Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied myocardial injury during acute coronary occlusion-reperfusion and atherosclerosis in rabbits fed a high cholesterol diet with or without fish oil supplementation. New Zealand white male rabbits were divided into 3 groups. Eight control rabbits fed with laboratory standard rabbit chow were group I. In addition to the standard chow, 15 rabbits fed with a 1% cholesterol-enriched diet for 6 weeks were group II, and 10 rabbits fed with a 1% cholesterol-enriched and 10% fish oil supplemented diet for 6 weeks were group III. Acute coronary occlusion was induced by ligating the marginal branch of the left circumflex coronary artery for 1 h, followed by reperfusion for 4 h. Myocardial injury was assessed by tissue creatine kinase activities and amino-nitrogen concentrations from the ischemic (infarct) and nonischemic (normal) myocardium, and the infarct area/risk area ratios of the left ventricle. The surface area of the atherosclerotic lesions of the aorta and pulmonary artery was measured by planimeter. There was significantly more myocardial loss of creatine kinase and amino-nitrogen in the cholesterol-fed rabbits than the controls (p less than 0.01 and 0.02, respectively). The cholesterol and fish oil-treated rabbits had a nonsignificant reduction in myocardial loss of both agents as compared to their corresponding cholesterol-fed ones. The same trend was also found in the infarct area/risk area ratio. Fish oil treated rabbits had a good effect on the reduction of atherosclerotic lesions and tissue cholesterol levels in the aorta and pulmonary artery, but not in the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dietary supplementation with fish oil on atherosclerosis and myocardial injury during acute coronary occlusion-reperfusion in diet-induced hypercholesterolemic rabbits. 161 95

This multicenter, double-blind, placebo-controlled, dose-response study was conducted in patients with primary hypercholesterolemia to examine the effects of pravastatin, a selective inhibitor of HMG-CoA reductase, on plasma lipids and lipoproteins. A total of 306 patients on cholesterol-lowering diets received twice daily doses of 5 mg, 10 mg, 20 mg pravastatin, or placebo for 12 weeks. Marked reductions in low density lipoprotein (LDL) cholesterol and total cholesterol were observed after 1 week of treatment; maximum lipid-lowering effects occurred at 4 weeks and were sustained for the duration of the trial. At week 12, pravastatin treatment resulted in dose-dependent mean reductions from baseline in LDL cholesterol of 17.5%, 22.9%, and 30.8% for the 3 doses tested (P less than or equal to 0001 compared with baseline and placebo). The reduction in LDL cholesterol was log-linear with respect to dose; each doubling of dose reduced LDL cholesterol an additional 6.5%. Dose-dependent reductions in total cholesterol from 12.9% to 23.3% also occurred (P less than or equal to 0.001). Triglycerides decreased by as 15.4% (P less than or equal to 0.001) and high-density lipoprotein (HDL) cholesterol increased approximately 7% (P less than or equal to 0.01), but these effects were not dose-dependent. No patient receiving pravastatin was discontinued during the 12-week trial. Transient episodes of rash and headache occurred. Slight increases in mean serum levels of ASAT and ALAT occurred, and 2% of both placebo- and pravastatin-treated patients reported myalgia although there was no clinically significant elevation of creatine kinase. These data indicate that pravastatin favorably affects all lipid parameters and is well tolerated.
Atherosclerosis 1990 Nov
PMID:Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. I. A dose-response study. 212 37

Hypercholesterolemia (type II hyperlipidemia) after cardiac transplantation is common and may play a role in the accelerated rate of coronary atherosclerosis seen following the procedure. However, conventional cholesterol-lowering drugs are either ineffective or contraindicated for use in transplant recipients. The presence of type II hyperlipidemia was identified in 11 cardiac transplant recipients during a mean follow-up period of 15 months (range 3 to 41) after transplantation. Lovastatin, at an initial dosage of 20 mg/day, was administered for a period of 1 year. The maximal dosage of lovastatin was 60 mg/day. All patients received maintenance dosages of immunosuppressive agents, including cyclosporine-A, prednisone and, in some instances, azathioprine. Lipid profiles, hepatic transaminases, serum creatinine, creatine kinase and cyclosporine-A serum trough levels were measured quarterly. Total cholesterol decreased by 27% (354 +/- 50 vs 258 +/- 36 mg/dl, p less than 0.01) after 3 months and remained stable thereafter. Similarly, low density lipoprotein cholesterol decreased by 34% (221 +/- 51 vs 146 +/- 40 mg/dl, p less than 0.01) after 3 months and remained constant. Triglycerides, high density lipoprotein, hepatic transaminases, creatinine, creatine kinase and trough cyclosporine-A levels remained stable during the 1-year follow-up period. Lovastatin was uniformly well tolerated in this study group. When given in modest dosages, lovastatin appears to be a safe, effective and well-tolerated therapy for hypercholesterolemia in cardiac transplant recipients.
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PMID:Lovastatin therapy for hypercholesterolemia in cardiac transplant recipients. 267 84

Hypercholesterolemia was induced in New Zealand white rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 2 wk. Half of the cholesterol-fed rabbits were given lovastatin, a potent inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate limiting enzyme in cholesterol biosynthesis, and the other half were given its vehicle (i.e., DMSO). At the end of 2 wk, the rabbits underwent experimental myocardial ischemia or a sham ischemia procedure. Ischemic animals fed the cholesterol-enriched diet for 2 wk experienced much greater cardiac damage than ischemic rabbits fed the control diet, despite the absence of any atherosclerosis. Lovastatin was shown to protect the ischemic rabbit myocardium by three different indices of ischemic damage: (a) maintenance of creatine kinase (CK) activity in the ischemic myocardium; (b) reduced loss of free amino-nitrogen containing compounds from the ischemic myocardium; and (c) blunting the rise of plasma CK activity. These effects were not due to differences in myocardial oxygen demand between the groups. Arteries isolated from animals fed the cholesterol-enriched diet developed defects in endothelium-dependent relaxation in both large vessels as well as coronary resistance vessels. Acute hypercholesterolemia increases the severity of myocardial ischemia while at the same time impairing endothelium-dependent relaxation. These deleterious changes can be significantly attenuated by treatment with lovastatin.
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PMID:Cardiovascular effects of acute hypercholesterolemia in rabbits. Reversal with lovastatin treatment. 291 50

Atherosclerosis was induced in New Zealand White rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 10-12 wk. Half of the cholesterol-fed rabbits were given BM 13505, a specific thromboxane A2/endoperoxide (TxA2/PGH2) receptor antagonist, and the other half were given its vehicle (i.e., 2% Na2CO3). At the end of 10-12 wk, the rabbits underwent experimental myocardial ischemia or an identical sham operation, except that the coronary artery was not occluded. BM 13505 was shown to protect the ischemic rabbit myocardium by three different methods: 1) maintenance of myocardial tissue creatine kinase (CK) activity in the ischemic myocardium; 2) reduced loss of free amino nitrogen-containing compounds from the myocardium; and 3) blunting the rise of plasma CK activity. Part of the mechanism for these effects may be due to inhibition of platelet aggregation and blockade of the vasoconstrictor effect of TxA2. However, these protective effects were not due to differences in myocardial oxygen demand among the groups. Finally, BM 13505 exhibited an antiatherogenic effect by reducing the deposition of cholesterol in the aortic wall and by retarding plaque formation in coronary arteries. However, it does not achieve this antiatherogenic effect by lowering plasma cholesterol concentrations or by scavenging superoxide free radicals. Thus blockade of TxA2 receptors exerts a variety of beneficial effects that reduce the severity of ischemic damage resulting from myocardial ischemia.
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PMID:Cardioprotective actions of thromboxane receptor antagonism in ischemic atherosclerotic rabbits. 297 Feb 33

A 37-year-old man with metastatic immature (malignant) teratoma with prominent rhabdomyosarcomatous elements had markedly increased activity of creatine kinase (EC 2.7.3.2) MB in serum. There was no electrocardiographic evidence of infarction or ischemia, and autopsy revealed no myocardial infarction, significant coronary atherosclerosis, myocarditis, or invasion of the heart by tumor. A high proportion of the creatine kinase activity in a homogenate of the tumor was attributable to the MB isoenzyme. Persistent increases of creatine kinase-MB and an unusually high MB isoenzyme activity, out of proportion to total creatine kinase activity, may indicate a nonmyocardial origin of this isoenzyme.
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PMID:Secretion of creatine kinase MB isoenzyme by an immature teratoma with predominant rhabdomyosarcomatous elements. 272 Sep 94

We investigated the effects of acute myocardial ischemia (MI) in a rabbit model of atherosclerosis to determine whether atherosclerosis augments the severity of damage produced in the ischemic myocardium. Normal rabbits were fed a control rabbit chow diet or a diet enriched with either 2% cholesterol or 0.5% cholesterol for 10-12 weeks prior to induction of MI. Plasma cholesterol concentrations in the cholesterol-fed rabbits were 1697 +/- 70 mg/dl (2%) and 1056 +/- 51 mg/dl (0.5%) vs. 61 +/- 12 mg/dl for the non-cholesterol-fed rabbits. All rabbits were observed for 5 h following induction of MI or sham MI. At the conclusion of the experiment, tissue biopsies from the MI region and non-MI (NMI) regions were taken and analyzed for two indicators of the severity of MI--myocardial creatine kinase (CK) activity and free amino-nitrogen concentration. Atherosclerosis was confirmed histologically in coronary artery and aortic specimens. No difference was found among any group with respect to heart rate (HR), mean arterial blood pressure (MABP), or pressure-rate index (HR x MABP/1000, a measure of myocardial oxygen demand). Myocardial CK loss (NMI - MI) was significantly greater for the 2% and 0.5% cholesterol groups (7.3 +/- 1.3 and 4.9 +/- 0.7 IU/mg protein, respectively, P less than 0.05) than in the nonatherosclerotic group (2.5 +/- 0.4 IU/mg protein; P less than 0.001 for 2% and P less than 0.01 for 0.5%). Increased severity of MI was confirmed by a significantly greater myocardial loss of free amino-nitrogen (NMI - MI) in the two atherosclerotic groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased severity of acute myocardial ischemia in experimental atherosclerosis. 369 58

In a group of 3000 hospital patients the prevalence of immunoglobulin bound creatine kinase (macro CK type 1) was 4.3%. The relative frequency was greater in the older age categories. The highest prevalence was found in patients with rheumatic and cardiac diseases. In a group of 556 cardiac patients selected for coronary angiography a prevalence of 13.8% was observed. No significant correlation was obtained between the findings of the coronary angiography and the activity of macro CK type 1. CK MB results determined by ion-exchange or immuno-inhibition techniques in macro CK type 1 positive patients are falsely positive. Macro CK type 1 may be seen as an antigen-antibody complex against CK BB, which originates at least partly from the vascular wall.
Atherosclerosis 1986 Jun
PMID:Macro CK type 1 as a marker for autoimmunity in coronary heart disease. 373 42

Nickel was measured, by electrothermal atomic absorption spectrophotometry, in sera from (a) 30 healthy adults, (b) 54 patients with acute myocardial infarction, (c) 33 patients with unstable angina pectoris without infarction, and (d) five patients with coronary atherosclerosis who developed cardiac ischemia during treadmill exercise. Mean (and SD) concentrations in Group a were 0.3 (0.3) microgram/L (range less than 0.05-1.1 microgram/L). Within 72 h after hospital admission, hypernickelemia (Ni greater than or equal to 1.2 microgram/L) was found in 41 patients of group b (76%) and in 16 patients of group c (48%). Hypernickelemia was found before and after exercise in one patient of Group d (20%). Peak values averaged 3.0 micrograms/L (range 0.4-21 micrograms/L) in Group b, 1.5 microgram/L (range less than 0.05-3.3 micrograms/L) in Group c. In Group b, the mean time interval between the peak values for creatine kinase activity and for nickel was 18 h. Serum nickel concentrations were unrelated to age, sex, time of day, cigarette smoking, medications, clinical complications, or outcome. Mechanisms and sources of release of nickel into the serum of patients with acute myocardial infarction or unstable angina pectoris are conjectural, but hypernickelemia may be related to the pathogenesis of ischemic myocardial injury.
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PMID:Nickel concentrations in serum of patients with acute myocardial infarction or unstable angina pectoris. 397 87

The incidence of perioperative myocardial infarction with noncardiac surgery varies by the type of procedure and the prevalence of coronary atherosclerosis in the study population. Incidence is < or = 1% with minor procedures and may exceed 10% with vascular operations. The case fatality rate continues to be 30% to 50%. Pathogenesis is not understood completely. Diagnosis is sometimes problematic, because less than 50% of patients complain of chest pain. In addition, a high frequency of notable but apparently innocent postoperative electrocardiograph changes limits the diagnostic use of the electrocardiogram. Fortunately, the creatine kinase MB isoenzyme retains its sensitivity and specificity for acute infarction in perioperative patients. Different approaches to preoperative risk assessment have been developed, including a summative cardiac risk index and a stratification system based on the likelihood that the most powerful risk factor (coronary artery disease) is present. Although many interventions have been recommended to lower perceived risk, none has been tested in a randomized controlled trial, and their comparative efficacy and safety is unknown.
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PMID:Perioperative myocardial infarction with noncardiac surgery. 801 Mar 37


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