Studies of autonomic properties after healing of experimental myocardial infarction

The link between healed myocardial infarction, sympathetic activation, and sudden death has led to a series of studies in a specifically designed animal model. Transmural and non-transmural infarcts were produced in cat hearts and the studies were performed few months later. Using direct stimulation of cardiac sympathetic nerves and measuring local refractory periods it was found that there was an exaggerated response in the border zone. Competitive binding studies revealed that there was a modest reduction in the number of beta-adrenergic receptors in tissue adjacent to the scar. In similar preparations the norepinephrine content, in hearts with healed transmural infarcts, was significantly reduced in areas adjacent to scars. In contrast, in hearts with non-transmural infarcts, the norepinephrine content was not different from normal controls. Phenylephrine and isoproterenol induced afterdepolarizations, blocked respectively by phentolamine and propranolol, in 34% of Purkinje fibers of the preparations with a healed infarct. Thus, afterdepolarizations and triggered activity may be mediated by both alpha- and beta-adrenergic activity in hearts with healed myocardial infarction. These data suggest the persistence, after healing of myocardial infarction, of regional abnormalities in autonomic function at a myocardial level. These regional disparities are likely to influence propensity to arrhythmias.