This review outlines the mechanisms of chemically induced cardiomyopathies, distinguishing between functional metabolic imbalances and direct cardiotoxicity, to aid detection in preclinical studies.
Distinguishes metabolic from direct cardiotoxicity mechanisms; leaves open clinical validation for patient monitoring.
Chemically induced cardiomyopathies are frequently the consequences of a cardiac metabolic imbalance brought about by exaggerated functional affects. The infarctlike lesions induced by adrenergic beta-receptor stimulants and the vasodilating antihypertensives serve as examples of this phenomenon. Direct cardiotoxic mechanisms not related to cardiovascular functional effects are responsible for another class of toxic cardiomyopathy. An example of this is the cardiomyopathy produced by the anthracycline antineoplastic agents. The pathogenesis, morphological changes and toxicologic features of these cardiomyopathies are described with particular reference to their detection in preclinical toxicity studies.
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Balázs et al. (1978) studied this question.
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