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Cardiomyopathy induced changes

Emetine emetine is still used at high doses for the treatment of patients with severe amebiasis. Muscle damage is uncommon but when it does occur can be a severe generalized necrotizing myopathy. The outcome is, at times, fatal, especially when an emetine-induced cardiomyopathy is also present. Despite the suggestion that there may be neuritic changes, there is no evidence that emetine damages peripheral nerve. The myopathy is usually painful but reversible. The mechanism of action of emetine is unknown. [Pg.344]

The main dose-limiting toxicity of all anthracyclines is myelosuppression, with neutropenia more commonly observed than thrombocytopenia. In some cases, mucositis is dose-limiting. Two forms of cardiotoxicity are observed. The acute form occurs within the first 2-3 days and presents as arrhythmias or conduction abnormalities, other electrocardiographic changes, pericarditis, and myocarditis. This form is usually transient and is asymptomatic in most cases. The chronic form results in a dose-dependent, dilated cardiomyopathy associated with heart failure. The chronic cardiac toxicity appears to result from increased production of free radicals within the myocardium. This effect is rarely seen at total doxorubicin dosages below 500-550 mg/m2. Use of lower weekly doses or continuous infusions of doxorubicin appear to reduce the incidence of cardiac toxicity. In addition, treatment with the iron-chelating agent dexrazoxane (ICRF-187) is currently approved to prevent or reduce anthracycline-induced cardiotoxicity in women with metastatic breast cancer who have received a total cumulative dose of doxorubicin of 300 mg/m2. All anthracyclines can produce "radiation recall reaction," with erythema and desquamation of the skin observed at sites of prior radiation therapy. [Pg.1301]

Syndrome X refers to the occurrence of effort angina and exercise-induced ECG changes with a normal coronary arteriogram and no evidence of structural (stenosis) or functional (spasm) abnormalities. Although the basis for this syndrome is not yet established, it is thought that syndrome X may be a result of inducible myocardial ischemia caused by impaired functional coronary reserve at the mi-crovascular level of intramural prearteriolar vessels. It has been proposed that this defect is caused by defective prearteriolar regulation of blood flow into the arteriolar bed with subsequent focal, sustained, compensatory release of adenosine excessive local concentrations of adenosine are then responsible for the pain seen in this syndrome. Cardiomyopathy and left bundle block may result from ischemia in some patients. Follow-up studies have shown that the occurrence of left bundle branch block in response to stress is associated... [Pg.286]

Chronic alcoholism produces pathologic changes such as chronic gastritis, cirrhosis of the Uver, alcoholic cardiomyopathy, Korsakoff s syndrome, bloatedness, flabby muscles, fine tremors, impaired physical capacity and stamina, diminished will power, and impaired memory. Accompanying malnutrition may contribute to alcohol-induced tissue injury. [Pg.257]


See other pages where Cardiomyopathy induced changes is mentioned: [Pg.35]    [Pg.35]    [Pg.119]    [Pg.4]    [Pg.332]    [Pg.307]    [Pg.309]    [Pg.102]    [Pg.345]    [Pg.221]    [Pg.597]    [Pg.497]    [Pg.305]    [Pg.305]    [Pg.538]    [Pg.103]    [Pg.307]    [Pg.341]    [Pg.1077]    [Pg.1082]    [Pg.471]    [Pg.480]    [Pg.383]    [Pg.333]   
See also in sourсe #XX -- [ Pg.34 ]




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