Nonhomogeneous electrophysiological changes and the bimodal distribution of early ventricular arrhythmias during acute coronary artery occlusion.

There is experimental evidence that the bimodally distributed ventricular arrhythmias (phases Ia and Ib) during the first 30 min after coronary occlusion (CO) in dogs are not due to the same mechanism. In 39 dogs we related the incidence of phases Ia and Ib to the time courses of excitation thresholds (ET), refractoriness (REFR), conduction times (CT) and effective refractory periods (ERP) at 6-12 epicardial electrode sites within the ischemic zone. The regional collateral myocardial blood flow (RMBF-tracer microsphere technique) was determined in 14 out of the dogs. This measurement only served for rough grouping into dogs with low and higher RMBF at the electrode sites during ischemia. REFR was determined as temporal recovery of excitability at a constant current strength of 4-6 times preocclusion ET. ERP was intermittently measured at 2.0-8.0 mA. At low RMBF ET, REFR and CT increased very inhomogeneously (dispersion of ET increased from 0.06 to 2.42 mA) 2-8 min after CO, leading to Ia-arrhythmias (also depending on infarct size) which terminated as ET, REFR and CT partially recovered 10-30 min after CO, their dispersions being still markedly elevated. With further recovery of these electrophysiological parameters the phases Ib subsided. On the other hand, the ERP diminished for the most part within the first 10 min after CO with only minor further decrease. Remarkably the dispersion of ERP did not significantly increase within the ischemic zone (from mean = 15 +/- 5 ms to 22 +/- 8 ms at low RMBF and from 14 +/- 6 ms to 18 +/- 9 ms at higher RMBF, p = ns). As a consequence of the homogeneous and constant shortening of the ERP, the time course of REFR mainly was determined by the nonhomogeneous alterations of ET. At a higher RMBF there were only minor electrophysiological alterations, and Ia- or Ib-arrhythmias did not emerge. These results indicate a strong relation of the Ia- and Ib-arrhythmias to the ischemia-induced time courses and dispersions of ET, REFR and CT but not of ERP within the ischemic area. Although the phases Ia relate to a strong increase of ET, REFR and CT and the Ib-arrhythmias to a partial recovery of these parameters, both the Ia- and Ib-arrhythmias seem to depend on a "critical" extent of electrophysiological inhomogeneity within a "critical" mass of ischemic but excitable myocardium.