Effects of canine myocardial infarction on sympathetic efferent neuronal function: scintigraphic and electrophysiologic correlates.

We studied the effects of nondecentralized left stellate ganglion stimulation on regional epicardial monophasic action potential duration at 50% (APD50) and 90% (APD90) repolarization from 104 sites in 10 surviving dogs with a chronic myocardial infarction model. These effects were correlated with thallium-201 and iodine-123 metiodobenzylguanidine (MIBG) imaging to identify areas of viable but denervated myocardium. Mean infarct size was 5.2% +/- 0.8% total heart weight, and the planimetered areas of denervation were always larger (18% +/- 4% total heart area). During constant ventricular pacing, stellate stimulation tended to shorten the APD90 only in normally innervated areas (364 +/- 5 to 358 +/- 5 msec) and to increase in denervated areas (358 +/- 5 to 362 +/- 5 msec), (p value not significant (NS) for prestellate and poststellate stimulation; p < 0.05 for difference between denervated vs innervated). The APD50 significantly shortened in innervated areas from 287 +/- 5 to 270 +/- 3 msec (p < 0.05) compared with denervated areas (283 +/- 4 to 274 +/- 5 msec, p = NS). We conclude that MIBG imaging demonstration of denervation identifies areas with impaired shortening of the epicardial APD50 in response to stellate stimulation and that nontransmural myocardial infarction produces areas of denervation larger than areas of necrosis.