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

Several recent autopsy reports indicate an increased prevalence of coronary atherosclerosis in ischemic heart disease temporally associated with cocaine abuse. The objective of this study was to conduct a retrospective analysis of sudanophilic lesions in young asymptomatic individuals who abused cocaine. Twenty-six cases (15-34-year-old black males) were examined from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study. Sixteen subjects (mean age 25 +/- 1 years) had a positive toxicologic screen for cocaine and/or its major metabolites at autopsy and were confirmed habitual cocaine abusers. The remaining 10 cases (mean age 24 +/- 2 years) were subjects with a negative toxicologic screen at autopsy and no history of illicit drug abuse. Post-mortem blood was collected for lipoprotein analysis and determination of smoking status. The aorta and right coronary arteries were stained with Sudan IV and the degree and extent of sudanophilia was quantitated by image analysis. Multiple linear regression analysis of cocaine, age, smoking status, VLDL+LDL-C/HDL-C ratio and HDL-C as predictor variables of percentage intimal surface involvement, revealed an association between cocaine abuse and the extent of sudanophilia in both the thoracic and abdominal aorta (P = 0.002 and 0.049, respectively). Analysis of risk factors or of cocaine abuse as predictors of sudanophilia did not achieve statistical significance in the right coronary artery. These preliminary results suggest that habitual use of cocaine, through unknown mechanism(s), increases aortic sudanophilia independent of traditional risk factors.
Atherosclerosis 1992 Nov
PMID:Cocaine: an independent risk factor for aortic sudanophilia. A preliminary report. 128 Jan 44

Cocaine abuse has been associated with sudden cardiac death with coronary artery thrombosis with or without underlying vessel disease. Additional vascular beds thus far implicated in cocaine-associated arteriopathy include thoracic and abdominal aorta, and pulmonary, cerebral, and placental vessels; abnormalities include vasospasm, thrombosis, and accelerated atherosclerosis. We report the case of an adult male cocaine user with severe arteriosclerosis of renal vessels, and suggest that cocaine may also affect the renal vasculature.
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PMID:Severe arteriosclerosis in the kidney of a cocaine addict. 144 65

With regard to cardiac findings in cocaine abuse, at autopsy the vast majority of patients dying with cocaine toxicity have either no pathologic change in the heart or only minimal changes that could not account for the patient's death. The second most frequent finding is underlying, mild-to-moderate coronary atherosclerosis, with or without coronary thrombosis. There may be acute or healed myocardial infarction or a sudden cardiac death without myocardial changes of ischemia. A high incidence of contraction band necrosis has been reported in the absence of coronary artery disease and may cause a sudden arrhythmic death. Myocarditis also has been described in a few cases as either lymphocytic or lymphocytic and eosinophilic infiltrate in the presence of myocyte necrosis. Usually, the foci are sparse and not always associated with contraction band necrosis. The underlying mechanisms are thought to be either direct effects of norepinephrine on myocytes or through vasospasm of resistance vessels and secondary myocardial ischemia. Cocaine rarely has been associated with aortic dissection, which is probably a result of cocaine's hypertensive effects.
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PMID:Cocaine-associated cardiovascular disease: clinical and pathological aspects. 174 14

From September 1983 through November 1986, autopsies were performed on 6810 patients at the Office of the Maryland Medical Examiners; of these 40 had detectable cocaine, its metabolites, or both in body fluids. These patients were divided into two groups: natural cocaine-associated deaths (31 patients, mean age 28 +/- 5 years, blood level of cocaine 5.3 +/- 8.1 mg/L) and homicide deaths with detectable cocaine (nine patients, mean age 33 +/- 8 years, blood level of cocaine 0.3 +/- 0.3 mg/L). Cocaine-associated deaths were compared to a control group of 27 victims of sudden traumatic death (mean age 34 +/- 5 years). Total thrombotic occlusion of the left anterior descending coronary artery overlying mild coronary atherosclerosis occurred in one patient with cocaine-associated death. Results of histologic examination showed myocarditis (mononuclear infiltrate) in 8 of 40 (20%) patients dying with detectable cocaine in body fluids compared to 1 of 27 victims of sudden traumatic death (3.7%, p less than or equal to 0.05). Contraction band necrosis occurred in 25% of cocaine-associated deaths compared to a 41% incidence among victims of sudden traumatic death. We conclude that myocarditis occurs frequently in patients dying of cocaine abuse and may represent microvascular injury.
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PMID:Cardiovascular effects of cocaine: an autopsy study of 40 patients. 272 73

Myocardial infarction is increasingly recognized as a complication of cocaine abuse. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients has remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse produced coronary artery spasm leading to coronary thrombosis and infarction.
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PMID:Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. 349 49

Several recent postmortem studies suggest an increased prevalence of atherosclerosis in young habitual cocaine abusers. However, little is known about the effects of cocaine abuse on the vascular endothelium and its relationship to atherosclerosis. Therefore, the consequence of chronic administration of intravenous cocaine on the induction of aortic sudanophilia was examined. Male New Zealand White rabbits were fed a 0.5% cholesterol diet for 10 wk. During this period, animals were randomized to receive either cocaine-hydrochloride (0.25 mg/kg) intravenously (n = 17) twice daily; or an equivalent volume of 0.9% physiologic saline, control group (n = 16). Mean values for total circulating leukocytes and platelets and total plasma cholesterol and triglycerides were similar in both groups throughout the protocol. At the completion of the study, aortic sudanophilia was measured and expressed as a percentage of regional involvement (R1 = proximal 4 cm, R2 = middle 6 cm, and R3 = distal 10 cm). Statistical significance among groups was achieved in the proximal thoracic aorta (p = 0.057). No significant differences in sudanophilia were noted in the middle and distal segments. When animals were placed in subgroups according to percent total plaque involvement, there was a significant increased distribution of rabbits with a greater extent of sudanophilia in the cocaine-treated group as compared with control (p = 0.01, chi-square analysis). Immunocytochemical studies using the macrophage-specific and muscle actin-specific monoclonal antibodies demonstrated that sudanophilic areas in both groups were predominantly composed of macrophage-derived foam cells. Evaluation of plaque morphology showed an increase in intimal plaque thickness and in the number of macrophages and smooth muscle cells in cocaine-treated animals; however, group differences were not statistically significant. Because no significant differences were found in the cellular composition of atherosclerotic plaques between groups, further studies were performed to assess the effects of cocaine on the permeability function of cultured endothelial cell monolayers as a possible mechanism of increased sudanophilia. Cocaine (100 microM)-treated endothelial cell monolayers demonstrated an increased permeability to horseradish peroxidase during all time intervals studied (0-6 hr). Permeability differences were statistically significant at 30 min and 1 hr (p = 0.003 and 0.02, respectively). Collectively, these observations suggest that administration of cocaine to cholesterol-fed rabbits increases the prevalence of aortic sudanophilia via at least one possible mechanism involving enhanced vascular permeability.
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PMID:Increased prevalence of aortic fatty streaks in cholesterol-fed rabbits administered intravenous cocaine: the role of vascular endothelium. 811 19

Between November 1992 and April 1993, 864 coronary angiographies were performed at our institution. In 14 patients (1.6%), no significant coronary disease (> 50% stenosis) was found despite documented myocardial infarction. Of these, 2 patients (0.2%), aged 46 and 33 years, had perfectly smooth coronary arteries at angiography. The most commonly postulated mechanism of myocardial infarction in such patients is coronary spasm with superimposed thrombosis. The same risk factors as those operative in atherosclerotic coronary artery disease are thought to play a role in this setting. The prognosis is good. In one of the patients with < 50% stenosis of coronary vessels, a history of cocaine abuse could be elicited as the possible causal factor of acute myocardial infarction. Cocaine-induced coronary spasm can lead to arrhythmias, myocardial infarction or accelerated coronary atherosclerosis even in patients with normal coronary arteries. Myocarditis must be considered in the differential diagnosis of acute myocardial infarction in young patients with chest pain, typical electrocardiographic and enzymatic changes but without risk factors.
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PMID:[Myocardial infarct in patients with normal coronary arteries]. 818 2

Cocaine use has been associated with ischemic syndromes, especially angor pectoris, myocardial infarction, cardiac arrhythmias and sudden death. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients have remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse probably produced coronary artery spasm leading to coronary thrombosis and infarction.
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PMID:[Acute myocardial infarction related to cocaine use. Report of a case]. 894 87

In summary, we report two cases of mesenteric ischemia following cocaine abuse in young women. In such cases it is always difficult to prove a direct causal relationship between the abuse of cocaine and mesenteric ischemia. Both our patients were relatively young (in their thirties) and did not have any history of atherosclerosis, and their urine toxicity screens were positive for the use of cocaine. Cocaine-related hospital visits are on the increase. Mesenteric ischemia should be considered in the differential diagnosis when evaluating a young patient with a history of cocaine abuse presenting with an acute abdomen.
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PMID:Mesenteric ischemia secondary to cocaine abuse: case reports and literature review. 917 33

Vaccine technology can be applied to targets of intervention that currently have not been considered preventable by immunization. Targets include some diseases caused by, or related to, infectious agents, and other conditions clearly unassociated with disease pathogens. This article considers vaccines for pregnancy, peptic ulcer disease, gastric cancer, cocaine abuse and atherosclerosis.
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PMID:Unconventional vaccine targets. Immunization for pregnancy, peptic ulcer, gastric cancer, cocaine abuse, and atherosclerosis. 1019 2


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