The deletion (D) allele of the insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene is strongly associated with an increased level of circulating ACE. The ACE gene polymorphism may influence the production of angiotensin II (Ang II). It has been shown that Ang II modulates fibrinolysis, that is, Ang II increases plasminogen activator inhibitor-1 (PAI-1) mRNA and plasma PAI-1 levels in vitro and in vivo. Considered together, we tested the hypothesis that the deletion allele of the ACE gene might be associated with increased levels of PAI-1. We related the ACE genotype to PAI-1 antigen levels in 603 men and 221 women attending a routine health screening. As a whole, the plasma PAI-1 level was not strongly associated with ACE genotype. Since the PAI-1 level was significantly influenced by well-known risk factors for coronary artery disease (CAD), we further analyzed the data after excluding subjects with major cardiovascular risk factors. In low-risk male subjects, the DD genotype had significantly higher levels of plasma PAI-1 (DD: 20.3 +/- 2.2; DI: 13.9 +/- 1.1; II: 13.6 +/- 1.3 ng/mL, P = .010 by ANOVA). In low-risk female subjects, the DD genotype showed a tendency to a high level of plasma PAI-1 without statistical significance. When analysis was restricted to postmenopausal women (age > or = 55 or FSH > or = 35 ng/mL), the DD genotype showed a significantly higher level of PAI-1 than subjects with the DI and II genotypes (27.7 +/- 6.2 versus 15.6 +/- 1.8 ng/mL, P = .028). The DD polymorphism of the ACE gene is associated with high PAI-1 levels in male and possibly in postmenopausal female subjects who have lower conventional cardiovascular risk factors. These results suggest that the increased ACE activity caused by DD polymorphism may play an important role in elevating the level of plasma PAI-1. Our data support the notion that the genetic variation of ACE contributes to the balance of the fibrinolytic pathway.
We experienced an unusual case of cardiac tamponde caused by a rupture of the coronary arteriovenous aneurysm in a 54-year-old woman. The patient was suffered from sudden chest pain and syncope, and was initially managed by pericardiocentesis following an echocardiogram which revealed a massive pericardial effusion with signs of cardiac tamponade. She was referred to our hospital under the impression of aortic dissection with cardiac tamponade. She underwent an emergency operation and was found to have a 2 x 2 cm sized bleeding cystic mass protruding from the proximal anterior descending coronary artery. The aneurysm was excised and the openings connected with the coronary artery and right ventricular outflow tract were closed with sutures from the inside of aneurysm. Subsequent coronary arteriography supported the diagnosis.
Background The analysis of ACE gene expression is vital to study the role of angiotensin converting enzyme ACE in the pathogenesis of cardiovascular disease. Traditionally, levels of individual mRNA expression have been analyzed by semiquantitative Northern blotting, which requires a large quantity of tissue. Therefore, gene expression of a little biopsy specimen from the human heart or atherectomy specimen from the blood vessel cannot be measured easily. Reverse transcriptionpolymerase chain reaction RT-PCR is very effective, sensitive and rapid method of detecting the expression of mRNA, but it is only used in qualitative analysis. Therefore, we established the method of quantitative RT-PCR QRT-PCR using recombinant RNA template as internal standard to measure the expression of ACE.Method Recombinant RNA rcRNA was designed to yield PCR product which differs in size by about 200bp from that of the target RNA. Initially, spacer gene, which was composed of ACE sense primer, antisense primer, T7 promoter and poly dT tail with glutathione transferase GSTM gene of 180bp in the middle, was constructed. Then, standard rcRNA was obtained by in vitro transcription. Target RNA was mixed with rcRNA and amplified by PCR, together with 32 P-dCTP. PCR products were analyzed by gel electrophoresis. For quantitation, either gel was cut and radioactivity was counted or gel was dried and exposed to X-ray film and density was measured using image densitometer. We carried out semiquantitative RT-PCR to study the modulation of ACE expression in vascular smooth muscle cell VSMC by dexame-thasone and basic FGF bFGF .
Background In patients with coronary artery disease CAD , atherosclerotic changes of carotid arteries CA often coexist with CAD itself. If the degree of carotid atherosclerosis can be estimated, it would be very helpful in the management of patients with CAD. Methods CA intima-media thickness IMT was evaluated by ultrasonography at 12 segments both proximal, middle, distal common CA, bifurcation, internal and external CA-of the extracranial CA on the 182 subjects whom underwent coronary angiograms. The subjects were divided into 4 groups according to the severity of CAD; control C, n 23 , single vessel disease , n 64 , two vessel disease , n 44 , three vessel disease , n 51. Results The means SD of maximal IMT, chosen from the 12 segments, of each group were 1.4 0.7mm C , 2.1 1.4mm , 2.2 1.2mm , and 2.9 1.7mm. The 4 groups showed significant differences between each other. The only conparison to yield unsignificant differences was between group I and group p 0.02 for C and , p 0.001 for C and , p 0.001 for C and , p 0.01 for and , p 0.04 for and. When multivariate analysis was used to assess which major risk factors for CAD age, male sex, smoking, hypertension, diabetes, cholesterol, triglycerides-and CAD groups affected CA IMT , group and increasing age were the most significant variables p 0.0001 and 0.0035, respectively. Conclusion It is necessary to evaluate the status of the extracranial carotid arterial system with
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