Recent clinical studies have revealed that the expression of
endoglin, an accessory
protein for the TGF-β 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-α 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.