Plasma endoglin as a marker to predict cardiovascular events in patients with chronic coronary artery diseases
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Tomokazu Ikemoto Yukihiro Hojo Hideyuki Kondo Nozomu Takahashi Masahiro Hirose Yoshioki Nishimura Takaaki Katsuki Kazuyuki Shimada K
- چاپ و سال / کشور: 2011
Description
Recent clinical studies have revealed that the expression of endoglin, an accessory protein for the TGF-b receptor, is increased in patients with atherosclerotic diseases. The plasma endoglin level is thought to represent endothelial activation, inflammation, and senescence. To clarify the significance of plasma endoglin in chronic coronary artery disease. Human umbilical vein endothelial cells (HUVECs) were cultured to examine changes in soluble endoglin (s-endoglin) levels caused by atherogenic stimulation in vitro. We studied 318 patients with stable coronary artery disease who underwent a successful percutaneous coronary intervention (PCI). Patients with acute coronary syndrome were excluded. Major adverse cardiovascular events (MACE) were congestive heart failure, acute myocardial infarction, stroke, and sudden cardiac death. All patients were followed-up to examine MACE after the procedure. We confirmed that the levels of s-endoglin was increased in the culture medium of HUVECs by senescence, tumor necrosis factor-a and hydrogen peroxide. In a clinical study, mean follow-up period was 1055 ± 612 days (49–2136 days) with 27 incidents of MACE (8.5%). We divided patients into three groups according to the plasma s-endoglin levels. Kaplan–Meier curves revealed that the highest endoglin group had a significantly higher MACE rate than the lowest endoglin group (log-rank test, p = 0.009). A Cox proportional hazards model showed that chronic kidney disease, left ventricular ejection fraction and s-endoglin level were significant factors to predict MACE. Plasma endoglin could be a marker to predict cardiovascular events in patients with chronic coronary artery disease after PCI.
Heart Vessels DOI 10.1007/s00380-011-0163-z Received: 14 October 2010 / Accepted: 20 May 2011
