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Introduction We aim to compare the midterm outcomes between coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) in diabetic patients who had multivessel coronary artery diseases (CAD). Material and methods A comprehensive literature search was conducted to identify the related clinical studies with a follow-up for 1 year at least. The endpoints were death, myocardial infarction, and major adverse cardiac and cerebrovascular events (MACCE). Results Finally, the analysis of ten studies involving 5,264 patients showed that patients with CABG had worse baseline characteristics, a higher rate of stable angina pectoris, a higher percentage of triple-vessel disease, higher incidence of chronic total occlusion and a higher SYNTAX score. However, there was no significant difference in mortality between the two groups. Additionally, the rates of myocardial infarction and MACCE were markedly decreased in the CABG group. Conclusions The strategy of CABG is better than PCI for diabetic patients with multivessel CAD. The CABG can significantly reduce the rates of myocardial infarction and MACCE and is comparable in mortality despite the worse baseline characteristics.

Aim: This study was to carry out exome sequencing in a Han Chinese family with venous thromboembolism. Methods: Three venous thromboembolism (VTE) patients and five members from a Han Chinese family were evaluated by exome sequencing. Results: Among the 3 VTE patients, mutations of 2 genes including PRF1 and HTR2A were identified and predicted to be functionally damaged to their encoded proteins. In addition, the PRF1 mutation and the HTR2A mutation identified in our study were absent in 100 non-related controls, indicating that venous thromboembolism has a genetic component. The R357W mutation is located in the membrane attack complex/perforin domain of PRF1 protein, which exists in both the perforin. The steps of killing foreign or pathological antigen cells by NK cells, CD8 +T cells and the membrane attack complex include membrane perforation and release of the granzyme, either of which is abnormal can lead to immune dysfunction. Conclusions: The mutations of immune related genes in familial VTE might provide new understanding of the pathogenesis of familial venous thromboembolism.

Background: To investigate the mechanism of smoking on cardiovascular diseases. Material and methods: 576 elderly patients with cardiovascular diseases in stable condition were consecutive recruited, asked about the living habits and smoking history in a way of face to face. Results: Of all the enrolled patients, current smoking rate was 34.8% for males and 3.4% for females. Average smoking quantity was 17 cigarettes per day and incidence of hyperhomocysteinemia was 38.0%. The homocysteine level in current smokers was significantly higher than that in never smokers (P = 0.004); while the serum folic acid and serum superoxide dismutase (SOD) level were significantly lower those in never smokers (P = 0.012; P = 0.004). The daily smoking consumption and the pack-years of smoking were significantly positively correlated with total homocysteine (tHcy) level (P = 0.020; P = 0.003). The reduced serum SOD level might be associated with increased risk of hypertension (P = 0.023), coronary heart disease (P = 0.018), and stroke (P = 0.035). However, the elevated serum tHcy level was not correlated with increased risk of hypertension and coronary heart disease, while may increase the risk of ischemic stroke (P = 0.075). Conclusions: Smoking status is still prevalent among Chinese elderly patients with cardiovascular diseases, which causes the increase of serum tHcy and the decrease of serum folate as well as SOD; smoking consumption per day and pack-years of smoking have indirect effects on tHcy. And decrease of serum SOD is a risk factor for cardiovascular diseases, increase of serum tHcy may be associated with changes of metabolism caused by oxidative damage.

Background: To compare different expression of core proteins among venous thromboembolism (VTE) and those with risk factor groups and analyze the relative risk for VTE after integrating integrin β1, β2 and β3 expression. Methods: A total of 1006 subjects were recruited and divided into VTE group, risk factor groups and control (non- risk factor) group. Flow cytometry was performed to detect the expression of integrin β1, β2 and β3. The relative risk for VTE was evaluated with independent, parallel and serial methods. Results: The expression of integrin β1 increased markedly in VTE patients, and those with risk factors (acute infection, malignancy, and autoimmune diseases), respectively (P < 0.001 or 0.01). The expression of integrin β1 in trauma/surgery group was not significantly different with control group (P > 0.05). The expression of integrin β2 or β3 significantly increased in VTE group, but that in risk factor groups was not significantly increased (P > 0.05). Multivariate analysis revealed the trauma/surgery groups had no significantly increased risk for VTE. Conclusions: VTE group patients have significantly increased expression of integrin β1, β2 and β3, and risk factor groups (acute infection, malignancy and autoimmune disease) have significantly increased expression of integrin β1. The significant increase in integrin β2, β3 expression is a marker differentiating of VTE group patients with other risk factor groups. Trauma/surgery group has no increased expression of integrin β1, β2 and β3 as other risk factors. Thus, that trauma/surgery may be not the “true” risk factor for VTE.

Aim: Poly-l-lactic acid (PLLA) based bioabsorbable stents with or without amorphous calcium phosphate (ACP) were implanted and compared the inflammation in coronary arteries. Methods: 6 PLLA and 6 PLLA/ACP based paclitaxel-eluting stents were randomly implanted into the coronary arteries of 12 healthy mini-pigs. The segments with stent were used to evaluate inflammation score and endothelialization score by hematoxylin-eosin staining. Results: At the 28th day after stent implantation, no in-stent restenosis or stent thrombosis was found in both PLLA and PLLA/ACP group. Histological analysis indicated that the inflammation score in PLLA/ACP group was less than that of in PLLA group (2.20±0.42 vs. 2.80±0.48, P

Objective: The high morbidity, mortality and misdiagnosis rate render pulmonary embolism (PE) as a worldwide health problem. However, the etiology and pathogenesis of this disease have not been well characterized. Increasing studies indicate infection and immunity play a crucial role in PE. Natural killer (NK) cells act as a bridge between the innate immune and acquired immune. This study aimed to investigate the possible function of NK cells in PE. Methods: Human cDNA microarray analysis was employed to detect genes associated with NK cells in peripheral blood mononuclear cells (PBMCs). Random variance model corrected t-test was used for statistical analysis of differential gene expression. Flow cytometry was performed to detect the CD16+CD56+ NK cells. Results: In the present study, based on gene expression microarray analysis, we showed four inhibitory receptors (KLRB1, KLRD1, KLRF1, KLRG1) and four activating receptors (KLRC1, KLRC3, KLRK1 and NCR1) on NK cells were remarkably down-regulated and the cytological experiment demonstrated the proportion of CD16+CD56+ NK cells among PBMCs decreased in the PE group. Conclusions: We confirmed the presence of reduced expression of critical activating as well as inhibitory NK cell receptors and low proportion of CD16+CD56+ NK cells in PE. The consistence between genomic and cytological examination suggests compromised NK cells may contribute to the pathogenesis of PE.