| Background:Coronary artery disease and ischemic stroke are serious diseases treaten the health of people worldwide. The atherosclerosis is the pathogenic basis of coronary artery disease and ischemic stroke. The inflammation plays a key role in the initiation and development of atherosclerosis. Previous case-control studies suggested that the single nucleotide polymorphism of cyclooxygenase-2 (COX-2) gene (G-765C) is associated with coronary artery disease (CAD) and ischemic stroke. Polymorphisms of Lymphotoxin-a (LTA) and galectin-2 (LGASL2) are associated with CAD and myocardial infarction. However, other studies do not confirm this relationship. Monocyte chemoattractant protein (MCP)-1 has been detected in atherosclerotic lesion and involved in the development of atherosclerotic plaques.Objectives:We used a meta-analysis to assess the relationship of COX-2 G-765C and CAD and ischemic stroke, the relationship of LTA A252G/LGALS2 C3279T and CAD. We used a case-control study and a meta-analysis to assess the relationship between MCP-1 gene and myocardial infarction. Databases, including PubMed, EMbase, CBM and CNKI, were searched to get the genetic association studies. Data were extracted by two authors and pooled odds ratio (OR) with 95%confidence interval (CI) was calculated.Results:For COX-2, the meta-analysis included 4930 CAD patients and 17997 controls,1628 ischemic stroke patients and 17653 controls. For CAD, the pooled OR of-765C was 0.80 (95%CI:0.65-0.98, p=0.03) compared to wild type allele in recessive model, and was 0.99 (95%CI:0.92-1.06, p=0.70) in dominant model. For ischemic stroke, the pooled OR of-765C was 1.11 (95%CI:0.88-1.42, p=0.38) in recessive model compared to wild type allele, and was 1.05 (95%CI:0.93-1.18, p=0.42) in dominant model. For LTA and LGALS-2, the meta-analysis included 20408 (LTA-A252G) and 10487 (LGALS2-C3279T) cases,14899 (A252G) and 10224 (C3279T) controls. The pooled OR of 252G was 1.02 (95%CI:0.98-1.07, p=0.41) compared to wild type allele in dominant model, and was 1.02 (95%CI:0.91-1.14, p=0.93) in recessive model. The pooled OR of 3279T was 0.96 (95%CI:0.88-1.06, p=0.07) compared to wild type allele in dominant model, and was 0.88 (95%CI: 0.77-1.01, p=0.06) in recessive model. For MCP-1,470 myocardial infarction patients and 522 healthy controls were recruited. Three tag single nucleotide polymorphisms, rs1024611, rs3760399 and rs3760396, were genotyped by polymerase chain reaction and restriction enzyme analysis. The association between rs1024611 and myocardial infarction was analyzed by meta-analysis. No association was found between polymorphisms rs1024611 (OR=1.19; 95%CI:0.84-1.70, P=0.31), rs3760399 (OR=1.29; 95%CI:0.91-1.82, P=0.13), rs3760396 (OR=1.27; 95%CI:0.83-1.96, P=0.23) and myocardial infarction was found in present case-control study. The meta-analysis included 1916 MI patients and 5538 controls. In dominant model, the pooled OR of G allele of rs1024611 was 1.05(95%CI:0.85-1.29, P=0.68) compared to wild type allele, and was 0.94(95%CI:0.80-1.10, P=0.41) in recessive model. No publication bias was found in this meta-analysis.Conclusion:The synthesis of available evidence supports that the COX-2-765C is a protective genetic factor for CAD, but not for ischemic stroke. No association was found in the polymorphisms of LTA gene, LGALS2-C3279T and MCP-1 gene and CAD. Background:Acute aortic dissection (AAD) is an uncommon lethal medical emergency, with a high mortality. D-dimer is a fibrin fragment and has been reported as a diagnostic marker for AAD. However, the differential diagnostic and prognostic roles of D-dimer in AAD remain controversial.Objective:To discuss the diagnostic and prognosis value of D-dimer in AAD, we evaluated the sensitivity, specificity and likelihood ratios of D-dimer in differential diagnosing AAD in this study.Methods:A total of 202 AAD patients with symptoms onset within 24 hours were enrolled. They were diagnosed by using enhanced computed tomography or magnetic resonance imaging. These patients were matched with 584 controls with symptoms clinically suspicious of AAD, including acute myocardial infarction (310), angina (136), pulmonary embolism (43), and other uncertain diagnosis (95). The plasma D-dimer was measured by stago-evolution (France). A total of six references were studied in this meta-analysis.Results:D-dimer level was significantly higher in AAD patients than in non-AAD controls (median 4.18 vs.0.45 ug/ml, P<0.05). D-dimer level in type A patients was significantly higher than that in type B patients (median 4.6 vs.3.64 ug/ml, P<0.05). D-dimer level was significantly higher in classic AAD than in aortic intramural hematoma patients (median 4.28 vs. 3.6 ug/ml, P<0.05). Receiver operating characteristic (ROC) curves analysis showed that D-dimer was a good predictor for ruling out AAD, with a sensitivity of 94.0%and the specificity of 57.0%. In cutoff value of 0.5 ug/ml, the negative likelihood ratio was 0.10, with positive likelihood ratio of 2.18. No difference was found in D-dimer levels between AAD died patients and survivors (median 4.13 vs.6.18 ug/ml, P>0.05). At the cut-off value of 0.5ug/ml, the pooled sensitivity was 0.95 (95%CI:0.92-0.97, P=0.06), the pooled specificity was 0.54 (95%CI: 0.51-0.57, P<0.05)。The pooled positive likelihood ratio was 1.98 (95%CI: 1.84-2.12,I2=82.2%, P=0.000), the pooled negative likelihood ratio was 0.10 (95%CI:0.07-0.15,I2=38.6%, P=0.15)Conclusion:D-dimer level is a useful marker to exclude AAD within 24 hours after symptoms onset, however, it is not associated with in-hospital mortality. |
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