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  • Title: New insights into the mechanism of the elevation of plasma brain natriuretic polypeptide levels in patients with left ventricular hypertrophy.
    Author: Murakami Y, Shimada T, Inoue S, Shimizu H, Ohta Y, Katoh H, Nakamura K, Ishibashi Y.
    Journal: Can J Cardiol; 2002 Dec; 18(12):1294-300. PubMed ID: 12518181.
    Abstract:
    BACKGROUND: Messenger RNA of brain natriuretic polypeptide (BNP) is detected in both the atrium and the ventricle in vitro. Clinical usefulness has been shown in assessment of BNP level in patients with left ventricular hypertrophy; however, few studies have reported the role of the atrium and ventricle separately in the secretion of BNP from the hypertrophied heart. OBJECTIVE: To investigate how the atrium and ventricle secrete natriuretic peptides by comparing the regional concentration of atrial natriuretic polypeptide (ANP) or BNP in the hypertrophied heart with clinical parameters. PATIENTS AND METHODS: ANP and BNP were measured in blood samples from the aortic root, the anterior interventricular vein (AIV) and the coronary sinus in 12 control subjects, 10 subjects with hypertensive hypertrophy and eight with non-obstructive hypertrophic cardiomyopathy. The difference in concentration between the aortic root and the AIV and that between the AIV and the coronary sinus was calculated to estimate ventricular and atrial secretion, respectively. RESULTS: Plasma BNP levels correlated significantly with left ventricular mass index, pulmonary artery wedge pressure, stroke volume and left atrial dimension. Stepwise multiple regression analysis identified BNP from the atrium, not the ventricle, as an independent predictor of left ventricular mass. CONCLUSIONS: These data suggest that atrium-derived BNP is a significant predictor of left ventricular mass index in patients with left ventricular hypertrophy. The atrium-derived component contributes significantly to the elevation of plasma BNP level, reflecting atrial pressure and volume loading in left ventricular hypertrophy without systolic dysfunction.
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