Unenhanced Whole-Heart Coronary MRA: Prospective Intraindividual Comparison of 1.5-T SSFP and 3-T Dixon Water-Fat Separation GRE Methods Using Coronary Angiography as Reference.

BACKGROUND. Coronary MRA is commonly performed at 1.5 T using SSFP acquisitions. Coronary MRA performed at 3 T using SSFP is limited due to impaired fat suppression and has been typically investigated using contrast-enhanced techniques. A Dixon fat-water separation gradient-recalled echo (GRE) method may enable high-quality unenhanced 3-T coronary MRA. OBJECTIVE. The purpose of this study was to compare 1.5-T SSFP and 3-T Dixon water-fat separation GRE methods for unenhanced whole-heart coronary MRA in patients with suspected coronary artery disease (CAD). METHODS. This prospective study included 44 patients (27 men and 17 women; mean age, 59 ± 8 [SD] years) with an intermediate to high risk of CAD who underwent both 1.5-T SSFP and 3-T Dixon GRE coronary MRA examinations before undergoing coronary angiography (CAG). Two radiologists independently assessed coronary arteries in terms of subjective image quality (on a scale of 1-5, with 5 denoting the highest image quality), number of visible segments, apparent contrast-to-noise ratio (CNR; vs myocardium), and presence of significant stenoses. Methods were compared using the mean of the readers' values for apparent CNR and using consensus interpretations for other measures. CAG served as the reference standard for detecting the presence of stenoses. RESULTS. Expressed as a kappa coefficient, interobserver agreement was 0.85 for image quality, 0.85 for segment visibility, and 0.83 for stenosis, and expressed as an intraclass correlation coefficient, interobserver agreement was 0.92 for apparent CNR. The mean overall image quality score was 4.0 ± 1.1 for 3-T Dixon GRE versus 3.0 ± 1.2 for 1.5-T SSFP. The percentage of visible segments for 3-T Dixon GRE versus 1.5-T SSFP was 96.7% versus 88.9% for all segments, 96.9% versus 90.1% for distal segments, and 93.1% versus 77.2% for branch segments. The mean overall apparent CNR was 93.2 ± 29.2 for 3-T Dixon GRE versus 80.8 ± 27.9 for 1.5-T SSFP. The 3-T Dixon GRE method, compared with the 1.5-T SSFP method, showed higher sensitivity and specificity in per-vessel analysis (87.9% vs 77.3% and 83.3% vs 60.6%, respectively), per-segment analysis (84.6% vs 74.8% and 90.9% vs 79.6%, respectively), and per-segment analysis of distal and branch segments (89.7% vs 75.9% and 89.7% vs 73.7%, respectively). CONCLUSION. For unenhanced coronary MRA, 3-T unenhanced Dixon GRE had better image quality and diagnostic performance than 1.5-T SSFP, particularly for distal and branch segments. CLINICAL IMPACT. The 3-T Dixon GRE technique may be preferred to the current clinical standard of the 1.5-T SSFP technique for unenhanced coronary MRA.

AGE/RAGE-Induced EMP Release via the NOX-Derived ROS Pathway.

OBJECTIVE: Diabetes is associated with accelerated formation of advanced glycation end products (AGEs) that are extensively found in circulating endothelial microparticles (EMPs). This study aimed to investigate whether AGEs have a direct effect on EMP formation and the possible underlying mechanism. METHODS: In vitro, cultured human umbilical vein endothelial cells (HUVECs) were incubated with AGEs (200 and 400 µg/ml) for 24 hours with or without pretreatment with anti-RAGE antibody, NOX inhibitor, or ROS scavenger. The number of CD31-positive EMPs was assessed by flow cytometry. RESULTS: The number of EMPs was significantly increased in HUVECs stimulated by AGEs in a dose-dependent manner. In addition, receptors for AGEs (RAGE), NAD(P)H oxidase (NOX), and reactive oxygen species (ROS) were increased by AGEs as compared to the control group. These changes could be reversed when HUVECs were pretreated with anti-RAGE antibody. Moreover, inhibition of NOX as well as antioxidant treatment reduced the release of EMPs induced by AGEs. CONCLUSION: Our study suggested that AGEs increased EMP generation, which was mediated by RAGE signaling through NOX-derived ROS.

Impact of multi-vessel therapy to the risk of periprocedural myocardial injury after elective coronary intervention: exploratory study.

BACKGROUNDS: Periprocedural myocardial injury (PMI) after elective percutaneous coronary intervention (PCI) significantly influences the prognosis of coronary artery disease (CAD). However, it was unclear whether the occurrence of PMI was associated with a series of controllable factors, such as PCI strategy or severity of CAD. METHODS: A total of 544 consecutive stable CAD patients underwent elective PCI were enrolled. The main outcome is PMI, defined as troponin T after PCI was at least one value above the 99th percentile upper reference limit. Major adverse cardiac events (MACE), including all-cause death, repeat myocardial infarction and target vessel revascularization were record in the period of follow-up. Univariate and multivariate analysis was applied to assess predictors for the occurrence of PMI. RESULTS: The incidence of PMI was 38.8% in the study. Compared with non-PMI patients (n = 333), PMI patients (n = 211) had more diseased vessels, higher Gensini and Syntax score. Meanwhile, there were higher incidence of MACE in PMI groups (9.5% vs. 3.2%, P < 0.01). We found that PMI patients underwent higher proportion of multi-vessel PCI simultaneously (32.2% vs. 10.5%, P < 0.01) and had more stents implanted (1.8 ± 0.8 vs. 1.4 ± 0.6, P < 0.01). Importantly, after simultaneously adjusted by other factors (such as age, diabetes, total cholesterol, number of diseased vessels, Gensini score and stent length), the risk of PMI was still increased 84% by multi-vessel PCI independently (OR = 1.654, 95% CI = 1.004-2.720, P < 0.05). CONCLUSIONS: The phenomenon of PMI occurred more commonly in stable CAD patients underwent multi-vessel PCI. Multi-vessel international therapy could increase the risk of PMI in elective PCI.

Establishment of a Novel Mouse Model of Coronary Microembolization.

BACKGROUND: Coronary microembolization (CME) has been frequently seen in acute coronary syndromes and percutaneous coronary intervention. Small animal models are required for further studies of CME related to severe prognosis. This study aimed to explore a new mouse model of CME. METHODS: The mouse model of CME was established by injecting polystyrene microspheres into the left ventricular chamber during 15-s occlusion of the ascending aorta. Based on the average diameter and dosage used, 30 C57BL/6 male mice were randomly divided into five groups (n = 6 in each): 9 µm/500,000, 9 µm/800,000, 17 µm/200,000, 17 µm/500,000, and sham groups. The postoperative survival and performance of the mice were recorded. The mice were sacrificed 3 or 10 days after the surgery. The heart tissues were harvested for hematoxylin and eosin staining and Masson trichrome staining to compare the extent of inflammatory cellular infiltration and fibrin deposition among groups and for scanning transmission electron microscopic examinations to see the ultrastructural changes after CME. RESULTS: Survival analysis demonstrated that the cumulative survival rate of the 17 µm/500,000 group was significantly lower than that of the sham group (0/6 vs. 6/6, P = 0.001). The cumulative survival rate of the 17 µm/200,000 group was lower than those of the sham and 9 µm groups with no statistical difference (cumulative survival rate of the 17 µm/200,000, 9 µm/800,000, 9 µm/500,000, and sham groups was 4/6, 5/6, 6/6, and 6/6, respectively). The pathological alterations were similar between the 9 µm/500,000 and 9 µm/800,000 groups. The extent of inflammatory cellular infiltration and fibrin deposition was more severe in the 17 µm/200,000 group than in the 9 µm/500,000 and 9 µm/800,000 groups 3 and 10 days after the surgery. Scanning transmission electron microscopic examinations revealed platelet aggregation and adhesion, microthrombi formation, and changes in cardiomyocytes. CONCLUSION: The injection of 500,000 polystyrene microspheres at an average diameter of 9 µm is proved to be appropriate for the mouse model of CME based on the general conditions, postoperative survival rates, and pathological changes.

Suppression of Bim by microRNA-19a may protect cardiomyocytes against hypoxia-induced cell death via autophagy activation.

Microvascular obstruction (MO), one of unfavorable complications of percutaneous coronary intervention (PCI), is responsible for the lost benefit of reperfusion therapy. Determination of microRNA-19a, a member of the miR-17-92 cluster, using quantitative real-time polymerase chain reaction (PCR) revealed notably down-regulated microRNA-19a, in myocardium with MO. Nonetheless, the role of miR-19a in MO and the underlying mechanism remains to be elucidated. To this end, an in vitro microembolization model in cardiomyocytes was used. Our data revealed that hypoxic exposure prompted cardiomyocyte apoptosis in a time-dependent manner accompanied by reduced miR-19a. miR-19a overexpression clearly ameliorated hypoxia-induced cell death (necrosis and apoptosis), at least in part, through switching on autophagy. Further dual-luciferase reporter assay and immunoblotting studies demonstrated that miR-19a-induced cytoprotection might be achieved in part through modulation of the specific target Bcl-2 interacting mediator of cell death, Bim, an apoptotic activator. Bim sufficiently interfered with miR-19a-induced LC3 conversion and increased cardiomyocyte apoptosis under hypoxia. Moreover, cardiomyocytes pretreated with 3-methyladenine conferred resistance to the cytoprotective effect of miR-19a and displayed notably increased TUNEL staining and caspase-3 activity. In conclusion, miR-19a protected cardiomyocytes against hypoxia-induced lethality at least in part via Bim suppression and subsequently autophagy activation.

Rapid predictors for the occurrence of reduced left ventricular ejection fraction between LAD and non-LAD related ST-elevation myocardial infarction.

BACKGROUNDS: Reduced left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI), which implies the occurrence of cardiac dysfunction, impacts cardiac prognosis, even after primary percutaneous coronary intervention (PCI). This study was designed to clarify the difference of clinical and angiographic predictors for reduced LVEF in ST-elevation myocardial infarction (STEMI) patients with left anterior descending artery (LAD) or non-LAD vessel as culprit artery. METHODS: This was a retrospective study to review a total of 553 patients of STEMI underwent primary PCI in our hospital. All patients underwent echocardiography. Univariate analysis, multivariate analysis and classification and regression tree (CART) were performed between LAD related AMI and non-LAD related STEMI. The primary outcome was the occurrence of reduced LVEF 4-6 days after PCI. RESULTS: In this study, culprit arteries of STEMI were 315 in LAD system (6 in left main artery, 309 in LAD) and 238 in non-LAD system (63 in left circumflex and 175 in right coronary artery). Compared with non-LAD group, post-MI LVEF was significantly reduced in LAD related STEMI group (52.4 ± 9.3% vs. 57.1 ± 7.8%, P < 0.01). Multivariate analysis indicated that elder (>65 years), time to hospital and proximal occlusion were associated with reduced LVEF (<55%) in LAD related STEMI patients. However, in non-LAD patients, time to hospital, multivessel stenosis and post-PCI blood pressure predicted the occurrence of reduced LVEF. Furthermore, CART analysis also obtained similar findings. CONCLUSIONS: Patients with LAD or non-LAD related STEMI could suffer reduced LVEF, while the clinical and angiographic predictors for the occurrence were different.

Assessment of the acute effects of glucocorticoid treatment on coronary microembolization using cine, first-pass perfusion, and delayed enhancement MRI.

PURPOSE: To assess the acute effects of methylprednisone treatment (MPT) on coronary microembolization (CME) by cardiac cine, first-pass perfusion, and delayed gadolinium enhancement magnetic resonance imaging (DE-MRI) in an experimental swine model. MATERIALS AND METHODS: Microembolization was established by intracoronary infusion of microspheres into the left anterior artery. Swine received placebo (n = 12) or methylprednisolone (n = 10, 30 mg/kg) intravenously 30 minutes before microembolization. Perfusion and DE-MRI was performed 6 hours after microembolization. Cine MR images of pre-/post-CME were obtained using 1.5T scanner. RESULTS: Cine MRI demonstrated relative amelioration of the post-CME myocardial contractile dysfunction in the glucocorticoid-treated group compared to the placebo group (P < 0.001). Post-CME target myocardial perfusion parameters decreased in both groups after microembolization. The extent of these decreases were the same for the embolized-to-control area ratio of maximum upslope (P = 0.245; 95% confidence interval of the difference [CID], -0.041/0.148) and time to peak ratio (P = 0.122; 95% CID, -0.201/0.026); however, the maximum signal intensity was higher in the glucocorticoid-treated group (P = 0.012; 95% CID, 0.023/0.156). DE-MRI revealed patchy hyperenhancement in all placebo pigs (n = 12/12) after microembolization, but no hyperenhanced regions in the glucocorticoid-pretreated pigs (n = 0/10). CONCLUSION: Standard, readily available, cardiac MRI techniques are useful in demonstrating post-CME myocardial dysfunction and the acute effects of glucocorticoid treatment on CME. Glucocorticoid pretreatment improves myocardial contractile dysfunction, prevents hyperenhancement, and partially ameliorates the decline of myocardial perfusion in the embolized area.

Exenatide Reduces Tumor Necrosis Factor-α-induced Apoptosis in Cardiomyocytes by Alleviating Mitochondrial Dysfunction.

BACKGROUND: Tumor necrosis factor-α (TNF-α) plays an important role in progressive contractile dysfunction in several cardiac diseases. The cytotoxic effects of TNF-α are suggested to be partly mediated by reactive oxygen species (ROS)- and mitochondria-dependent apoptosis. Glucagon-like peptide-1 (GLP-1) or its analogue exhibits protective effects on the cardiovascular system. The objective of the study was to assess the effects of exenatide, a GLP-1 analogue, on oxidative stress, and apoptosis in TNF-α-treated cardiomyocytes in vitro. METHODS: Isolated neonatal rat cardiomyocytes were divided into three groups: Control group, with cells cultured in normal conditions without intervention; TNF-α group, with cells incubated with TNF-α (40 ng/ml) for 6, 12, or 24 h without pretreatment with exenatide; and exenatide group, with cells pretreated with exenatide (100 nmol/L) 30 mins before TNF-α (40 ng/ml) stimulation. We evaluated apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and flow cytometry, measured ROS production and mitochondrial membrane potential (MMP) by specific the fluorescent probes, and assessed the levels of proteins by Western blotting for all the groups. RESULTS: Exenatide pretreatment significantly reduced cardiomyocyte apoptosis as measured by flow cytometry and TUNEL assay at 12 h and 24 h. Also, exenatide inhibited excessive ROS production and maintained MMP. Furthermore, declined cytochrome-c release and cleaved caspase-3 expression and increased bcl-2 expression with concomitantly decreased Bax activation were observed in exenatide-pretreated cultures. CONCLUSION: These results suggested that exenatide exerts a protective effect on cardiomyocytes, preventing TNF-α-induced apoptosis; the anti-apoptotic effects may be associated with protection of mitochondrial function.

The influence of aortic valve calcification on the risk of periprocedural myocardial injury after elective coronary intervention.

BACKGROUND: Aortic valve calcification (AVC) is a common progressive condition that involves several inflammatory and atherosclerotic mediators. However, it is unclear whether the occurrence of periprocedural myocardial injury (PMI) after elective coronary intervention is associated with AVC in stable coronary artery disease (CAD) patients. METHODS: A total of 530 stable CAD patients who underwent elective coronary intervention were enrolled in this clinical study. High sensitive cardiac troponin T (hs-cTnT) was detected before and after the procedure. PMI was defined as hs-cTnT after coronary intervention higher than 99th percentile upper reference limit (URL). All patients underwent echocardiography to detect the occurrence of AVC. Univariate and multivariate analyses were applied to analyze risk factors of PMI. RESULTS: A total of 210 patients (39.6 %) were diagnosed with PMI after elective coronary intervention. Compared with non-AVC patients (n = 386), AVC patients (n = 144) had higher rate of PMI (64.6 vs. 30.3 %, P < 0.01). CAD patients with AVC had higher Gensini score (39.9 ± 26.6 vs. 34.2 ± 22.1, P < 0.05) and more number of implanted stents (1.7 ± 0.8 vs. 1.5 ± 0.7, P < 0.05). After stratification by classic risk factors of CAD (such as age, male gender and diabetes) in subgroup analyses, we found that AVC patients had increased risk of PMI compared with non-AVC patients. Importantly, even after being adjusted by multivariate analysis, AVC still independently increased the risk of PMI (OR = 3.329, 95 % CI = 2.087-5.308, P < 0.01). CONCLUSION: AVC significantly increased the risk of PMI after elective coronary intervention. It could be one of the independent predictors for PMI in stable CAD patients.

Association of indoxyl sulfate with heart failure among patients on hemodialysis.

BACKGROUND AND OBJECTIVES: Indoxyl sulfate, a protein-bound uremic toxin, may be associated with cardiovascular events and mortality in patients with CKD. This study aimed to investigate the relationship between indoxyl sulfate and heart failure in patients on hemodialysis. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Patients on hemodialysis for >6 months were enrolled within 6 months. Patients with congestive heart failure, angina pectoris, acute myocardial infarction, cerebral infarction, or cerebral hemorrhage within 3 months before the study or those <18 years old were excluded. The primary end point was first heart failure event during follow-up. RESULTS: In total, 258 patients (145 men) with a mean age of 57.0 ± 14.6 years old were enrolled. Median plasma indoxyl sulfate level was used to categorize patients into two groups: the low-indoxyl sulfate group (indoxyl sulfate ≤ 2.35 µg/ml) and the high-indoxyl sulfate group (indoxyl sulfate >32.35 µg/ml). Then, patients were prospectively followed up for a median of 48.0 (interquartile range: 33.5-48.0) months. During follow-up, 68 patients experienced episodes of first heart failure. Kaplan-Meier analysis revealed the incidence of first heart failure event in the high-indoxyl sulfate group was significantly higher than in the low-indoxyl sulfate group (log rank P<0.001). Cox regression analysis showed indoxyl sulfate was significantly associated with first heart failure event (indoxyl sulfate as the continuous variable: hazard ratio, 1.02; 95% confidence interval [95% CI], 1.01 to 1.03; P=0.001; indoxyl sulfate as the dichotomous variable: hazard ratio, 3.49; 95% CI, 1.97 to 6.20; P<0.001). After adjustment for other confounding factors, the results remained significant (indoxyl sulfate as the continuous variable: hazard ratio, 1.04; 95% CI, 1.02 to 1.06; P<0.001; indoxyl sulfate as the dichotomous variable: hazard ratio, 5.31; 95% CI, 2.43 to 11.58; P<0.001). CONCLUSIONS: Plasma indoxyl sulfate was associated with first heart failure event in patients on hemodialysis. Whether indoxyl sulfate is only a biomarker or involved in the pathogenesis of heart failure in hemodialysis warrants additional study.

TNF-α-induced cardiomyocyte apoptosis contributes to cardiac dysfunction after coronary microembolization in mini-pigs.

This experimental study was designed to clarify the relationship between cardiomyocyte apoptosis and tumour necrosis factor-alpha (TNF-α) expression, and confirm the effect of TNF-α on cardiac dysfunction after coronary microembolization (CME) in mini-pigs. Nineteen mini-pigs were divided into three groups: sham-operation group (n = 5), CME group (n = 7) and adalimumab pre-treatment group (n = 7; TNF-α antibody, 2 mg/kg intracoronary injection before CME). Magnetic resonance imaging (3.0-T) was performed at baseline, 6th hour and 1 week after procedure. Cardiomyocyte apoptosis was detected by cardiac-TUNEL staining, and caspase-3 and caspase-8 were detected by RT-PCR and immunohistochemistry. Furthermore, serum TNF-α, IL-6 and troponin T were analysed, while myocardial expressions of TNF-α and IL-6 were detected. Both TNF-α expression (serum level and myocardial expression) and average number of apoptotic cardiomyocyte nuclei were significantly increased in CME group compared with the sham-operation group. Six hours after CME, left ventricular end-systolic volume (LVESV) was increased and the left ventricular ejection fraction (LVEF) was decreased in CME group. Pre-treatment with adalimumab not only significantly improved LVEF after CME (6th hour: 54.9 ± 2.3% versus 50.4 ± 3.9%, P = 0.036; 1 week: 56.7 ± 4.2% versus 52.7 ± 2.9%, P = 0.041), but also suppressed cardiomyocyte apoptosis and the expression of caspase-3 and caspase-8. Meanwhile, the average number of apoptotic cardiomyocytes nuclei was inversely correlated with LVEF (r = -0.535, P = 0.022). TNF-α-induced cardiomyocyte apoptosis is likely involved in cardiac dysfunction after CME. TNF-α antibody therapy suppresses cardiomyocyte apoptosis and improves early cardiac function after CME.

Validation of a novel clinical prediction score for severe coronary artery diseases before elective coronary angiography.

OBJECTIVES: Coronary artery disease (CAD) severity is associated with patient prognosis. However, few efficient scoring systems have been developed to screen severe CAD in patients with stable angina and suspected CAD before coronary angiography. Here, we present a novel scoring system for CAD severity before elective coronary angiography. METHODS: Five hundred fifty-one patients with stable angina who were admitted for coronary angiography were enrolled in this study. Patients were divided into training (n = 347) and validation (n = 204) cohorts. Severe CAD was defined as having a Gensini score of 20 or more. All patients underwent echocardiography (ECG) to detect ejection fraction and aortic valve calcification (AVC). Multivariable analysis was applied to determine independent risk factors and develop the scoring system. RESULTS: In the training cohort, age, male sex, AVC, abnormal ECG, diabetes, hyperlipidemia, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were identified as independent factors for severe CAD by multivariable analysis, and the Severe Prediction Scoring (SPS) system was developed. C-indices of receiver operating characteristic (ROC) curves for severe CAD were 0.744 and 0.710 in the training and validation groups, respectively. The SPS system also performed well during calibration, as demonstrated by Hosmer-Lemeshow analysis in the validation group. Compared with the Diamond-Forrester score, the SPS system performed better for severe CAD prediction before elective coronary angiography. CONCLUSIONS: Severe CAD prediction was achieved by analyzing age, sex, AVC, ECG, diabetes status, and lipid levels. Angina patients who achieve high scores using this predicting system should undergo early coronary angiography.

Coronary artery angiography and myocardial viability imaging: a 3.0-T contrast-enhanced magnetic resonance coronary artery angiography with Gd-BOPTA.

With improving MR sequence, phase-array coil and image quality, cardiac magnetic resonance imaging is becoming a promising method for a comprehensive non-invasive evaluation of coronary artery and myocardial viability. The study aimed to evaluate contrast-enhanced whole-heart coronary MR angiography (CE WH-CMRA) at 3.0-Tesla for the diagnosis of significant stenosis (≥50%) and detection of myocardial infarction (MI) in patients with suspected coronary artery disease (CAD). CE WH-CMRA was performed in consecutive 70 patients with suspected CAD by using a 3.0-T MR system. A respiratory-gated, electrocardiography-triggered, inversion-recovery, segmented fast low angle shot sequence (TI = 200 ms) was used. Data acquisition began 60 s after the slow injection of Gd-BOPTA (0.2 mmol/kg body weight, at an injection rate 0.3 ml/s). At last, breath-hold 2D-PSIR-SSFP sequence was performed. Diagnostic accuracy of CE WH-CMRA in detecting significant stenosis (≥50%) was evaluated using invasive coronary angiography as the referenced standard. The MI region appearing as high signal intensity visualized on CEWH-CMRA and 2D-PSIR-SSFP images were compared and analyzed. CE WH-CMRA correctly identified 42 of 44 patients with significant CAD. The overall sensitivity, specificity, negative predictive value, positive predictive value and accuracy for diagnosing significant CAD was 83.6, 95.8, 96.0, 82.8 and 93.4% respectively. The MI region detected by WH-CMRA and 2D-PSIR-SSFP were consistent in 10 patients and these segments manifested with transmural or subendocardial enhancement patterns. Only one MI patient was judged inconsistent between WH-CMRA and 2D-PSIR-SSFP, who was confirmed by clinical and electrocardiogram results. The enhancement pattern in this patient was spotted and focal in 2D-PSIR-SSFP, but was dismissed by WH-CMRA. It is feasible to obtain information about coronary artery stenosis and myocardial viability in a single CE WH-CMRA with administration of Gd-BOPTA.

Risk factors of cardiac troponin T elevation in patients with stable coronary artery disease after elective coronary drug-eluting stent implantation.

BACKGROUND: Cardiac troponin T elevation after coronary intervention has been demonstrated to be associated with the prognosis of coronary artery disease (CAD). However, there were few studies about comprehensive risk factors analysis of troponin T elevation after elective drug-eluting stent (DES) implantation. HYPOTHESIS: The prognosis of CAD after coronary interventions was associated with clinical and procedural risk factors of CAD, such as age, hypertension, severity extent of CAD and so on. METHODS: From March to December in 2010, patients with stable CAD were admitted for elective coronary intervention in our hospital. They were divided into an elevated troponin T group and a normal troponin T group by postprocedural troponin T. Clinical factors, laboratory-test factors, and angiographic factors (such as gender, age, cholesterol, Gensini score, and others) were analyzed. RESULTS: A total of 209 patients with an average age of 64.0 ± 9.9 years were enrolled in the study: 70 patients with elevated troponin T (≥0.03 ng/mL) after DES implantation and 139 patients with normal troponin T (<0.03 ng/mL). After univariate analysis, we found that age, hypertension, total cholesterol, low density lipoprotein-cholesterol (LDL-C), Gensini score, number of stenosed vessels, and total implanted stents were associated with postprocedural troponin T elevation. According to the results of multivariate analysis, we found that age, total cholesterol, number of stenosed vessels, and number of implanted stents were independent risk factors of postprocedural troponin T elevation. CONCLUSIONS: Age, serum total cholesterol, number of stenosed vessels, and number of implanted stents could be independent risk factors of troponin T elevation after elective DES implantation.

Prevalence and severity of coronary artery disease in diabetic patients with aortic valve calcification.

OBJECTIVE: Aortic valve calcification (AVC) is common in the elderly and associated with increased cardiovascular mortality, while diabetes is one of the confirmed risk factors for coronary artery disease (CAD). In this study, we aimed to evaluate the prevalence and severity of CAD in type-2 diabetic patients with AVC. METHODS: From June to December in 2007, a total of 325 consecutive patients with chest pain or chest distress were admitted for coronary angiography. The severity of CAD was evaluated by the Gensini score and the number of stenosed vessels. All patients underwent transthoracic echocardiography for detecting AVC. RESULTS: Compared with the patients without diabetes (n = 221), the type-2 diabetic patients (n = 104) had a similar prevalence of CAD (66.5% vs. 72.1%, P = 0.312). Further classified by the presence of AVC, patients with AVC had a higher prevalence of CAD, average Gensini score and the number of stenosed vessels, both in the group with and without diabetes. It was also demonstrated that the odds ratio (OR) of AVC for CAD in the diabetic patients was higher than in the non-diabetic ones (3.405 vs 2.515) after chi-square analysis (single-variable). However, at multivariable logistic regression analysis for CAD, the OR of AVC was 3.757 (P = 0.03) in diabetic group, while it did not achieve statistical significance in the non-diabetic group (OR = 2.130, P= 0.074). CONCLUSIONS: Type-2 diabetic patients with AVC had a higher prevalence of and more severe CAD.

Spatio-temporal distribution of malaria in Yunnan Province, China.

The spatio-temporal distribution pattern of malaria in Yunnan Province, China was studied using a geographic information system technique. Both descriptive and temporal scan statistics revealed seasonal fluctuation in malaria incidences in Yunnan Province with only one peak during 1995-2000, and two apparent peaks from 2001 to 2005. Spatial autocorrelation analysis indicated that malaria incidence was not randomly distributed in the province. Further analysis using spatial scan statistics discovered that the high risk areas were mainly clustered at the bordering areas with Myanmar and Laos, and in Yuanjiang River Basin. There were obvious associations between Plasmodium vivax and Plasmodoium falciparum malaria incidences and climatic factors with a clear 1-month lagged effect, especially in cluster areas. All these could provide information on where and when malaria prevention and control measures would be applied. These findings imply that countermeasures should target high risk areas at suitable times, when climatic factors facilitate the transmission of malaria.

Acute hyperenhancement on delayed contrast-enhanced magnetic resonance imaging is the characteristic sign after coronary microembolization.

BACKGROUND: Detection of coronary microembolization is of clinical importance for patient management and prediction of long-term outcome. However, there are few studies of the changes of magnetic resonance imaging after coronary microembolization. This study was designed to investigate the imaging of the left ventricle using delayed contrast enhanced magnetic resonance imaging as well as the left ventricular ejection fraction after coronary microembolization in animal models. METHODS: Eight miniswine, of either sex (body weight 21-25 kg), were used to make the coronary microembolization model. After coronary angiography, a 2.8F infusion catheter was placed in the left anterior descending artery with the tip located between the second and third diagonal branches. Microspheres with the diameter of 42 microm and mean dosage of 1.2 x 10(5) were selectively infused into the left anterior descending artery. First pass and stressed first pass perfusion scan were performed after cine images were acquired. Then a second bolus of 0.15 mmol/kg gadolinium DTPA was given at a rate of 2 ml/s. Ten minutes later, delayed contrast enhanced magnetic resonance images of the left ventricular wall were evaluated. Serum changes of tumor necrosis factor alpha (TNF-alpha) were evaluated by enzyme-linked immunosorbent assay (ELISA). RESULTS: Hypoenhancement was not observed at first pass perfusion at the anterior wall of the left ventricle. Hyperenhancements of the anterior-septal and anterior wall of the left ventricle was in evidence on delayed enhancement images 6 hours after microembolization and disappeared one week later. The characteristic change of coronary microembolization on delayed contrast enhanced magnetic imaging was non-enhanced regions within the hyperenhancement zone. Left ventricular ejection fraction measured by magnetic resonance imaging decreased significantly from 0.451 +/- 0.063 at baseline to 0.362 +/- 0.070 at the sixth hour (P < 0.01), and recovered to 0.431 +/- 0.053 one week later (P < 0.01 vs 6th hour). Compared with baseline values, the left ventricular end systolic volume enlarged significantly at 6th hour and at one week after microembolization (P < 0.05 and P < 0.01 respectively). Serum TNF-alpha increased significantly at 6th hour (22.62 +/- 6.96) pg/ml compared with baseline (16.83 +/- 3.45) pg/ml (P < 0.05) and it further increased to (27.44 +/- 3.97) pg/ml at one week after coronary microembolization and was significantly higher than that at baseline (P < 0.01). CONCLUSIONS: On delayed contrast enhanced magnetic resonance imaging, hyperenhancement of the anterior-septal and anterior wall of the left ventricle show at 6th hour but not at one week after coronary microembolization. This might represent the characteristic imaging after coronary microembolization. The left ventricular ejection fraction decreased at 6th hour and recovered one week later after coronary microembolization. Although impairment of left ventricular function could be recovered at 1 week after coronary microembolization, the left ventricular remodeling process still continued in concert with continuously elevation of serum TNF-alpha.