[Cardiac lesions in methamphetamine abusers].

Various cardiac lesions such as hypertrophy, disarray and fibrosis similar to HCM, were often found in the heart of methamphetamine (MA) abusers. Myolysis, eosinophilic changes, contraction band necrosis and small round cell infiltration were also observed. Male ddy mouse were administered MA 1 mg/kg subcutaneously every day for 4 weeks. Their hearts revealed many cardiac changes such as hypertrophy, myolysis, contraction band necrosis, disarrangement of myofibers, saw-like cytoplasm, side-to-side connection of cardiac cells and vascuolative degeneration microscopically, and crysterosis of mitochondria, enlargement of sarcoplasmic reticulum and hypercontraction electronmicroscopically. These changes are thought to be similar to that of MA abusers, so it is certified that MA has toxic effect on the heart. Moreover, these changes could not be found when beta-blocker or calcium antagonist was premedicated. To elucidate the mechanisms of MA cardiac toxicity, we have designed some experiments. When MA (15 mg or 20 mg/kg) was administered on rats, cardiac lipid peroxidates, as a marker of free radical, increased rapidly. When rats were feeded for 7 weeks with Vitamin E deficient diet, 10 mg/kg MA administration was enough to increase lipid peroxidates. Simultaneous ECG observation revealed various arrhythmia such as VPB, A-V block and intraventricular conduction delay. In the investigation of contractile protein, although we could not find differences in the isozyme pattern of myosin heavy chain between MA groups (1 mg/kg for 8 and 12 weeks) and control group, Mg2+ ATPase activity of myocardial actomyosin at 0.1 microM Ca2+ increased significantly in 12 weeks MA group. We also found MA induced cardiac toxicity in cultured myocytes. Primary cultured adult rat myocytes were exposed to MA (1 x 10(-5) M and 1 x 10(-3) M) for 1 to 24 h in the presence and absence of 1 x 10(-5) M propranolol. After 24-h MA treatment, cellular granulation, swelling and hypercontraction and release of CPK were observed both with and without propranolol treatment. These findings suggest that MA may exert direct toxic effects on the heart.