摘要
Background Cathepsin S and its endogenous inhibitor cystatin C are implicated in the pathogenesis of atherosclerosis, especially in the plaque destabilization and rupture leading to acute coronary syndrome. However, whether circulating cathepsin S and cystatin C also change in association with coronary plaque morphology is unknown yet. Methods We recruited 98 patients with unstable angina （UA, n=56） or stable angina （SA, n=-42） who had a segmental stenosis resulting in 〉20% and 〈70% diameter reduction in one major coronary artery on coronary angiography. Thirty-one healthy subjects served as controls. Intravascular ultrasound （IVUS） was used to evaluate plaque morphology. Plasma cathepsin S and cystatin C were measured as well. Results At the culprit lesion site, plaque area （（7.85±2.83） mm^2 vs （6.53±2.92） mm^2, P=0.027）, plaque burden （（60.92±11.04）% vs （53.87±17.52）%, P=0.025）, remodeling index （0.93±0.16 vs 0.86±0.10, P=0.004） and eccentricity index （0.74±0.17 vs 0.66±0.21, P=0.038） were bigger in UA group than in SA group. Plasma cathepsin S and cystatin C were significantly higher in patients than in controls （P〈0.01）. Plasma cathepsin S was higher in UA group （（0.411±0.121） nmol/L） than in SA group （（0.355±0.099） nmol/L, P=0.007）, so did the plasma cystatin C （（0.95±0.23） mg/L in UA group, （0.84±0.22） mg/L in SA group; P=0.009）. Plasma cathepsin S positively correlated with remodeling index （r=0.402, P=0.002） and eccentricity index （r=0.441, P=0.001）, and plasma cystatin C positively correlated with plaque area （r=0.467, P 〈0.001） and plaque burden （r=0.395, P=0.003） in UA group but not in SA group. Conclusions Plasma cathepsin S and cystatin C increased significantly in UA patients. In angina patients, higher plasma cathepsin S may suggest the presence of vulnerable plaque, and higher plasma cystatin C may be a clue for larger atherosclerotic coronary plaque.
Background Cathepsin S and its endogenous inhibitor cystatin C are implicated in the pathogenesis of atherosclerosis, especially in the plaque destabilization and rupture leading to acute coronary syndrome. However, whether circulating cathepsin S and cystatin C also change in association with coronary plaque morphology is unknown yet. Methods We recruited 98 patients with unstable angina （UA, n=56） or stable angina （SA, n=-42） who had a segmental stenosis resulting in 〉20% and 〈70% diameter reduction in one major coronary artery on coronary angiography. Thirty-one healthy subjects served as controls. Intravascular ultrasound （IVUS） was used to evaluate plaque morphology. Plasma cathepsin S and cystatin C were measured as well. Results At the culprit lesion site, plaque area （（7.85±2.83） mm^2 vs （6.53±2.92） mm^2, P=0.027）, plaque burden （（60.92±11.04）% vs （53.87±17.52）%, P=0.025）, remodeling index （0.93±0.16 vs 0.86±0.10, P=0.004） and eccentricity index （0.74±0.17 vs 0.66±0.21, P=0.038） were bigger in UA group than in SA group. Plasma cathepsin S and cystatin C were significantly higher in patients than in controls （P〈0.01）. Plasma cathepsin S was higher in UA group （（0.411±0.121） nmol/L） than in SA group （（0.355±0.099） nmol/L, P=0.007）, so did the plasma cystatin C （（0.95±0.23） mg/L in UA group, （0.84±0.22） mg/L in SA group; P=0.009）. Plasma cathepsin S positively correlated with remodeling index （r=0.402, P=0.002） and eccentricity index （r=0.441, P=0.001）, and plasma cystatin C positively correlated with plaque area （r=0.467, P 〈0.001） and plaque burden （r=0.395, P=0.003） in UA group but not in SA group. Conclusions Plasma cathepsin S and cystatin C increased significantly in UA patients. In angina patients, higher plasma cathepsin S may suggest the presence of vulnerable plaque, and higher plasma cystatin C may be a clue for larger atherosclerotic coronary plaque.
