Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has long been unclear how exercise training improves myocardial perfusion in patients with stable CAD. Regression of coronary atherosclerosis and collateral formation have been favorite theories; however, angiographic techniques have so far failed to document any significant increase in coronary collaterals at rest. Although net regression of stenotic lesions may be achieved in high-intensity exercise training, it is unlikely that it causes the significant improvement in myocardial perfusion that is seen much earlier than plaque regression. The novel tools to examine coronary endothelial function in vivo and in vitro have now made it clear that exercise training enhances myocardial perfusion by increasing both eNOS and ecSOD expression, which attenuates the premature breakdown of NO by ROS. These increases in local NO production and half-life improve endothelium-dependent vasodilation in response to flow or acetylcholine. These functional changes will occur rather rapidly after the initiation of an exercise training program, although no studies are available on their precise time course. Anatomic changes, such as augmentation of the capillary bed and slowing of the progression of coronary atherosclerosis, may require more extended periods of training (Fig. 4). Recently, first reports about a possible association between endothelial dysfunction and the frequency of clinical events has been documented. Further prospective studies are needed to establish whether endothelial dysfunction is just an indicator of plaque instability or an independent prognostic marker. If it turns out to be the latter, exercise training may be promoted from a symptomatic intervention to a preventive strategy with long-term prognostic benefits.
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PMID:Effects of exercise training on vascular function and myocardial perfusion. 1157 Jan 10

eNOS affects the NO level in the blood vessel wall, and therefore eNOS might be considered as a candidate gene for CAD. In this cross-sectional case-control association study we tested the hypothesis whether the eNOS 4alb gene polymorphism is a genetic marker for premature CAD in Slovene men. The eNOS 4a/b gene polymorphism was tested in 403 Slovene men: 215 cases with premature CAD and 188 subjects with no history of CAD. The frequency of 4a/b genotypes did not differ between patients and controls: in CAD patients the frequencies of the 4aa, 4ab, or 4bb genotype were 5.0%, 27.9%, or 67.1%, respectively, and in controls the genotype frequencies were 5.3%, 30.9%, or 63.8%, respectively. In this study the aa genotype of the eNOS 4a/b polymorphism was not associated with premature CAD (OR = 1, 95% CI 0.4-2.3, P = 0.9). Moreover, there were no differences in lipid parameters (total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides) between the subjects with the aa genotype and the subjects with the ab or bb genotype. In conclusion, we failed to demonstrate that the eNOS 4a/b gene polymorphism was a genetic marker for premature CAD in Slovene men.
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PMID:The eNOS gene polymorphism does not have a major impact on lipid parameters and premature coronary artery disease in Slovene men (Caucasians). 1591 34

In chronic heart failure of CAD, therapeutic approach will be available either with drugs or exercise. With exercise, coronary risk factors such as BP, lipid, DM and obesity will be controlled. In addition, ischemia will also be controlled by decreasing oxygen demand related to BP and HR, and with increasing oxygen supply by increased ECNOS gene expression, collateral formation and regression of coronary stenosis. Infarct size is also reported to be decreased by increasing MnSOD in the cell by exercise. Prognosis of CHF is also good in various evidence of exercise therapy. Recent advances of molecular biology have revealed various mechanisms of exercise effect. Thus, exercise if properly prescribed without provoking ischemia will be basically and clinically effective therapy for patients with CHF.
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PMID:[Exercise therapy for heart failure]. 1668 81