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This study aimed to evaluate the relationship between grayscale intravascular ultrasound-attenuated plaque (AP) and poststenting plaque prolapse (PP) as well as their influence on creatine kinase-myocardial band (CK-MB) elevation after drug-eluting stent (DES) implantation.The relationship between baseline AP and poststenting PP and their impacts on percutaneous coronary intervention (PCI) are not well known.A total of 141 single, native, de-novo coronary lesions in 141 patients with normal pre-PCI CK-MB levels who underwent intravascular ultrasound before and after DES implantation were studied.AP was found in 72 (51.1%) lesions and PP occurred in 43 (30.5%) lesions. Baseline AP was associated with greater plaque area, lesion eccentricity, and positive remodeling, and was associated with higher frequency of poststenting PP (47.2 vs. 13.0%, P0.001) as well as greater poststenting PP volume (2.2±1.3 vs. 1.9±1.1 mm, P=0.045). Elevated CK-MB levels were observed in 34 (24.1%) lesions and significantly more frequently in patients with baseline AP and poststenting PP than without both of these findings. Multivariate analysis indicated that AP with PP was the predictor of post-PCI CK-MB elevation.Baseline AP was associated with high-risk characteristics, higher frequency, and greater volume of poststenting PP accompanied by CK-MB elevation in patients with DES implantation.

There is no reliable way to identify the high-risk patients with intermediate coronary artery lesions (diameter stenosis 20%-70%) in early stage. Soluble CXC chemokine ligand 16 (CXCL16) is a newly discovered chemokine that can mediate inflammatory responses. It is released by proteolytic cleavage of its membrane-bound form, named scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX) that can promote the uptake of oxidized low-density lipoprotein cholesterol by macrophages. We have hypothesized that CXCL16 is an indicator of the prognosis of intermediate coronary artery lesions, and thus assessed the association between plasma CXCL16 concentrations and the 2-year prognosis in 616 patients with intermediate coronary artery lesions. The primary endpoint was a composite of all-cause death, non-fatal myocardial infarction, revascularization and angina pectoris requiring re-hospitalization. During the median follow-up time of 24 months, 69 events occurred. The plasma concentrations of CXCL16 (median 7712.88 pg/ml vs. 6792.43 pg/ml, P = 0.014) and high-sensitivity C-reactive protein (hs-CRP) (median 2.82 mg/L vs. 1.68 mg/L, P < 0.001) were higher in patients with events than patients without events. Cox hazard proportion analysis showed patients in upper CXCL16 quartile were more likely to suffer from adverse outcome than patients in lower quartile (RR = 1.271, P = 0.029, 95% CI: 1.025-1.577) after adjusting for sex, age, smoking, hypertension, diabetes, fat, dyslipidemia, hs-CRP, and medication use. In conclusion, plasma level of CXCL16 is an independent predictor of the prognosis of the patients with intermediate coronary lesions. Elevated plasma CXCL16 is associated with higher risk for these patients.

Percutaneous coronary intervention with drug-eluting stents (DES) may achieve midterm outcomes comparable to coronary artery bypass grafting (CABG) for unprotected left main coronary artery disease, but few real-world, long-term studies have been reported. In this study, 376 patients with unprotected left main coronary artery disease who underwent DES implantation (n = 131) or CABG (n = 245) were evaluated, and outcomes were compared using propensity analyses to adjust for baseline differences. Overall, 367 patients (98%) had complete clinical follow-up for a median of 4.0 years (interquartile range 3.2 to 4.7). Although the overall sample size was limited, there was a trend toward lower mortality with DES versus CABG in unadjusted (hazard ratio [HR] 0.50, 95% confidence interval [CI] 0.20 to 1.22, p = 0.13), multivariate-adjusted (HR 0.37, 95% CI 0.13 to 1.09, p = 0.07), and propensity score-adjusted (HR 0.34, 95% CI 0.12 to 1.03, p = 0.06) analyses. Treatment with DES was associated with a higher rate of target-vessel revascularization (TVR; 18% vs 9%, p = 0.02). However, ischemic TVR was not significantly different between the 2 groups (25% vs 39%, p = 0.15) in patients who received angiographic follow-up. No differences were detected in the occurrence of composite major adverse cardiac and cerebrovascular events between DES and CABG (27% vs 22%, p = 0.42). In conclusion, during 4-year follow-up, overall composite major adverse cardiac and cerebrovascular events were similar after DES and CABG treatment of unprotected left main coronary artery disease, with a trend toward lower mortality after percutaneous coronary intervention with DES. DES were associated with a higher rate of TVR compared to CABG, but ischemic TVR was not significantly different between the 2 groups.

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 follow‐up, 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. Copyright © 2009 Wiley Periodicals, Inc.

To assess the relationship between pregnancy associated plasma protein-A (PAPP-A) and culprit coronary plaque morphology in patients with unstable angina (UA).Sixty-eight UA patients undergoing diagnostic coronary angiography and intravascular ultrasound were included in this study. A sandwich enzyme-linked immunosorbent assay technique was used to assay the circulating PAPP-A. Plaque characteristics of culprit lesion were analyzed for UA patients with various PAPP-A levels.PAPP-A level was significantly higher in high-risk UA than in non-high-risk UA [(19.9 ± 20.1) mIU/L vs. (6.9 ± 5.7) mIU/L, P = 0.002]. Optimal threshold of PAPP-A to predict high-risk UA was determined as 11.0 mIU/L with a sensitivity of 78.6% and a specificity of 77.5%. Patients with higher PAPP-A level (≥ 11.0 mIU/L) was associated with larger external elastic membrane cross-sectional area, plaque area and more plaque burden compared with patients with lower PAPP-A level (all P0.01). Positive remodeling, attenuated plaque and plaque rupture were significantly more often in patients with higher PAPP-A than in patients with lower PAPP-A level (all P0.01). PAPP-A ≥ 11.0 mIU/L (OR = 5.921, P = 0.014) and attenuated plaque (OR = 7.541, P = 0.038) were independent risk predictors for high-risk UA.PAPP-A was associated with instability of culprit plaque in UA patients. PAPP-A ≥ 11.0 mIU/L and attenuated plaque were independent predictors for high-risk UA.

To evaluate the accuracy of quantitative coronary angiography (QCA) assessment on target lesion and reference vessel in patients with diabetes mellitus with intravascular ultrasound (IVUS) measurements as golden standard.QCA and IVUS were performed in 52 diabetes mellitus patients [35 males, mean age (62.3 +/- 7.1) years]. Regression equation was ascertained with the IVUS derived plaque burden as dependent and QCA derived vessel stenosis as independent variable. The measurement results derived from the two modalities on proximal and distal reference vessels were compared.The regression equation (constant = 0.8286, P = 0.001) of plaque burden and vessel stenosis derived from two modalities were significantly correlated (r = 0.691, P0.001) but QCA overestimated the stenosis severity (57.9% +/- 15.5% vs. 53.5% +/- 12.9%, P0.01). Target vessels negative remodeling index in these patient was 0.87 +/- 0.23. QCA significantly underestimated the proximal and distal reference segments vessel diameters [(0.81 +/- 0.24) mm, (0.64 +/- 0.17) mm, all P0.05] as compared to IVUS results.Due to the significant negative vessel remodeling, QCA overestimated the stenosis severity and underestimated the reference segments vessel diameters in patients with diabetes mellitus.

To develop a simple risk score model of in-hospital major adverse cardiac events (MACE) including all-cause mortality, new or recurrent myocardial infarction (MI), and evaluate the efficacy about revascularization on patients with different risk.The basic characteristics, diagnosis, therapy, and in-hospital outcomes of 1512 ACS patients from Global Registry of Acute Coronary Events (GRACE) study of China were collected to develop a risk score model by multivariable stepwise logistic regression. The goodness-of-fit test and discriminative power of the final model were assessed respectively. The best cut-off value for the risk score was used to assess the impact of revascularization for ST-elevation MI (STEMI) and non-ST elevation acute coronary artery syndrome (NSTEACS) on in-hospital outcomes.(1) The following 6 independent risk factors accounted for about 92.5% of the prognostic information: ageor =80 years (4 points), SBPor =90 mm Hg (6 points), DBPor =90 mm Hg (2 points), Killip II (3 points), Killip III or IV (9 points), cardiac arrest during presentation (4 points), ST-segment elevation (3 points) or depression (5 points) or combination of elevation and depression (4 points) on electrocardiogram at presentation. (2) CHIEF risk model was excellent with Hosmer-Lemeshow goodness-of-fit test of 0.673 and c statistics of 0.776. (3)1301 ACS patients previously enrolled in GRACE study were divided into 2 groups with the best cut-off value of 5.5 points. The impact of revascularization on the in-hospital MACE of the higher risk subsets was stronger than that of the lower risk subsets both in STEMI [OR (95% CI) = 0.32 (0.11, 0.94), chi2 = 5.39, P = 0.02] and NSTEACS [OR (95% CI) = 0.32 (0.06, 0.94), chi2 =4.17, P = 0.04] population. However, both STEMI (61.7% vs. 78.3%, P = 0.000) and NSTEACS (42.0% vs 62.3%, P = 0.000) patients with the risk scores more than 5.5 points had lower revascularization rates.The risk score provides excellent ability to predict in-hospital death or (re) MI quantitatively and accurately. The patients undergoing revascularization with risk score greater than 5.5 have lower incidence rates of endpoint.

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.