Electrophysiologic basis for arrhythmias in ischemic heart disease.

Substantial gains have been made toward clarifying the mechanisms of arrhythmia in ischemia in animal models. After coronary occlusion in the dog, ischemic myocardial cells have reduced resting potential and slowed and diminished upstrokes of action potentials due to depression of fast channels. As a result, conduction is slow and irregular, especially at shorter cycle lengths, because refractoriness is altered by a delay in recovery of the fast channels beyond the completion of repolarization. These abnormalities occur during the acute phase of arrhythmia in the first half hour after occlusion and persist in surviving the subepicardial layers of myocardial cells for days to weeks. Reentry has been mapped in these surviving layers. Reentrant circuits form around regions of functional block formed by interfaces between responding and refractory myocardium. Standard antiarrhythmic agents generally are fast-channel blockers that further depress conduction and prolong refractoriness in ischemic tissue, causing block in slow conducting segments of the reentry circuits. However, antiarrhythmic agents may cause or accentuate reentrant arrhythmias by virtue of the same depressant actions. The greater likelihood of antiarrhythmic agents suppressing rather than producing reentrant arrhythmias may be due to enhanced depressant effects of antiarrhythmic agents on very slowly conducting tissues that are involved in reentry circuits. After the acute phase, arrhythmias occurring 1 to 4 days after coronary occlusion are probably largely automatic, although the potential for reentry remains if the cycle length is shortened. Abnormally enhanced automaticity and triggered activity are demonstrable in the surviving Purkinje network in regions of infarction, but the role of these phenomena in vivo has not been clarified.(ABSTRACT TRUNCATED AT 250 WORDS)