致死性不整脈の成立機序

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This study was aimed to investigate the mechanisms of life-threatening ventricular tachyarrhythmias complicated with the acute and chronic phase of ischemia, and to find clues to develop pharmacologic and non-pharmacologic treatments for such arrhythmias.In acute ischemia, potassium ion (K^+) was released from ATP-depleted myocytes by opening the ATP-dependent potassium channel and inhibition of Na-K pump, and was thus accumulated in the extracellular space. Such K^+ accumulation was not homogeneous but dependent on the severity of the ischemia, thereby leading to re-entrant arrhythmias caused by inhomogeneous depression of excitability and conductivity in the ischmic region. Administration of Mg ion or potassium channel opener could prevent such ventricular arrhythmias experimentally, but a further study should be done before clinical application.In the chronic phase of ischemia, inhomogeneities of excitiation couduction were developed through remodelings of failing heart such as healing and/or apoptotic processes of muscle fibers in association with reactive proliferation of connective fibers. Thus, such complicated processes and reactions of the cardiac tissue shoud be taken into account in order to develop new pharmacological and non-pharmacological treatments for ventricular arrhythmias in the chronic phase of ischemia.