Background: Endothelial nitric oxide synthase (eNOS) could be a candidate gene for coronary artery disease (CAD). This study investigated the relationship of the eNOS Glu 298 3 Asp and T 786 3 C polymorphisms with the presence and severity of CAD in the Italian population. Methods: We enrolled 415 unrelated individuals who underwent coronary angiography. The severity of CAD was expressed by means of the Duke score. The eNOS Glu 298 3 Asp and T 786 3 C variants were analyzed by PCR. Results: There was significant linkage disequilibrium between the two eNOS polymorphisms (P <0.0001). Both variants were significantly associated with the occurrence and severity of CAD (P ؍ 0.01 and 0.004 for Glu 298 3 Asp and T 786 3 C, respectively). The risk of CAD was increased among individuals homozygous for the C allele of the T 786 3 C polymorphism compared with individuals homozygous for the T allele (odds ratio ؍ 2.5; P <0.01) and was independent of the other common risk factors (P ؍ 0.04). Moreover, individuals with both the Asp/Asp genotype of the Glu 298 3 Asp polymorphism and at least one C allele of the T 786 3 C variant in the promoter region of the eNOS gene had an increased risk of CAD (odds ratio ؍ 4.0; P <0.001) and a significantly higher mean Duke score (26.2 ؎ 2.9 vs 45.2 ؎ 3.7; P ؍ 0.002) compared with individuals with the TT genotype and the Glu allele.
Conclusions:The present study provides evidence that the Glu 298 3 Asp and T 786 3 C polymorphisms of the eNOS gene are associated with the presence and sever-
"Degenerative" aortic valve stenosis appears to be a chronic inflammatory process associated with atherosclerotic risk factors. The coexistence of neoangiogenesis, T-lymphocyte infiltration, adhesion molecules, and hsp60 gene expression indicates an active immunomediated process in the final phases of the disease.
To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.
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