[Association of cathepsin L with coronary heart disease and its risk factors].

OBJECTIVE: To explore the relationship of cathepsin L (CatL) with coronary heart disease (CHD), severity of coronary stenosis and risk factors of CHD. METHODS: A total of 137 CHD patients and 48 controls were included in the study, to determined the serum levels of CatL, high sensitive C reactive protein (hs-CRP), fasting glucose (FBS), total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1(Apo-A1) and apolipoprotein B. All the subjects were invited for a coronary angiography, using the sum of the Gensini scores to assess the severity of coronary artery stenosis. RESULTS: Serum CatL levels were significantly higher in CHD patients (5.63 +/= 0.12 microg/L) than non-CHD subjects (3.93 +/= 0.22 microg/L, P<0.01). CatL was an independent risk factor of CHD in Logistic regression analysis [Exp(B)=2.341, 95%CI 1.567 approximately 3.496, P<0.01]. Serum CatL levels were associated positively with the Gensini scores(r=0.228, P<0.01); In fact, CatL was an independent correlator of Gensini scores (P<0.05). CatL inversely associated with HDL-C (r=-0.228, P<0.01) and ApoA1(r=-0.187, P<0.05), and positively with FBS(r=0.161, P<0.05). CONCLUSION: CatL is involved in the pathogenesis of CHD. Serum CatL levels could reflect the severity of coronary luminal narrowings. CatL might participate in glucose and lipid metabolic disorders.

Usefulness of serum cathepsin L as an independent biomarker in patients with coronary heart disease.

Higher levels of cysteinyl cathepsin L were detected in human atherosclerotic lesions than in healthy aortas. However, a link between human coronary heart disease (CHD) and systemic cathepsin L levels remains unknown. A total of 137 volunteers with diagnosed acute and previous myocardial infarction (MI) and stable and unstable angina pectoris in addition to 48 controls were asked to undergo coronary angiography. Serum cathepsin L, high-sensitivity C-reactive protein, fasting glucose, and lipid protein profiles were measured. Serum cathepsin L levels were significantly higher in patients with CHD than in those without CHD (p <0.001). The significance persisted after adjusting for most major confounders. Patients with unstable angina pectoris had higher serum cathepsin L levels than those with stable angina pectoris (p = 0.02). Of patients with acute coronary syndrome, those with acute MI had higher serum cathepsin L levels than those with unstable angina pectoris (p <0.05) and patients with previous MI had the highest levels. Importantly, serum cathepsin L associated positively with number of coronary branch luminal narrowings (R = 0.38, p <0.001), Gensini scores (R = 0.44, p <0.001), high-sensitivity C-reactive protein (R = 0.32, p <0.001), fasting glucose (R = 0.16, p <0.03), and cigarette smokers (R = 0.27, p <0.001), but inversely with high-density lipoprotein (R = -0.23, p = 0.002) and apolipoprotein A1 (R = -0.19, p = 0.01) in all subjects. In conclusion, after adjusting for these confounders, we found that serum cathepsin L correlated positively and independently with Gensini score, suggesting that serum cathepsin L serves as a novel and independent biomarker for CHD.