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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

The causal link between smoking, atherosclerosis and an increased risk for acute platelet mediated coronary events such as acute platelet thrombus formation, myocardial infarction, and sudden coronary death is not clear. Our studies suggest that there may be a transient increase in in vivo platelet activity with each exposure to cigarette smoke or elevated plasma nicotine. It is thought that platelets may contribute to the acceleration of the atherosclerotic process by several mechanisms (5). Thus it may be that each time a person increases their platelet activity, by smoking or some other means, and given other predisposing conditions such as elevated lipids and/or acute intimal damage, such as rupture of an atherosclerotic plaque, the atherosclerotic process may be enhanced. In addition it appears that cigarette smoke makes a developing thrombus more adherent and less likely to embolize distally, although the effect is transient. Finally, cigarette smoke may provide the final stimulus for an occlusive coronary thrombus in a stenosed coronary artery already predisposed to thrombosis by other risk factors. This may account for the fact that the risk of coronary occlusion and myocardial infarction decreases markedly in the first year after quitting (65). It may be that smoking has a greater likelihood of precipitating a fatal thrombus than it does of accelerating the altherosclerotic process. This would be reflected in the inability of aspirin to prevent the smoking induced enhancement of CFR's in our model (23) or the enhancement of platelet function in men with coronary artery disease (66).
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PMID:Effects of cigarette smoke and nicotine on platelets and experimental coronary artery thrombosis. 228 88

Plasma levels of dehydroepiandrosterone sulfate (DHEA-S), testosterone, dihydrotestosterone (DHT) androstenedione, sex hormone-binding globulin (SHBG), lipoproteins, apolipoproteins and high density lipoprotein (HDL) subfraction were measured in 32 men aged 26-40 years after myocardial infarction (MI) suffered at least 3-4 months prior to the study, who were normocholesterolemic and had angiographically demonstrated coronary occlusion. The control group consisted of 76 healthy men aged 25-40 years. Blood samples were obtained in the morning from fasting subjects. A significant decrease in plasma DHEA-S and DHT levels were found in MI patients. Also, a significant decrease in HDL-cholesterol, HDL2-cholesterol (HDL2-C) and apolipoprotein A-I, an increase in apolipoprotein B and LDL-cholesterol (LDL-C) levels were observed in those patients as compared with healthy men. However, there were no differences in testosterone, androstenedione and SHBG concentrations between the groups. Significant correlations between testosterone and HDL2-C (r = 0.46, P less than 0.01), as well as between DHEA-S and HDL3-C (r = 0.39, P less than 0.05) levels in MI patients were observed. These results suggest that decreased levels of plasma DHEA-S and DHT may promote the development of coronary atherosclerosis in men.
Atherosclerosis 1989 Oct
PMID:Decreased plasma dehydroepiandrosterone sulfate and dihydrotestosterone concentrations in young men after myocardial infarction. 253 16

Among 144 patients with hypertrophic cardiomyopathy, eight (58.3 +/- 7.0 years, M:F = 7:1) had complicating myocardial infarction, which was diagnosed clinically and by elevated cardiac enzymes or new Q-waves on electrocardiography. Coronary occlusion or stenosis evidenced by coronary angiography and nuclear cardiological findings were investigated. In six of the eight patients, coronary atherosclerosis caused infarction. These patients had many coronary risk factors compared to the other two patients. Sixteen of the 144 patients (11%) with hypertrophic cardiomyopathy had coronary atherosclerosis, the rate of which is reportedly 10 to 20%. Two of the eight patients had no coronary atherosclerosis. One patient had a diffusely spastic diathesis provoked by the intravenous administration of ergonovine maleate during coronary angiography, suggesting that coronary spasm caused myocardial infarction. The other patient had recurrent episodes of supraventricular tachyarrhythmia and no evidence of spasm during coronary angiography, suggesting coronary embolism as a cause of myocardial infarction. Myocardial infarction in patients with hypertrophic cardiomyopathy and normal coronary arteries as advocated by Maron et al. may have such pathogenesis. We conclude that coronary angiography may be mandatory in patients with hypertrophic cardiomyopathy, especially those who have many coronary risk factors and anginal symptoms. In these patients, ST-T changes and abnormal Q-waves on electrocardiography sometimes may be misleading when diagnosing the occurrence of acute myocardial infarction by electrocardiography alone. In such cases, infarct-avid scintigraphy with 99 m-Tc pyrophosphate is preferable.
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PMID:[Clinical diagnosis and pathogenesis of myocardial infarction complicated by hypertrophic cardiomyopathy: review of eight cases]. 256 22

Percutaneous transluminal coronary angioplasty (PTCA) is indicated for many patients with symptomatic coronary atherosclerosis. It can be safely used in patients with unstable angina pectoris, multivessel coronary disease (in selected instances), multiple stenoses in single vessels, stenoses in coronary artery bypass grafts, and recent total coronary occlusion. PTCA may be useful in reestablishing coronary flow after acute myocardial infarction with coronary occlusion and in association with thrombolytic therapy for acute myocardial infarction. The primary success rate of PTCA in experienced hands should be approximately 90%. If restenosis occurs after successful PTCA, a second procedure can be used to dilate the segment with restenosis and the success rate is high. Acute coronary events are the major complications of PTCA. Less than 5% of patients need emergency coronary surgery. Mortality for PTCA is less than 1%. Complications of PTCA diminish with increasing operator experience. PTCA is not indicated for patients with long-standing complete coronary occlusions, diffuse atherosclerotic coronary stenoses without discrete stenotic segments, multiple sites of total occlusions, or "skip" areas in vessels served by bridging collaterals. Patients with main left coronary stenoses and stenoses involving both sides of large-vessel bifurcations are not considered for PTCA in most centers. The choice for or against PTCA should be made after careful assessment of the risk/benefit ratio of PTCA vs coronary bypass surgery.
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PMID:Percutaneous transluminal coronary angioplasty: role in the treatment of coronary artery disease. 293 84

The death rate due to myocardial infarction appears to vary with dietary consumption of Mg. This could be due to effects on atherosclerosis, coronary artery spasm, altered pathogenesis of myocardial infarction, increased vulnerability to arrhythmia, or some combination of these. Mg deficiency (MD) has been found to increase the severity of a coronary occlusive event in terms of the amount of necrosis produced by a given occlusion. MD is also associated with increased likelihood of arrhythmia development. In addition, reduced extracellular magnesium concentration (Mgo) is associated with contraction of vascular smooth muscle that may be the equivalent of arterial spasm. In hamsters, MD leads to fibrinoid necrosis thought to be secondary to Ca overload. These 3 effects: coronary artery spasm, cardiac arrhythmia, and increased vulnerability to myocardial necrosis following coronary occlusion, may all be dependent on changes in myocardial and vascular smooth muscle electrolyte metabolism that follow from the reduced Mgo that is associated with MD.
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PMID:Effects of magnesium deficiency on the pathogenesis of myocardial infarction. 301 33

Cigarette smoking is believed to cause harmful cardiovascular and atherogenic effects resulting from changes in lipid metabolism. Intravenous nicotine and smoking raise plasma free fatty acid (FFA) levels through enhanced lipolysis resulting from sympathoadrenal stimulation. The study reported here investigated FFA-stimulated myocardial oxygen consumption (MVO2) in intact dogs. It was found that about half of the nicotine-induced rise in MVO2 resulted from metabolic stimulation by high concentrations of FFA, and the remainder was a result of enhanced mechanical activity of the heart directly produced by nicotine. In intact dogs, the increase in myocardial oxygen requirement resulting from excess myocardial FFA uptake also increased the severity of myocardial ischemic injury after acute coronary occlusion. Human studies with men who had smoked for more than 10 years showed that smokers had lower plasma high-density lipoprotein cholesterol fractions 2 and 3. High-density lipoprotein fraction 2 is reported to be antiatherogenic. Thus smoking appears to have at least two lipid effects that may promote coronary heart disease and atherosclerosis: increased plasma FFA and decreased plasma high-density lipoprotein cholesterol fraction 2.
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PMID:Lipid effects of smoking. 333 94

The relation of the Type A behaviour pattern to coronary atherosclerosis was assessed in a sample of 519 coronary angiography patients. Type A measures were the Structured Interview and the Framingham questionnaire. Angiographic indices included a composite coronary occlusion index and number of coronary vessels significantly diseased. Univariate analysis involving the entire sample showed no significant relation between Type A and severity of coronary vessel disease. Analyses for two subsamples, namely males currently employed in white collar occupations and persons found to have significant disease at angiography, also failed to indicate a relationship between Type A and coronary disease. Multivariate analysis revealed sex, cholesterol and age to be risk factors for atherosclerosis; Type A behaviour was not. The implications of these findings are discussed.
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PMID:Type A behaviour and coronary atherosclerosis. 340 92

Coronary artery occlusion and reperfusion in the anesthetized rat was used as a whole animal model of arrhythmia and sudden cardiac death to examine the influence of long-term dietary lipid modulation of myocardial membrane fatty acids on the development of cardiac arrhythmias. Feeding rats a diet supplemented with tuna fish oil significantly reduced the incidence and severity of arrhythmias, preventing ventricular fibrillation during both occlusion and reperfusion. Dietary sunflower seed oil reduced arrhythmias during occlusion but not in reperfusion. Dietary fat can modify the vulnerability of the myocardium to arrhythmic stimuli. The efficacy of tuna fish oil in reducing vulnerability to both ischemic and reperfusion arrhythmias suggests a potential beneficial effect of dietary n-3 fatty acids in addition to their influence on hemostasis, plasma lipids, and atherosclerosis that may contribute to their proposed role in lowering cardiovascular disease mortality and morbidity.
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PMID:Dietary fish oil prevents ventricular fibrillation following coronary artery occlusion and reperfusion. 341 86

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35


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