Izumi Furuno

Electrophysiological and Anatomical Substrates for Late Potential Recorded by Signal Averaging in Seven‐Day‐Old Myocardial Infarction in Dogs

A filtered QRS (fQRS) was recorded by signal averaging in 7‐day‐oJd myocardial infarction (MI) in dogs to detect late potential (LP). The criteria for the LP included a duration of fQRS (D) ≥ 60 msec and a voltage in the last 15 msec (VI5) ≤ 10 μV. These parameters were determined from the control data from 15 dogs without infarction (D: 45 to 60 msec and V15: 12.0 to 83.6 μV). On the seventh day of infarction, the D had increased from 53.5 ± 4.7 to 62.2 ± 9.6 msec (P < 0.05) and the V15 decreased from 38.6 ± 19.5 to 18.4 ± 16.0 μV (P < 0.01). Of 23 dogs, 14 met the LP criteria (group A) and 9 did not (group B). Sustained ventricular tachycardia (SVT) was induced in 12 group A dogs and in none of the group B dogs. The delayed epicardial activation (DEA) was recorded after the end of QRS at 5.1 ± 4.7 sites in group A dogs and 1.3 ± 1.8 sites in group B dogs (P < 0.05). The maximum value of epicardial activation time was more prolonged in group A than in group B (70.0 ± 28.3 vs 44.4 ± 9.8 msec, P < 0.01). The area of MI was more extensive in dogs with DEA than those without (24.9 ± 5.8% vs 10.3 ± 9.0% of the total left ventricular weight, P < 0.01). In 72 of 90 sites with DEA, the thickness of the surviving epicardial muscle was ≤1 mm. The sensitivity and specificity of the criteria for LP in detecting DEA were 71.4% and 55.6%, and 100% and 81.8% for predicting inducibility of SVT. It was thus concluded that LP, reflected the DEA, was identified from infarct areas of slow conduction within a reentry circuit of SVT.

Sympathetic denervation of the epicardial border zone in the genesis of dispersion of refractoriness and arrhythmogenesis in a 7-day-old canine myocardial infarction model

BackgroundThe purpose of this study was to clarify whether sympathetic denervation occurs in the infarcted heart and contributes to the dispersion of the effective refractory period (ERP) and arrhythmogenesis. MethodsERP was measured at 47 epicardial sites in 13 dogs with 7-day-old infarctions after proximal ligation of the left anterior descending artery. To delineate the sympathetic innervation, the effects of ansae subclaviae stimulation (ASS), norepinephrine infusion, and prazosin infusion on ERP were tested. ResultsThe per cent change in ERP (AERP) induced by ASS was significantly lower at test sites where the surviving epicardial myocardial thickness (Th) was 2mm or less than at those with a Th of more than 2 mm and the normal zone. Eleven out of 179 sites (6.1%) overlying the infarct showed no ERP change after ASS. ASS paradoxically prolonged ERP at 29 sites (16.2%). In contrast, norepinephrine infusion produced a greater AERP in the infarct zone than in the normal zone. Prazosin shortened ERP at sites where ASS prolonged it, but had no effect at sites where ASS shortened ERP. ASS increased both the degree of ERP dispersion and inducibility of ventricular tachycardias or ventricular fibrillation (VTNF), whereas norepinephrine increased VTNF inducibility despite a reduction in ERP dispersion. ConclusionsWe conclude that heterogeneous sympathetic denervation contributed to a prolongation and dispersion of ERP in the surviving epicardium overlying the infarct. Furthermore, a supersensitive response to norepinephrine with resultant ERP shortening and a paradoxical ERP prolongation during ASS caused by a-receptor mechanisms that may be related to increased electrical instability were observed.

Rate-dependent anisotropic conduction property in the epicardial border zone of canine myocardial infarcts and its modification by moricizine

SummaryWe evaluated anisotropic conduction properties, different conduction velocities depending on fiber orientation, in normal and infarcted myocardium and the effects of moricizine on anisotropic conduction. Various cycle lengths of stimulation were applied to 15 mongrel dogs, and epicardial mapping was performed using a 96-channel mapping electrode. Moricizine was then administered to seven dogs and the same procedure was performed. Conduction velocities were calculated from these maps. Programmed electrical stimulations were performed before and after moricizine administration to induce ventricular arrhythmias. Before moricizine administration, a rate-dependent decrease in longitudinal conduction velocity was observed in the infarcted zone. Moricizine suppressed longitudinal conduction in the normal zone significantly at 300 msec pacing, but not at slower rates. Moricizine at a dose of 4 mg/kg, on the other hand, suppressed longitudinal conduction in the infarcted zone significantly at all pacing cycle lengths. The effect of moricizine on transverse conduction was inconsistent. In three dogs, sustained ventricular tachycardia (VT) was induced either before or after moricizine administration. The mean cycle length of sustained VT was prolonged from 202 msec to 291 msec after 4 mg/kg of moricizine. Thus, the changes in cycle length of ventricular tachycardia observed were most likely the result of slowing of conduction velocity, especially in the longitudinal direction, in the infarcted myocardium. We conclude that the electrophysiologic nature of the subacute ischemic model was modified by moricizine, leading to depression of the conduction velocity of longitudinal conduction and the inducibility of ventircular arrhythmias.