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Background: The association between interleukin-8 (IL-8) gene polymorphism −251 A>T and susceptibility to coronary artery disease (CAD) has been investigated previously; however, results remain controversial. Thus, a meta-analysis was conducted to reassess the effects of this polymorphism on CAD risks. Methods: The PubMed, Cochrane Library, China National Knowledge Infrastructure, and Wanfang databases were searched for relevant studies published up to December, 2018. The pooled odds ratios (OR) were calculated using STATA 13.0 software for allelic (A vs T) as well as homozygote (AA vs TT), heterozygote (AT vs TT), recessive (AA vs AT + TT), and dominant (AA + AT vs TT) genotype models, respectively. Results: Ten case-control studies (3744 cases and 3660 controls) were included. Overall, a significant association of IL-8 gene −251 A > T polymorphism with an increased risk of CAD was only observed in the dominant genotype model (OR = 1.48), but not others. In the subgroup analysis, significantly increased risks were also found for Chinese (OR = 1.64), polymerase chain reaction-restriction fragment length polymorphism genotyping (OR = 1.61), acute coronary syndrome (ACS) type (OR = 1.92 for 3 datasets; OR = 1.88 for 4 datasets), high quality (OR = 1.64), and age/gender matching status (OR = 1.55) under the dominant model. Furthermore, significantly increased risks were also found for ACS type under allelic (OR = 1.32 for 3 datasets; OR = 127 for 4 datasets), homozygote (OR = 1.64 for 3 datasets; OR = 1.50 for 4 datasets), heterozygote (OR = 1.32 for 3 datasets; OR = 1.30 for 4 datasets), and recessive (OR = 1.40 for 3 datasets; OR = 1.28 for 4 datasets) models. Conclusion: This meta-analysis suggests that Chinese patients carrying −251A allele of IL-8 may have an increased risk for the development of CAD, especially ACS.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that hydrolyzes oxidized phospholipids to generate bioactive proatherogenic products. Nonculprit lesions have been assumed to contribute to the pathogenesis of recurrent acute coronary syndrome (ACS). The role of LP-PLA2 in the progression of nonculprit coronary lesions after successful percutaneous coronary intervention (PCI) remains unclear. Our study included 123 patients with ACS who underwent initial PCI and a long-term follow-up (mean interval, one year) with coronary angiography. Among them, 19 patients were diagnosed as the progression of nonculprit lesions, based on the presence of at least one of the following factors: (1) ≥ 10% reduction in the diameter of a preexisting ≥ 50% stenosis; (2) ≥ 30% reduction in the diameter of a < 50% stenosis; and (3) early-onset stenosis with ≥ 30% reduction in the diameter of a segment that was normal on the primary angiogram. Blood sampling was drawn from all patients at 12-14 hours after PCI. The ACS patients with progression had higher total cholesterol (4.47 ± 1.02 mmol/L vs. 3.59 ± 0.57 mmol/L, P < 0.05), higher levels of Lp-PLA2 activity (14.39 ± 6.13 nmol/min/ml vs. 8.86 ± 3.14 nmol/min/ml, P < 0.001) and a higher proportion of multi-vessel disease than those without progression. Multivariate logistic regression analysis showed that Lp-PLA2 activity (β = 0.024, P = 0.005) was an independent predictor for rapid progression of nonculprit coronary lesions. In conclusion, elevated Lp-PLA2 activity is associated with rapid progression of nonculprit coronary lesions in ACS patients who underwent PCI.

OBJECTIVE To investigate the effects of salvianolic acid B (SA-B) on cardiovascular endothelial cell function and platelet activation during myocardial ischemia-reperfusion in rabbits. METHODS A total of 24 New Zealand white rabbits were randomly divided into sham-operated group, ischemia-reperfusion group (untreated group) and SA-B group. The hearts of rabbits in untreated group and SA-B group underwent half an hour of left anterior descending coronary artery (LADCA) occlusion via ligation technology, which was followed by 4 hours of reperfusion to prepared ischemia-reperfusion injury model in vivo. For sham-operated group, the animals were not subjected to occlusion of LADCA. In SA-B treatment group the rabbits were intravenously administered SA-B immediately after LADCA occlusion, and the other two groups were given normal saline in the same way instead of SA-B. The jugular vein bloods of animals were collected before LADCA ligation, half an hour after ligation and after 1-, 4-hour reperfusion, respectively. The content of plasma nitric oxide (NO) was determined by nitrate reductase process. Radioimmunoassay was applied to detect the endothelin (ET) content in plasma and the count of alpha-granule membrane protein-140 (GMP-140) on platelet surface to identify the activation of the platelet. RESULTS No significant difference was observed before and after sham LADCA occlusion in sham-operated group in the contents of NO and ET in plasma (P>0.05), neither was the count of GMP-140 on platelet surface (P>0.05). The content of NO in plasma detected 0.5 h after LADCA occlusion was significantly decreased in untreated group compared with the sham-operated group at the corresponding time, and they were also much lower than that before LADCA occlusion in the sham-operated group (P

Introduction: Aortopulmonary window (APW), a large aortopulmonary septal defect (APSD), is a serious and rare defect within congenital heart diseases. Case report: In this study, we reported an APW case with severe pulmonary arterial hypertension. This patient was successfully treated by transcatheter closure with a muscular ventricular septal defect (VSD) occluder. Conclusion: We had a successful experience with transcatheter closure of a large APW using a muscular VSD occluder. There was no residual shunt or complications during the 6-month follow-up.

A 3-month-old female of 5 kg presented with a 4.23 mm isolated perimembranous ventricular septal defect (pmVSD) which was confirmed by transoesophageal echocardiography (TEE) ( Panel A ). Before that, she had suffered from pneumonia twice. Systolic murmurs of Grade 3 could be heard in the third intercostal space, with intense pulmonary second heart sound. As determined with transthoracic echocardiography (TTE) analysis, the dimensions of the pmVSD were 4.5 mm, with enlarged left atria and ventricles. A 46 mmHg pulmonary artery systolic pressure was estimated by TTE. Cardiomegaly (cardiothoracic ratio: 0.65) and pulmonary congestion were demonstrated on chest X-ray film. All the above features strongly indicated …