High PLTP activity is associated with depressed left ventricular systolic function

Abstract

Phospholipid transfer protein (PLTP) modulates lipoprotein metabolism and plays an important role in inflammation and oxidative stress. High PLTP activity is associated with atherosclerosis and its risk factors, which also predispose to left ventricular systolic (LV) dysfunction and/or congestive heart failure. However there are few data linking PLTP activity directly to LV function. According, we sought to determine the relation between PLTP activity and LV ejection fraction (EF) in a Chinese cohort of 732 patients referred for coronary angiography. Weak but significant correlations of PLTP activity levels were found with age (r = −0.09, p = 0.017), male gender (r = 0.09, p = 0.019), diabetes (r = 0.08, p = 0.036), TG (r = 0.11, p = 0.003), HDL-C (r = −0.18, p = <0.001), apo A (−0.30, p < 0.001) apo B (r = 0.20, p < 0.001), fibrinogen (r = 0.32, p < 0.001) and LVEF (r = −0.12, p = 0.003). Median PLTP activity levels were higher among patients with reduced than in normal LV systolic function (LVEF <50%) [26.7 pmol/microl/h (IQR 20.2, 38.6) vs. 19.9 pmol/microl/h (IQR 12.2, 31.0), p < 0.001]. There was a step-wise increase in median PLTP levels in patients with normal, mild, and moderate-severe degrees of LV dysfunction (19.9 pmol/microl/h vs. 25.1 pmol/microl/h vs. 34.7 pmol/microl/h, p < 0.001). Median PLTP activity levels were higher among patients with unstable rather than stable AP and non-CHD patients (25.9 pmol/microl/h vs 20.2 vs 21.9, p = 0.012). On multivariate analyzes, higher median PLTP activity levels were associated with depressed LV systolic function as a dichotomous variable and with lower LVEF as a continuous variable. In conclusion, higher PLTP activity is associated with depressed LV systolic function in a dose-dependent manner independent of coronary heart disease as well as to unstable CHD.