Relation of baseline plasma phospholipid transfer protein (PLTP) activity to left ventricular systolic dysfunction in patients referred for coronary angiography.
Relation of baseline plasma phospholipid transfer protein (PLTP) activity to left ventricular systolic dysfunction in patients referred for coronary angiography.
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DOI：
10.1016/j.atherosclerosis.2009.04.011
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发表时间：
2009-11
期刊：
影响因子：
5.3
通讯作者：
Jiang, Xian-Cheng
中科院分区：
文献类型：
--
作者：
Cavusoglu, Erdal;Marmur, Jonathan D.;Chhabra, Sandeep;Chopra, Vineet;Eng, Calvin;Jiang, Xian-Cheng
磷脂转移蛋白（PLTP）是脂蛋白之间磷脂转移和交换的重要调节剂，在炎症和氧化应激中也起作用。因此，PLTP与动脉粥样硬化的发展有关。左心室（LV）收缩功能障碍在动脉粥样硬化患者中很常见，炎症和氧化应激也参与了其发展和进展。本研究的目的是探讨血浆PLTP水平与左室收缩功能之间的关系。在389例因各种适应症接受冠状动脉造影的男性患者中测量基线血浆PLTP活性。详细的临床、血管造影和实验室特征可用于患者。与LV功能正常的患者（定义为心室造影射血分数>=55%）相比，任何程度LV功能障碍的患者PLTP活性升高（中位PLTP 17.8 pmol/ul/h vs 15.9 pmol/ul/h，p=0.0038）。使用多变量分析，并调整已知影响LV功能和PLTP活性的各种混杂变量，PLTP活性是整个人群中存在任何左心室收缩功能障碍的独立预测因子（OR 1.47，95%CI 1.12-1.93，p=0.0052）。此外，PLTP活性是存在左室功能障碍的独立预测因素，无论患者是否存在心肌梗死（OR分别为2.39，95% CI 1.18-4.86，p=0.0161和OR 1.41，95% CI 1.05-1.89，p=0.0206）。总之，PLTP活性可能是已知或疑似冠状动脉疾病患者左室收缩功能障碍的一种新标志物。
Phospholipid transfer protein (PLTP) is an important modulator of phospholipid transfer and exchange among lipoproteins and also plays a role in inflammation and oxidative stress. Accordingly, PLTP has been implicated in the development of atherosclerosis. Left ventricular (LV) systolic dysfunction is common in patients with atherosclerosis, and both inflammation and oxidative stress have also been implicated in its development and progression. The goal of the present study was to examine the relation between plasma levels of PLTP and LV systolic function. Baseline plasma PLTP activity was measured in 389 male patients referred for coronary angiography for a variety of indications. Detailed clinical, angiographic and laboratory characteristics were available for the patients. Compared to those patients with normal LV function (defined as an ejection fraction of >=55% on ventriculography), patients with any degree of LV dysfunction had elevated PLTP activity (median PLTP 17.8 pmol/ul/h versus 15.9 pmol/ul/h, p=0.0038). Using multivariate analysis, and adjusting for a variety of confounding variables known to affect both LV function and PLTP activity, PLTP activity was an independent predictor of the presence of any left ventricular systolic dysfunction in the entire population (OR 1.47, 95% CI 1.12–1.93, p=0.0052). Furthermore, PLTP activity was an independent predictor of the presence of LV dysfunction in both patients with and without myocardial infarction on presentation (OR 2.39, 95% CI 1.18–4.86, p=0.0161 and OR 1.41, 95% CI 1.05–1.89, p=0.0206, respectively). In conclusion, PLTP activity may represent a novel marker of LV systolic dysfunction in patients with known or suspected coronary artery disease.
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