Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of fluvastatin and bezafibrate on lipids, lipoproteins, and apoproteins (apo) were investigated in a multicenter randomized, double-blind, parallel-group study. After 8 weeks of strictly controlled (computer-based assessment) dietary stabilization, patients with primary hypercholesterolemia (low-density lipoprotein cholesterol [LDL-C] > or = 160 mg/dL; triglycerides < or = 300 mg/dL) were enrolled into a 6-week placebo phase. Altogether, 131 patients were randomized to receive either fluvastatin at 40 mg once daily (n = 64; mean age 53 years) or bezafibrate at 400 mg once daily (n = 67; mean age 52 years) for 12 weeks. Compliance with the diet was monitored (3-day food records) after 6 and 12 weeks. Fluvastatin led to significant reductions in LDL-C (-23%), total cholesterol (-17%), LDL-C/high-density lipoprotein cholesterol (HDL-C) (-24%) and apo B (-19%). Fluvastatin significantly increased LpA-I (+8%) and apo E (+20%). Bezafibrate produced significant reductions in LDL-C (-17%), total cholesterol (-13%), LDL-C/HDL-C (-24%), triglycerides (-28%), apo B (-15%), and LpA-I (-10%) and significantly increased HDL-C (+12%), apo A-I (+9%), apo A-II (+30%), apo E (+14%), and Lp(a) (+3%). No clinically notable increases in levels of liver enzymes or creatine phosphokinase were observed with either treatment. Both treatments were well tolerated. There was a low incidence of adverse events that tended to be mild and included headache, muscular pain, angina, and dyspepsia. The frequency of adverse events was similar in both treatment groups, and no significant differences in dietary behavior were observed. In conclusion, fluvastatin is a well tolerated 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment of primary hypercholesterolemia. Effects of fluvastatin on LpA-I occur irrespective of changes in HDL-C.
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PMID:Treatment of primary hypercholesterolemia: fluvastatin versus bezafibrate. 801 68

Since Mg(2+)-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg(2+) on lipoproteins with those of the statin drugs is warranted. Formation of cholesterol in blood, as well as of cholesterol required in hormone synthesis, and membrane maintenance, is achieved in a series of enzymatic reactions that convert HMG-CoA to cholesterol. The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA. The statins and Mg inhibit that enzyme. Large trials have consistently shown that statins, taken by subjects with high LDL-cholesterol (LDL-C) values, lower its blood levels 35 to 65%. They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality. These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation, Mg has effects that parallel those of statins. For example, the enzyme that deactivates HMG-CoA Reductase requires Mg, making Mg a Reductase controller rather than inhibitor. Mg is also necessary for the activity of lecithin cholesterol acyl transferase (LCAT), which lowers LDL-C and triglyceride levels and raises HDL-C levels. Desaturase is another Mg-dependent enzyme involved in lipid metabolism which statins do not directly affect. Desaturase catalyzes the first step in conversion of essential fatty acids (omega-3 linoleic acid and omega-6 linolenic acid) into prostaglandins, important in cardiovascular and overall health. Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker. More recent work shows that Mg also acts as a statin.
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PMID:Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals. 1546 51

In spite of a large number of studies on the use of HMG-CoA-reductase inhibitors (statins) in treatment of different forms of coronary artery disease, the efficacy of their early administration in acute coronary syndrome (ACS) is still unclear. The purpose of the present investigation was to study the effects of medium doses (40 mg per day) of simvastatin on the clinical course of ACS and blood levels of C-reactive protein (CRP) and lipids in ACS patients to whom the drug was administered on the first day of the disease. One hundred and eight patients with ACS were randomized into two groups: the control group receiving standard therapy, and the main group receiving in addition 40 mg of simvastatin beginning on the first day of the disease. Blood levels of lipids and CRP were measured by a precise qualitative technique on the first and fourteenth days of the disease. The clinical course of the disease was evaluated during six months from the first day of hospital stay. Mean CRP level decreased significantly within two weeks in the group of patients receiving simvastatin (from 14.9 +/- 9.7 to 7.6 +/- 6.0 mg/l; p = 0.02). In the control group CRP concentration decreased less and not significantly (from 16.1 +/- 7.3 to 13.2 +/- 6.8 mg/l; p = 0.18). Two main types of the dynamics of CRP level were revealed in the ACS patients. Most patients in both groups displayed a decrease in CRP level by the fourteenth day of the disease. At the same time, in some patients CRP level grew during this period, and these patients had stenocardia and required repeated hospital admissions due to ACS recurrence significantly more frequently during the following six months (relative risk 1.4; 95% confidence interval 1.1 to 1.8). The frequency of postinfarction stenocardia was the most substantial and significant clinical difference between the groups (50.9% in the control group, and 23.6% in the main group, p = 0.04). Thus, early therapy with simvastatin in ACS lowers SRP level and the frequency of postinfarction stenocardia. The elevation of CRP level during the first two weeks of the disease is a poor prognostic sign.
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PMID:[The effects of early application of simvastatin on C-reactive protein level, blood lipids, and the clinical course of acute coronary syndrome]. 1821 56

The number of patients with limited organ function is steadily increasing due to the aging of the population. Consequently, a growing number of patients needing surgery is accompanied by serious comorbidities. These patients are at high risk of perioperative organ dysfunction. In this context cardiac events (e.g. cardiac arrhythmias, angina or myocardial infarction) play a major role with significant impact on postoperative care, long term outcome and economic sequelae. Thus, anaesthesiologists must prevent such events in the perioperative period. Besides general measures such as adequate analgesia, protection from stressful events and sufficient volume replacement, medical intervention with beta-blockers or HMG-CoA-reductase-inhibitors (statins) are necessary to reduce the incidence of perioperative cardiac events. Both beta-blockers and HMG-CoA-reductase-inhibitors are known to exhibit pleiotropic effects (defined as additional cardioprotective effects) besides the primary blockade of the beta-adrenergic receptor or the inhibition of the synthesis of serum cholesterol, respectively. Both groups of drugs improve cardiac function, decrease inflammatory response, decrease activation of blood coagulation and stabilize endothelial plaques. Based on the current literature the following recommendations are published concerning the perioperative administration of beta-blockers: (i) Patients who are on beta-blockers on a regular basis following guidelines concerning chronic treatment of cardiovascular diseases should continue this medication throughout the perioperative period; (ii) a sufficient indicator of an adequate therapy is the baseline heart rate. It should not exceed 60-70bpm at rest; (iii) the Revised Cardiac Risk Index (RCRI) is a widely accepted score to estimate the patient's perioperative cardiac risk; (iv) patients with a RCRI > or =3 should not be scheduled for routine surgery without sufficient beta-adrenergic-receptor blockade; (v) in patients at high cardiac risk based on the RCRI who are scheduled for emergency surgery beta-blocker-therapy should not be initiated de novo perioperatively. However, for perioperative treatment of tachycardia or hypertension beta-blockers are the drug of first choice. Concerning perioperative statin-therapy the following recommendations are suggested: (i) chronic statin-therapy should be continued throughout surgery and the perioperative period; (ii) in patients without chronic statin-therapy scheduled for vascular surgery this treatment should be started perioperativly; (iii) no data is available concerning other patient populations; (iv) if statin-therapy is indicated it should be started independently from baseline serum LDL-C-concentration; (v) side effects of statin-therapy are rare and usually not live threatening, thus treatment is considered to be without serious risks to the patient.
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PMID:[Organprotection in cardiac risk patients--rational of perioperative beta-adrenoceptor-antagonists and statins]. 2038 81