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

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

The injury-vasospasm hypothesis of IHD was discussed in relation to coronary artery autoregulation and the anoxic-feedback mechanism. Observations in the recent literature, not usually attributed to spasm, were examined in light of this phenomenon. This includes reperfusion models of experimental AMI, the association of AMI with myocarditis, and findings in AMI and SCD as necrotic microlesions, prodromata, and epicardial arterial plaque rupture and hemorrhage. The disparity between the severity of coronary disease and the occurrence of the various types of IHD suggest that atherosclerosis itself does not precipitate attacks of chest pain. It was emphasized that plaque rupture due to spasm might help induce CAT. With exercise, the possible importance of the autoregulatory system was explored in the prevention and induction of AMI and SCD, and the improvement of AP. The role of spasm in IHD should be defined.
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PMID:The injury-vasospasm hypothesis of ischemic heart disease, revisited. 33 91

Thromboses are a classical complication of sickle cell disease in the severe homozygous form. In the heterozygous individual, although the risk of severe thromobotic episodes is small, it must nevertheless be recognised. The authors report two cases of myocardial infarction in patients whose coronary arteries were relatively free from atherosclerosis; they were young men, with the heterozygous form of sickle cell disease AS. The part played by inheritance, the factors favouring vascular occlusion, and the possibility of preventing such episodes are all discussed.
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PMID:[Myocardial infarction and heterozygous sickle cell anemia. Apropos of 2 cases]. 40 90

Stroke is increasingly becoming a major cause of death and morbidity in African population among most of which the frequencies of hypertension are considerable, although hard data based on community surveys are lacking and most of the information available is from hospital data. The epidemiology of stroke in the Africans is reviewed. The frequencies in hospital populations varied from 0.9% to 4.0% and stroke accounted for 0.5% to 45% of neurological admissions. There is male predominance in published series. The main risk factors are hypertension, diabetes mellitus and homozygous sickle cell disease (in children only). Ischaemic stroke is by far the commonest clinical type encountered. These conclusions are further supported by experience at Ibadan, of over 1100 Africans seen over 18 years reported briefly in this communication. The results of the first community study over a 2-year period on the incidence of stroke in an African Urban (Ibadan) Community are presented. The study was carried out as part of a multinational multicentric study initiated and sponsored by the World Health Organization. The male to female ratio was five to two. Incidence rates reached peaks in the eighth decade in males and in seventh decade in females and were higher in males in all age groups, and the rates are comparable with those recorded in European populations, except in those under the age of 40 in Ibadan, in which age-specific incidence rates are considerably lower than in European and Japanese populations. Hypertension, diabetes mellitus constituted the main risk factors. Mortality and recurrence rates are described and are similar to experience in the Caucasians. Hypertension in the Nigerians predispose to a high frequency of cerebrovascular disease other than through mainly cerebral atherosclerosis. With increasing longevity of Nigerians and other Africans, the mortality and morbidity caused by cerebrovascular disease would probably become of enormous dimensions and adequate control of high blood pressure on a community basis may be the only way of preventing this: this would be desirable as myocardial infarction in contradistinction to hypertensive heart disease is an uncommon complication of high blood pressure in the Africans and prevention of hypertensive heart disease as shown by experience elsewhere can be achieved by control of high blood pressure, which does not seem to prevent ischaemic myocardial disease.
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PMID:Stroke in the Africans. 41 66

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.
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PMID:[Cerebral ischemia in young adults]. 193 40

From 1982 to 1986, there were 1230 sudden death cases autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were classified cardiac deaths (SCDs) such as coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours after the appearance of the fatal symptoms, and most of them (72%) were supposed to be instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%) or at work (8%). 34% of them were thought to be healthy by themselves or by their family members before their deaths. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were their major past histories recorded. Cardiac lesions such as myocardial hypertrophy, fibrosis and atherosclerosis of coronary artery were frequently admitted in SCD. SCD has been vigorously studied for a long time in various fields including legal medicine, and it has also attracted a great deal of public attention recently. To clarify the causes and the mechanisms of SCD, investigations of the actual situation of SCD cases is essential. Therefore, 1230 autopsy cases of SCD in Osaka Medical Examiner's Office for recent five years were statistically investigated.
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PMID:A statistical study of sudden cardiac death for past five years in Osaka medical, investigated at the Osaka Medical Examiner's Office. 252 Jun 96

Endothelial cell damage is considered to be the initial step in the genesis of thrombosis and atherosclerosis. Recently, the adhesion of erythrocytes from patients with diabetes or sickle cell anemia to endothelial cells was found to be increased and correlated with the severity of vascular complications. We have measured by radioimmunoassay the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) as an index of prostacyclin (PGI2) production, during red cell adhesion to endothelial cells in culture. The amount of 6-keto-PGF1 alpha released after incubation with normal red cells was similar to that observed with buffer (1.07 +/- 0.32 nmol/10(6) endothelial cells). However, after the adhesion of erythrocytes from patients with diabetes or sickle cell anemia, the amount of 6-keto-PGF1 alpha produced was significantly increased (P less than 0.01) and was correlated with the extent of erythrocyte adhesion (P less than 0.05). Tritium-labeled PGI2 was found to bind to erythrocytes, and the binding was time and concentration dependent. PGI2 release was inhibited by the cyclooxygenase inhibitor (flurbiprofen), whereas red cell adhesion remained unchanged. Fibrinogen potentiated erythrocyte adhesion and PGI2 production. The increase in PGI2 production after the adhesion of red cells from patients with diabetes or sickle cell anemia to endothelial cells indicates that endothelium may be damaged by abnormal erythrocyte adhesion.
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PMID:Release of prostacyclin after erythrocyte adhesion to cultured vascular endothelium. 308 70

A 30-year-old black man with proven sickle cell anemia died after five years of progressive heart failure and three clinically distinct episodes of myocardial infarction. Autopsy revealed massive ventricular myocardial fibrosis, a large left ventricular aneurysm, and an organized nonatherosclerotic thrombosis of the left coronary artery. Myocardial infarction, unassociated with atherosclerosis, has very rarely been reported in sickle cell anemia. A toxic/lethal level of amitriptyline was found at autopsy.
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PMID:Massive nonatherosclerotic myocardial infarction in sickle cell anemia. 338 95

A review of the electrocardiograms (ECG) of 108 patients with sickle cell anemia found only 3 with patterns consistent with myocardial infarction. Two of the 3 patients with ECG infarct patterns had postmortem examination confirmation of the infarction. These two patients had no significant coronary atherosclerosis nor did the other six autopsied patients in the present series. Literature reports of postmortem examinations on patients with sickle cell anemia confirm the scarcity of coronary atherosclerosis and myocardial infarction in these patients. Forty of the 108 ECGs showed signs of left ventricular hypertrophy and 20 others had nondiagnostic ST and T wave abnormalities. Nine showed first degree AV block and four right bundle branch block.
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PMID:Myocardial infarction in sickle cell anemia. 623 6

Endothelial cell alterations are considered to be a primary event in thrombosis and atherosclerosis. The adhesion of red cells from diabetic patients or patients with sickle cell anemia was measured using endothelial cell culture and a radiometric technique. The adhesion was significantly increased (P less than 0.001). Ultrastructure observation of red cells adhering to endothelial cells showed endothelial cell deformations, membrane modifications and formation of an anchoring device. Morphological changes support the hypothesis of an endothelial cell stimulation or damage during adhesion already suggested by the increased prostacyclin release during red cell adhesion.
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PMID:[Endothelial cells and adhesion of red cells in diabetes and sickle cell anemia. Quantitative and qualitative aspects]. 652 43


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