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  • Title: Increased serum N-terminal pro-B-type natriuretic peptide and left ventricle diastolic dysfunction in patients with hepatitis C virus infection.
    Author: Che W, Liu W, Wei Y, Xu Y, Hou L, Matsumori A, Hu D.
    Journal: J Viral Hepat; 2012 May; 19(5):327-31. PubMed ID: 22497811.
    Abstract:
    Prior studies demonstrated that patients with hepatitis C virus (HCV) infection had higher plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, which may indicate the presence of a subclinical cardiac dysfunction. However, there are few data regarding the echocardiographic assessment in HCV-infected patients. The objectives of this study were to investigate changes in the left ventricle (LV) with echocardiography and to identify echocardiographic correlates of serum NT-proBNP levels in HCV-infected patients. Ninety HCV-infected patients and 90 age and gender-matched healthy controls were included. The level of serum NT-proBNP was higher in the patient group (P < 0.001). The proportion of patients whose serum NT-proBNP levels were higher than 125 pg/mL was greater than that of controls (15.56%vs 3.33%, P = 0.011). Echocardiography did not show any significant difference of cardiac structural abnormalities between groups. In the patient group, E, E' and E/A were lower, and E/E' was higher. The proportion of patients (13, 14.44%) with impaired diastolic filling (E/A ≤ 0.75; 0.75 < E/A < 1.5 and E/E' ≥ 10) was greater than that of the control group (3, 3.33%; P = 0.018). Simple regression analysis demonstrated a statistically significant linear correlation between NT-proBNP levels and left ventricular diastolic diameter (LVDd) (r = 0.178, P = 0.013), left ventricular posterior wall diastolic thickness (LVPWd) (r = 0.147, P = 0.023) and mitral E/E' (r = 0.414, P = 0.027). Independent correlates of NT-proBNP levels (R(2) = 0.34) were older age (β' = 0.034, P = 0.011) and E/E' ratio (β' = 0.026, P = 0.018). In conclusion, the combined analysis of NT-proBNP and echocardiography showed a possible subclinical left ventricular diastolic dysfunction as evidence of a pathogenic link between HCV and CVD.
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