serum markers of collagen synthesis and echo parameters of left ventricular diastolic function (LVdf) in 22 male athletes. METHODS Twenty-two highly competitive male athletes (10 cyclists, 12 soccer players) were studied with full history, clinical examination, Doppler echocardiogram, and serum concentration of the carboxyl-terminal propeptide of collagen type I (PIP). They were divided into two groups: normal left ventricular mass (N) with left ventricular mass index (LVMI) < 125 g/m2 (14 athletes) and LVH with LVMI > 125 g/m2 (8 athletes). RESULTS Age, body surface area, blood pressure, heart rate, and systolic function were not different between the groups. Serum concentration of PIP (N: 163 +/- 44.1 microg/l, LVH: 172.7 +/- 61.2 microg/l--NS) and LVdf (early to atrial peak mitral flow velocity ratio: [E/A] N: 1.77 +/- 0.47, LVH: 1.98 +/- 0.70--NS, and early to atrial peak mitral annulus velocity ratio: [Ea/Aa] N: 2.63 +/- 0.70, LVMI: 2.55 +/- 0.90 LV 1.61--NS) were similar in both groups. CONCLUSIONS Normal serum concentration of PIP in athletes with LVH in association with normal LVdf indicates the possibility that in this type of physiologic hypertrophy there is mainly an increase of myocyte size without interstitial fibrosis.
منابع مشابه
Transforming growth factor beta in hypertensives with cardiorenal damage.
We investigated whether a relationship exists between circulating transforming growth factor beta -1 (TGF-beta(1)), collagen type I metabolism, microalbuminuria, and left ventricular hypertrophy in essential hypertension and whether the ability of the angiotensin II type 1 receptor antagonist losartan to correct microalbuminuria and regress left ventricular hypertrophy in hypertensives is relat...
متن کاملToward the biochemical assessment of myocardial fibrosis in hypertensive patients.
The serum concentrations of amino-terminal procollagen type III and carboxy-terminal procollagen type I-derived peptides, which have been proposed as useful markers of the tissue synthesis of collagen types III and type I, respectively, were abnormally increased in patients with essential hypertension and became normal after angiotensin-converting enzyme (ACE) inhibition. An association was fou...
متن کاملMyocardial fibrosis as an early manifestation of hypertrophic cardiomyopathy.
BACKGROUND Myocardial fibrosis is a hallmark of hypertrophic cardiomyopathy and a proposed substrate for arrhythmias and heart failure. In animal models, profibrotic genetic pathways are activated early, before hypertrophic remodeling. Data showing early profibrotic responses to sarcomere-gene mutations in patients with hypertrophic cardiomyopathy are lacking. METHODS We used echocardiography...
متن کاملDiastolic heart failure: evidence of increased myocardial collagen turnover linked to diastolic dysfunction.
BACKGROUND The pathophysiology of diastolic heart failure (DHF) is poorly understood. One potential explanation is an active fibrotic process that produces increased ventricular stiffness, which compromises filling. The present study investigates collagen metabolism in hypertensive patients in different phases of diastolic function with and without proven DHF. METHODS AND RESULTS We studied 8...
متن کاملAssociation of cardiotrophin-1 with myocardial fibrosis in hypertensive patients with heart failure.
Cardiotrophin-1 has been shown to be profibrogenic in experimental models. The aim of this study was to analyze whether cardiotrophin-1 is associated with left ventricular end-diastolic stress and myocardial fibrosis in hypertensive patients with heart failure. Endomyocardial biopsies from patients (n=31) and necropsies from 7 control subjects were studied. Myocardial cardiotrophin-1 protein an...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Clinical cardiology
دوره 27 8 شماره
صفحات -
تاریخ انتشار 2004