Automaticity, triggered activity, and responses to adrenergic stimulation in cat subendocardial Purkinje fibers after healing of myocardial infarction

We studied automaticity, triggered activity, and responses to α- and β-adrenergic stimulation in subendocardial Purkinje fibers overlying healed infarct scars (infarct preparation) and from remote normal zones (noninfarct preparation) of cat left ventricles. The preparations were studied 2 to 4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex arteries. Subendocardial Purkinje fibers from corresponding areas of normal hearts served as control samples (control preparation). Transmembrane action potential characteristics and rates of automaticity (spontaneous phase 4 depolarization) did not differ among control, noninfarct, and infarct preparations. However, overdrive at cycle lengths of less than 400 msec suppressed automaticity to a greater degree in Purkinje fibers of infarct preparations than those of control and noninfarct preparations. Changes in automatic rate during superfusion with isoproterenol (10^-10 M to 10^-6 M) were not different among the three groups of preparations, but exposure to phenylephrine (10^-9 M to 10^-5 M) in the presence of 5 x 10^-7 M propranolol reduced the automatic rate to a greater degree in Purkinje fibers of infarct preparations than those of control or noninfarct preparations. Triggered activity arising from delayed afterdepolarizations was recorded in 10 of 29 infarct preparations (34%), but not in 12 control and 10 noninfarct preparations. These afterpotentials were augmented by increasing extracellular Ca⁺⁺ concentration, 10^-7 M isoproterenol, and 10^-5 M phenylephrine in the presence of 5 x 10^-7 M propranolol. We conclude that Purkinje fibers overlying healed infarct scars have altered physiology of spontaneous automaticity, enhanced responses to α-adrenergic interventions, and a tendency to triggered activity, and that both α- and β-adrenergic effects may result in worsening of arrhythmias by augmentation of afterpotentials in healed myocardial infarction.