| Background:Coronary artery disease (CAD) has complex pathophysiology generated by interactions of genes and the environment. It has greatly threatened human health in last decades. With the continuous development of the gene sequencing level, the association between gene polymorphism and disease susceptibility has become a research hot spot. It was reported that thrombospondin gene single nucleotide polymorphisms were associated with CAD risk. It has been widely discussed whether thrombospondin is closely associated with CAD risk since the results were not the same.Objective:This study aimed to systematically assess the association between single nucleotide polymorphisms in thrombospondin-1 (THBS1), thrombospondin-2 (THBS2), thrombospondin-4 (THBS4) and CAD risk through meta analysis.Methods:Electronic databases:PubMed, Embase, Web of Science and Cochrane Library were systematically searched before June,2014 to obtain articles associated with thrombospondin polymorphisms and CAD risk. After obtaining case-control studies through the including and excluding criteria, we extracted data and assessed the quality of studies. The meta-analysis was conducted by STATA 11.2 software:odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to pool effect sizes. Different effect models were used according to heterogeneity. Meta-regression and sensitivity analyses were performed to examine the heterogeneity source. Subgroup analysis was applied to investigate the influence of races. Begg’s funnel plot and Egger’s test were conducted for publication bias.Results:A total of 13 studies involving 10,801 cases and 9,381 controls were included. Associations were observed between the THBS1 N700S polymorphism and CAD risk in general population(heterozygote model:OR=1.14,95% CI:1.03-1.26; dominant model:OR=1.13,95% CI:1.00-1.29), European population (heterozygote model: OR=1.13,95% CI:1.00-1.27) and Asian population (heterozygote model:OR=1.57, 95% CI:1.01-2.44; dominant model:OR=1.56,95% CI:1.00-2.43). The THBS2 3’ untranslated region (UTR) polymorphism and THBS4 A387P polymorphism were not associated with overall CAD risk. However, an association was observed between the THBS4 A387P polymorphism and CAD risk in the American population (allele model:OR=1.09,95% CI:1.00-1.18; homozygote model:OR=1.29,95% CI: 1.04-1.61; recessive model:OR=1.27,95% CI:1.02-1.58). The Begg’s funnel plot and Egger’s test both showed no evidence of publication bias.Conclusions:The THBSl N700S polymorphism was associated with increased CAD risk, especially in Asian and European populations. No association was observed between the THBS2 3’UTR polymorphism and CAD risk. The THBS4 A387P polymorphism was associated with increased CAD risk in the American population.Objective:To study the pathogenesis, clinical manifestation, diagnosis and treatment of accessory mitral valve (AMV).Materials and methods:A case of AMV was reported, which was admitted and treated in Qilu hospital of Shandong University. Combining with literatures obtained through PubMed database searching, retrospective analysis of the epidemiological characters, clinical presentations, diagnosis and treatment of accessory mitral valve was conducted.Results:A case of 46-year-old woman with a two-month history of chest congestion and palpitation admitted to the hospital was reported. Physical examination showed the border of cardiac dullness enlarged and a 3/6 grade systolic ejection murmur was audible in aortic valve area. The echocardiography showed a mobile 17mm×15mm mass in the left ventricular outflow tract (LVOT), attaching to the LVOT front wall with a 4 mm long pedicle. The cardiac magnetic resonance imaging (MRI) showed a 1.6cm X 2.0cm X 1.7cm round-like mass in the LVOT. The long T1 and slight long T2 signal subaortic mass attached to the front wall of LVOT. The mass slightly deformed during the cardiac cycle. After admitted to hospital, the operation was performed. Resection specimen pathology reported for fibrous connective tissue with hyaline degeneration and mucous degeneration.A total of 149 cases of AMV including the present one were obtained through database searching. There were 91 males and 47 females, with the average diagnosed age 27.5 years old. The main clinical manifestations of AMV were asymptomatic, dyspnea on exertion, palpitation, chest pain, syncope and so on. The common abnormal physical examination was the systolic murmur audible in aortic valve area. Echocardiography showed a floating mass or membrane-like echo in the LVOT. Most AMV patients were associated with other cardiac anomalies, such as atrioventricular septal defect, transposition of great arteries, bicuspid aortic valve. Patients with severe left ventricular outflow tract obstruction (LVOTO), obvious symptoms and other cardiac anomalies could take operations and the rest were advised to take oral anticoagulants and antibiotics to follow up with echocardiography on regular.Conclusion:1. AMV is a rare congenital cardiac malformation which could cause LVOTO and is commonly associated with other cardiac anomalies or solitary.2. Patients with AMV may be asymptomatic with the presence of a murmur at the very beginning. With the progress of disease, the obstruction of LVOT has become severer and patients begin to produce clinical manifestation such as dyspnea on exertion, palpation, fatigue and the presence of heart failure.3. Since AMV is relatively rare and often accompanied with other cardiac anomalies, it is frequently misdiagnosed. Nowadays, the main preoperative diagnosis of AMV depends on echocardiography. With the development of radiological technology, 3-dimension echocardiograpy and MRI have played great roles in the diagnosis of AMV.4. The treatment of AMV is mainly divided into surgical treatment and conservative treatment. Which one to choose mainly depends on the clinical manifestation, the condition of LVOTO and accompany of other cardiac anomalies. |
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