Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within the framework of clinical tests of the preparation Gevilon (gemfibrosil tablets 450 mg) of Parke-Davis Co. this hypolipidaemic preparation was administered to 28 patients with different types of hyperlipoproteinaemia. One-month administration of gemfibrosil, 900 mg per day, significantly influenced some parameters of the lipid and lipoprotein metabolism. Plasma cholesterol declined by 20%, triglycerides by as much as 60%. On the other hand, the HDL cholesterol level did not change. The concentration of the "risk" apolipoprotein B declined by 11%, that of apolipoprotein A1 which is considered protective from the aspect of ischaemic heart disease increased by 21%. There is a significant decline of lipoprotein Lp(a) which was not described in hypolipidaemic drugs of the clofibrate type. Treatment with Gevilon led also to a marked decline of the serum uric acid level. Gemfibrisol is according to the authors' experience as well as according to the results of other authors an effective hypolipidaemic agent suitable for the majority of patients with hyperlipoproteinaemia. Treatment with gemfibrosil leads to a significant decline of the prevalence of ischaemic heart disease.
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PMID:[Gemfibrozil in the treatment of hyperlipoproteinemia]. 261 83

In a double-blind, placebo-controlled study, 47 patients with ischemic heart disease and acute myocardial infarction were allocated to 3 months' treatment with peroral magnesium (15 mmol/d) or placebo. Before, during, and after treatment, blood samples were taken to determine serum concentrations of cholesterol; triglyceride; high-density, low-density, and very-low-density lipoprotein; apolipoprotein A1 and B; and magnesium. We found a 13% increase in molar ratio of apolipoprotein A1:apolipoprotein B after magnesium treatment, as compared with a 2% increase in the placebo group (for mean differences between changes of the magnesium and the placebo groups). This increase was caused by a decrease in apolipoprotein B concentrations, which were reduced by 15% from 1.44 to 1.23 mmol/L in the magnesium group as compared with a slight increase in the placebo group. Triglyceride, and thereby very-low-density lipoprotein concentrations decreased by 27% after magnesium treatment (from 2.41 to 1.76 mmol/L, and from 1.1 to 0.79 mmol/L, respectively) as compared with much smaller decrements in the placebo group. Likewise, we found tendencies toward an increase in high-density lipoprotein cholesterol and in high-density lipoprotein cholesterol ratio/(low-density lipoprotein cholesterol:very-low-density lipoprotein cholesterol) after magnesium treatment. The observed findings support the hypothesis that magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis.
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PMID:Influence of magnesium substitution therapy on blood lipid composition in patients with ischemic heart disease. A double-blind, placebo controlled study. 271 98

During the year 1982 serum cholesterol and apolipoprotein A1 and B levels were measured in 1319 male subjects (mean age 20 years) from different provinces of Belgium. The serum cholesterol level and the apolipoprotein B level were distinctly lower in Dutch-speaking than in French-speaking subjects. An increase of 1.1 mg% of total cholesterol was found per kg per consumer unit per year of butter consumed and a decrease of 1.1 mg% per kg per consumer unit per year of margarine consumed. The higher cholesterol value in French-speaking subjects correlated significantly with a high regional mortality from all causes and from ischaemic heart disease in male subjects of the 45-64-year age group. A 10 mg% difference in serum cholesterol at the age of 20 years corresponds with an increase in mortality from all causes of 20% and from ischaemic heart disease of 21%. A significant difference in log GGT (gamma glutamyl-transpeptidase)--possibly due to differences in alcohol consumption--was observed between the provinces of Belgium. The difference in cholesterol and apolipoprotein B level remained significant after adjustment for log GGT.
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PMID:Serum lipid distribution and mortality in Belgium. 614 37

The aim of this study was to compare apolipoprotein A1 (ApoA1) and B (ApoB) with high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) as markers for cardiovascular mortality and morbidity in elderly men. We analyzed serum ApoA1, ApoB, total cholesterol, HDL-C, and LDL-C in a group of 77-year-old men (n = 785). The results were correlated with data from the Swedish cause of death registry. Receiver-operating characteristic curves showed that, of the studied serum markers, ApoA1 was the best predictor for ischemic heart disease mortality (area under the curve = 0.724, 95% confidence interval, 0.691-0.755). There were also significant correlations between the apolipoproteins and other known risk markers for cardiovascular disease such as triglycerides, high-sensitivity C-reactive protein (hsCRP), and cystatin C. Serum ApoA1 is a better risk marker than are ApoB, ApoB/ApoA1 ratio, HDL-C, and LDL-C for cardiovascular disease and mortality in elderly men.
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PMID:Apolipoprotein A1 is a stronger prognostic marker than are HDL and LDL cholesterol for cardiovascular disease and mortality in elderly men. 1723 19

HDL and apolipoprotein A1 (apoA1) concentrations inversely correlate with risk of death from ischemic heart disease; however, the role of apoA1 in the myocardial response to ischemia has not been well defined. To test whether apoA1, the primary HDL apolipoprotein, has an acute anti-inflammatory role in ischemic heart disease, we induced myocardial infarction via direct left anterior descending coronary artery ligation in apoA1 null (apoA1(-/-)) and apoA1 heterozygous (apoA1(+/-)) mice. We observed that apoA1(+/-) and apoA1(-/-) mice had a 52% and 125% increase in infarct size as a percentage of area at risk, respectively, compared with wild-type (WT) C57BL/6 mice. Mitochondrial oxidation contributes to tissue damage in ischemia-reperfusion injury. A substantial defect was present at baseline in the electron transport chain of cardiac myocytes from apoA1(-/-) mice localized to the coenzyme Q (CoQ) pool with impaired electron transfer (67% decrease) from complex II to complex III. Administration of coenzyme Q10 (CoQ10) to apoA1 null mice normalized the cardiac mitochondrial CoQ pool and reduced infarct size to that observed in WT mice. CoQ10 administration did not significantly alter infarct size in WT mice. These data identify CoQ pool content leading to impaired mitochondrial function as major contributors to infarct size in the setting of low HDL/apoA1. These data suggest a previously unappreciated mechanism for myocardial stunning, cardiac dysfunction, and muscle pain associated with low HDL and low apoA1 concentrations that can be corrected by CoQ10 supplementation and suggest populations of patients that may benefit particularly from CoQ10 supplementation.
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PMID:Apolipoprotein A1 regulates coenzyme Q10 absorption, mitochondrial function, and infarct size in a mouse model of myocardial infarction. 2475 32