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.

Coronary collateral blood flow and its changes during the first 30 min of acute coronary artery occlusion were studied in 34 anesthetized dogs to clarify its influence on the vulnerability of the heart in this first arrhythmic phase. Collateral flow was determined with 9-micron tracer microspheres (TM) injected at 1, 10 and 30 min after acute proximal occlusion of the left circumflex (LCX, n = 30) or left anterior descending (LAD, n = 4) coronary artery. The post-mortem selective retrograde coronary angiography was used to evaluate the functional extent of preexisting coronary collaterals. After acute LCX occlusions collateral flow increased significantly (p less than 0.05) from 17.8 +/- 2.7 ml.(min.100 g)-1 (mean +/- SE; n = 13) at 1 min to 29.3 +/- 5.1 ml . (min . 100 g)-1 at 30 min of occlusion in animals with well-formed preexisting coronary collaterals (group 1), whereas it was very low (4.7 +/- 0.6 ml . (min . 100 g)-1; n = 13) and changed only slightly in dogs with poor collaterals (group 2). Most of these animals died by ventricular fibrillation (VF) before a second measurement could be carried out. In four dogs with poor collaterals but an unusually small LCX area (group 3), flow remained almost constant (11.0 +/- 4.7 versus 11.0 +/- 4.4 ml . (min . 100 g)-1) during this period. Similar results were obtained in animals with acute LAD occlusion (group 4). Ventricular extrasystoles (VES) mainly developed in animals with poor collaterals and respective low and almost unchanging collateral flow (group 2,3,4) while none or only a few VES occurred in dogs in which flow initially was clearly higher and increased significantly (group 1). The animals of group 1, 3 and 4 all survived the first arrhythmic phase, whereas all the animals of group 2 died by VF, either in the arrhythmic subphase Ia (n = 7) or Ib (n = 6). The results of the present study show that only the initial magnitude of flow is decisive for the development of VES and VF during the first arrhythmic phase, whereas the subsequent increase in flow is of no importance to the bimodal vulnerability in the first arrhythmic phase (subphases Ia and Ib). The in vivo measured critical minimal collateral flow of about 5 ml . (min . 100 g)-1 corresponds well with the survival limit (border between collateral state III and IV) previously determined by post-mortem retrograde coronary angiography.