2013年美国心力衰竭管理指南(心衰指南)-英文

myocardial hypertrophy with interstitial fibrosis, lympho-mononuclear infiltration, myocyte necrosis, and biventricular concentric hypertrophy (135).

5.4. Toxic Cardiomyopathy

5.4.1. Alcoholic Cardiomyopathy

Chronic alcoholism is one of the most important causes of DCM (136). The clinical diagnosis is suspected when biventricular dysfunction and dilatation are persistently observed in a heavy drinker in the absence of other known causes for myocardial disease. Alcoholic cardiomyopathy most commonly occurs in men 30 to 55 years of age who have been heavy consumers of alcohol for >10 years (137). Women represent approximately 14% of the alcoholic cardiomyopathy cases but may be more vulnerable with less lifetime alcohol consumption (136, 138). The risk of asymptomatic alcoholic cardiomyopathy is increased in those consuming >90 g of alcohol per day (approximately 7 to 8 standard drinks per day) for >5 years (137). Interestingly, in the general population, mild to moderate alcohol consumption has been reported to be protective against development of HF (139, 140). These paradoxical findings suggest that duration of exposure and individual genetic susceptibility play an important role in pathogenesis. Recovery of LV function after cessation of drinking has been reported (141). Even if LV dysfunction persists, the symptoms and signs of HF improve after abstinence (141).

5.4.2. Cocaine Cardiomyopathy

Long-term abuse of cocaine may result in DCM even without CAD, vasculitis, or MI. Depressed LV function has been reported in 4% to 18% of asymptomatic cocaine abusers (142-144). The safety and efficacy of beta blockers for chronic HF due to cocaine use are unknown (145).

5.4.3. Cardiotoxicity Related to Cancer Therapies

Several cytotoxic antineoplastic drugs, especially the anthracyclines, are cardiotoxic and can lead to long-term cardiac morbidity. Iron-chelating agents that prevent generation of oxygen free-radicals, such as dexrazoxane, are cardioprotective (146, 147), and reduce the occurrence and severity of anthracycline-induced cardiotoxicity and development of HF.

Other antineoplastic chemotherapies with cardiac toxicity are the monoclonal antibody trastuzumab

(Herceptin), high-dose cyclophosphamide, taxoids, mitomycin-C, 5-fluorouracil, and the interferons (148). In contrast to anthracycline-induced cardiac toxicity, trastuzumab-related cardiac dysfunction does not appear to increase with cumulative dose, nor is it associated with ultrastructural changes in the myocardium. However, concomitant anthracycline therapy significantly increases the risk for cardiotoxicity during trastuzumab

treatment. The cardiac dysfunction associated with trastuzumab is most often reversible on discontinuation of treatment and initiation of standard medical therapy for HF (149). The true incidence and reversibility of