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ACTH, hydrocortisone and cyclic nucleotides levels, beta-receptors sensitivity, lipid peroxidation (LPO), antioxidant system, hemodynamics were investigated in 93 coronary patients without myocardial infarction in the presence of cardiac arrhythmia and after its correction. The clinical and laboratory findings indicate that it is primarily LPO activation and LPO products excessive accumulation in the blood that are responsible for arrhythmia emergence. Experimental data support these results by showing possibility of cardiac arrhythmia onset due to LPO products which raise the density of Na-Ca channels and inhibit the activity of Ca-dependent ATPase.
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