Background: This article aims to investigate the changes of plasma cystatin C concentration (PcyC), and to evaluate the relationship between PcyC and acute coronary syndrome. Methods: A total of 126 consecutive patients with coronary artery disease (CAD) were enrolled in this study, consisting of 34 patients with stable angina pectoris (SAP), 56 patients with unstable angina pectoris (UAP), 36 patients with acute myocardial infarction (AMI), and 34 healthy subjects as controls. Plasma cystatin C, high sensitivity C-reactive protein (hs-CRP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and uric acid (UA) in all subjects were determined. All patients were followed up for 6 months and adverse cardiovascular events were recorded. Results: Plasma cystatin C was elevated in CAD. Cystatin C levels were significantly higher in UAP patients than those in SAP patients and controls (2013.83 ± 633.85 ng/mL vs 1348.41 ± 369.62 ng/mL and 1509.99 ± 408.65 ng/mL, P < 0.05), but were much lower than those in AMI patients (2013.83 ± 633.85 ng/mL vs 2873.55 ± 1149.48 ng/mL, P < 0.05). Patients with AMI also exhibited significantly higher cystatin C levels than SAP patients and the control group (2873.55 ± 1149.48 ng/mL vs 1348.41 ± 369.62 ng/mL and 1509.99 ± 408.65 ng/mL, P < 0.01). Much higher hs-CRP concentrations were found in UAP patients (1.58 ± 2.81 mg/L, P < 0.05) and AMI patients (20.68 ± 18.98 mg/L, P < 0.01). Cystatin C was positively and significantly correlated with age, hs-CRP, white blood cells (WBC), creatinine, and UA (r > 0, P < 0.05), whereas a significantly negative correlation was observed with HDL-C (r = −0.227, P < 0.05). These coefficients were clearly high for creatinine (r = +0.612) and WBC (r = +0.459). During the 6 month followup, 26 patients were found with adverse cardiovascular events and had significantly higher cystatin C levels than the 22 control patients at admission (2356.73 ± 897.64 ng/mL vs 1469.51 ± 574.83 ng/mL, P < 0.01). Conclusions: Cystatin C plays an important role in the development of CAD and PcyC is a strong predictor for risk of cardiovascular events.
Our aim in this study was to investigate the changes of serum high-sensitive C-reactive protein (hs-CRP) and uric acid (UA), and evaluate the synergistic effect of amlodipine and atorvastatin on blood pressure and left ventricular remodeling in hypertensive patients with primary hypercholesterolemia. One hundred and twenty-six hypertensive patients with hypercholesterolemia were randomized into amlodipine group (10 mg/day, group A, n = 65) and amlodipine (10 mg/day) plus atorvastatin group (20 mg/day, group B, n = 61), treated for 4 months continuously. Serum concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were determined, and blood pressure of both groups was examined before and after treatment. Left ventricular posterior wall thickness and interventricular spectum thickness were measured by echocardiography, and left ventricular mass index (LVMI) was calculated. After 4-months of treatment with atorvastatin, serum concentrations of total cholesterol, low-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were significantly decreased in group B (P < 0.05, P < 0.01), while serum concentrations of high-density lipoprotein cholesterol was elevated (P < 0.05). Meanwhile, systolic blood pressure and diastolic blood pressure were reduced in both groups (P < 0.05), and blood pressure in group B was markedly lower than that in group A after treatment (P < 0.05). Compared with that before treatment, LVMI in both groups decreased (P < 0.05), to a significantly lower degree in group B than in group A (P < 0.05). Atorvastatin can decrease serum concentrations of hs-CRP and UA. The amlodipine-atorvastatin combination markedly reduces blood pressure and reverses left ventricular hypertrophy more than amlodipine monotherapy. The positive effect suggests that in hypertensive and hypercholesterolemic patients, the combination of amlodipine and atorvastatin could be the treatment of choice.
Pregnancy-associated plasma protein-A (PAPP-A) level is an independent predictor of acute cardiovascular event occurrence. To test the hypothesis that increased PAPP-A levels would be associated with a higher burden of coronary thin-cap fibroatheroma (TCFA) thereby underlying the heightened risk for cardiovascular events in patients with coronary artery disease; 154 patients (462 vessels and 975 plaques) with stable angina or non-ST-segment elevation acute coronary syndrome (NSTE-ACS) referred for percutaneous coronary intervention were assessed using 3-vessel virtual histology (VH)-intravascular ultrasound (IVUS). Thin-cap fibroatheroma virtual histology was defined as focal, necrotic core (NC)-rich (≥10% of cross-sectional area) plaques in contact with the lumen, and plaque burden ≥40%. Pregnancy-associated plasma protein-A levels were determined by sandwich enzyme-linked immunosorbent assay, and patients were divided into 3 groups based on PAPP-A level tertiles. Although the highest PAPP-A level tertile was not associated with 3-vessel plaque number, it was associated with 3-vessel VH-TCFA number and necrotic core volume. Patients with ≥3 VH-TCFAs had a higher PAPP-A level than patients with 1 to 3 VH-TCFAs or without any VH-TCFA (13.3 ± 11.8 versus 7.8 ± 4.7 versus 7.4 ± 4.7 mIU/L, P < 0.001, respectively). Moreover, PAPP-A level was an independent predictor of higher total number of VH-TCFAs (OR 1.18; 95% CI 1.07–1.29, P = 0.001). This VH-IVUS study demonstrated, for the first time to our knowledge, that higher PAPP-A levels are associated with higher 3-vessel TCFA burden in patients with coronary artery disease. Pregnancy-associated plasma protein-A, therefore, might be a useful serum biomarker to predict increased coronary TCFA burden and plaque instability.
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