Cardiotoxicity may be defined as a drug action producing abnormalities in cardiac function, such as transitory disturbances or rhythm, conduction or contractility. Clearance of the drug is followed by recovery of the initial function. Cardionecrosis is the irreversible consequence of cardiotoxicity. Its appearance depends not only upon the toxicological potency of a given compound but may also depend upon the pathophysiological state of the heart. Therefore, two main categories may be recognized considering the influence of this state. Drugs may act on the processes controlling cellular structure such as protein biosynthesis in the case of antibiotics of the anthracycline group. Drugs may act at the level of metabolic regulation through a membranal or an intracellular action; in this case, the functional state of the heart plays a major role. This is mainly observed with sympathomimetics and with drugs interacting with the function of catecholamines. The cardiotoxicity observed in such conditions mimics the action of anoxia or of ischemia. The main determinant of the cardiac lesion is probably the disturbance of cellular calcium metabolism. This situation may be prevented (or treated) by the use of calcium entry blockers (calcium antagonists). A great part of this report will deal with the second group of drugs, because of their potential importance as a chemical hazard for the population and because of a possible preventive protection by calcium entry blockers (calcium antagonists).
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