Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven hundred fifty-two cases of instantaneous sudden cardiac death were studied. Alcoholic cardiomyopathy was found in 127 cases (16.9%), predominantly in men under age 50 (73%). The heart was enlarged, with an average mass of 441 +/- 8 g. Light microscopy revealed uneven thinning and atrophy of the cardiomyocytes, with fatty infiltration and development of fatty tissue around the vessels of the left ventricle and interventricular septum, up to the subendocardial areas. In the majority of cardiomyocytes, electron microscopy showed atrophy of the myofibrils, pronounced dilation of the sarcoplasmic reticulum, lipids in the cytoplasm, mitochondriosis and an increased number of lysosomes and alterations of the mitochondria. Unchanged cardiomyocytes were characterized by hypertrophy and numerous ribosomes, and had developed a granular endoplasmic reticulum. Also observed were interstitial edema, an enlarged cardiomyocyte-capillary space, thinning of the capillary walls, flattening of the endothelium and a plethora and aggregation of erythrocytes. Decreases in mitochondrial enzyme activity were studied by enzyme histochemistry. Analogous pathologic changes may be individually present in other types of myocardial disease, but the complex of changes is specific for alcoholic cardiomyopathy. The frequency of alcoholic cardiomyopathy among victims of sudden death suggests that alcoholic cardiomyopathy is a risk factor for sudden cardiac death.
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PMID:Alcoholic cardiomyopathy and sudden cardiac death. 371 41

Dilated cardiomyopathy (DCM) is a disorder of unknown aetiology characterized by the left ventricular cavity enlargement and wall thinning associated with reduced left ventricular wall motion. DCM in chronic alcoholics is supposed to be caused by alcohol induced myocardial damage (alcoholic cardiomyopathy). Nevertheless, cardiotropic viruses, such as enteroviruses have long been suspected as causative agents for at least some forms of DCM. In the present study, 13 cases of DCM in chronic alcoholics were investigated with qualification and quantification of infiltrating leucocytes using immunohistological antibodies against leucocyte common antigen (LCA), T-lymphocytes (CD3) and macrophages (CD68). In addition, the expression of tenascin, playing a role in the initiation of fibrotic changes, was examined. All antigens were known to be possibly enhanced in cases of chronic myocarditis. Using these immunohistological techniques, 2 out of 13 cases had evidence for chronic inflammatory myocardial alterations in the sense of lymphocytic infiltrates (>2.0 CD3 T-lymphocytes/visual field at 400 x (HPF); >7 CD3 T-lymphocytes per mm(2)). These cases were diagnosed as having inflammatory cardiomyopathy. The other cases without myocardial inflammation were diagnosed as idiopathic/alcoholic DCM.
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PMID:Alcoholic cardiomyopathy versus chronic myocarditis--immunohistological investigations with LCA, CD3, CD68 and tenascin. 1195 34

In the United States, in both sexes and all races, long-term heavy alcohol consumption (of any beverage type) is the leading cause of a nonischemic, dilated cardiomyopathy, herein referred to as alcoholic cardiomyopathy (ACM). ACM is a specific heart muscle disease of a known cause that occurs in two stages: an asymptomatic stage and a symptomatic stage. In general, alcoholic patients consuming > 90 g of alcohol a day (approximately seven to eight standard drinks per day) for > 5 years are at risk for the development of asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. ACM is characterized by an increase in myocardial mass, dilation of the ventricles, and wall thinning. Changes in ventricular function may depend on the stage, in that asymptomatic ACM is associated with diastolic dysfunction, whereas systolic dysfunction is a common finding in symptomatic ACM patients. The pathophysiology of ACM is complex and may involve cell death (possibly due to apoptosis) and changes in many aspects of myocyte function. ACM remains an important cause of a dilated cardiomyopathy, and in latter stages can lead to heart failure. Alcohol abstinence, as well as the use of specific heart failure pharmacotherapies, is critical in improving ventricular function and outcomes in these patients.
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PMID:Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. 1268 36