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)

Extracorporeal procedures to eliminate LDL from plasma now allow us to drastically lower the plasma LDL-concentrations to virtually every desired level. In a new therapeutic approach the combination of HMG-CoA reductase inhibitors with an LDL/fibrinogen apheresis procedure (the HELP-system) was evaluated in hypercholesterolemic CAD-patients. HELP treatment alone can lower the mean plasma LDL-cholesterol by about 50-60%, HMG-CoA reductase inhibitor therapy reduces the LDL-cholesterol by about 40%. The combination of both treatments resulted in a lowering of mean LDL-cholesterol to about 80% of baseline values. Improvement of blood rheology by lowering plasma viscosity and inhibiting erythrocyte aggregation became apparent. No relevant adverse effects were noted over a period of two years. This therapeutic strategy for maximal LDL-cholesterol lowering may be useful in secondary prevention of coronary heart disease in hypercholesterolemic patients if plasma LDL-C cannot be reduced by diet and drug treatment to desirable plasma levels (LDL-cholesterol less than 120 mg/dl). Preliminary data show an improvement in the symptoms of our CAD-patients treated with this combined therapy. Furthermore, within the near future a combined HELP and dialysis unit will be available for patients with terminal renal insufficiency and progressive atherosclerosis.
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PMID:[Maximal therapy of hypercholesterolemia in coronary heart disease]. 237 8

Coronary artery disease mortality can be reduced by aggressive lipid lowering. The reduction in cardiovascular events observed in the recent major lipid lowering trials is dramatically better than that seen in the classic studies of medically or surgically managed CAD from the 1970s. One postulated mechanism for this improvement is restoration of normal endothelial function through cholesterol lowering. By restoring endothelial dependent vasodilation, cardiovascular events and ischemia can be reduced. PTCA has variable effects on endothelial function. Lipid lowering is beneficial in combination with invasive CAD interventions. The appropriate management of coronary artery disease should consider the advance in medically managed outcomes provided by HMG CoA reductase inhibitors (statins).
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PMID:Medical management of coronary artery disease revisited: the endothelial factor. 931 36

The increased risk of cardiovascular disease in diabetic patients is well documented. A greater appreciation for the importance of this fact and regular use of secondary prevention strategies, including aggressive use of HMG-CoA reductase inhibitors or other lipid-lowering agents to reduce cholesterol levels, are clearly indicated for diabetic patients with CAD. If no contraindications exist, ACE inhibitors, beta blockers, and aspirin also should be considered for these high-risk patients.
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PMID:Coronary artery disease and diabetes. 1002 4

Use of lipid-lowering drugs in both primary and secondary prevention of cardiovascular disease (CVD) decreases significantly risk of myocardial infarction, stroke, incidence of cardiovascular events, reduces the cardiovascular mortality and morbidity as well as total mortality. HMG-CoA reductase inhibitors (statins) are most potent cholesterol-lowering drugs. Statins act by inhibition of HMG-CoA reductase activity, a rate--limiting step in synthesis of cholesterol and important metabolites of mevalonate--isoprenoids. The mechanisms by which favourable antiatherogenic actions of statins occur are complex. Statins inhibit proliferation and migration of vascular smooth muscle cells, reduce free-radicals generation and LDL modification, lower Lp(a) concentration, inhibit macrophage-derived foam cells accumulation and inhibit activation of platelets, thromboxane and PAI-1 synthesis. Use of statins in the therapy of hypercholesterolemia is presently recommended by NCEP, especially in high-risk groups (diabetes, post-CABG and PTCA, kidney and heart transplantation). Nevertheless, patients with CAD and moderately elevated LDL-C levels also benefit from the treatment with statins. Because of high costs of the therapy, statins of most favourable pharmacoeconomic profile should be used.
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PMID:[HMG-CoA reductase inhibitors in prevention of cardiovascular diseases: new mechanisms, aspects and trials]. 1105 20

Rosuvastatin (ZD4522) and pitavastatin (NK-104) are novel HMG-CoA reductase inhibitors with a peculiar pharmacological profile. In particular, they show a high potency in decreasing LDL-C and their catabolism is not mediated by the cytochrome P-450 3A4, thus reducing the potential for drug-drug interaction and improving the management of blood cholesterol. As the magnitude of LDL-C reduction is directly associated with the decrease in the incidence of myocardial infarction and mortality for CAD, statins with increased LDL-C lowering potency may ensure the achievement of target LDL-C levels and offer a more aggressive cholesterol control, further improving CAD morbidity and mortality.
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PMID:Novel statins: pharmacological and clinical results. 1237 4

Statins, inhibitors of HMG-CoA reductase, have pleiotropic benefits independent of cholesterol levels, including anti-oxidant and anti-inflammatory effects. Here, we investigate the effect of statins on myeloperoxidase (MPO) expression. MPO, expressed in foam cell macrophages, was recently shown to oxidize the ApoA-1 component of HDL, impairing ABCA-1 mediated cholesterol efflux. High levels of serum MPO correlate with increased risk of CAD events. Findings here show that statins strongly inhibit MPO mRNA expression in human and murine monocyte-macrophages. Suppression was reversed by downstream intermediates of HMG-CoA reductase, mevalonate, and geranylgeranylpyrophosphate, but not farnesylpyrophosphate. An inhibitor of geranylgeranyltransferase, GGTI-286, mimics the effects of statins, indicating geranylgeranylation is key to MPO expression. Reduction of MPO mRNA levels was observed in vivo in leukocytes from statin-fed mice, correlating with reductions in MPO protein and enzyme activity. These findings suggest that the pleiotropic protections afforded by statins may be due in part to suppression of MPO expression.
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PMID:Statins downregulate myeloperoxidase gene expression in macrophages. 1585 Jul 79