SYMPATHETIC REINNERVATION AFTER ACUTE MYOCARDIAL INFECTION

Myocardial infarction produces sympathetic denervation of the necrotic myocardium and noninfarcted myocardium apical to the injury. Proof of sympathetic reinnervation after myocardial infarction has, however, r emained elusive. In this study, we investigated whether cardiac sympat hetic reinnervation occurs in men recovering from myocardial infarctio n. I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid, and Tc-99m sestamibi scintigraphic imaging were conducted in 13 men 3 and 12 months after a first myocardial infarction to determine the extent of denervated myocardium, the size of the infarct, and the size of the myocardium with reduced perfusion, respectively. A defect was determined as regional uptake of less than or equal to 30% of the maximal myocardial activity. The size of the MIBG defect was not signi ficantly different between 3 and 12 months after infarction (17 +/- 8% and 18 +/- 8% of left ventricular mass, respectively) There was also no significant change in the extent of viable but denervated myocardiu m at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). M IBG activity of the infarct zone (expressed as ct percentage of MIBG a ctivity of the myocardium with normal perfusion) did not change (17 +/ - 3% and 20 +/- 16%), whereas MIBG activity of the periinfarct zone in creased during follow-vp (32 +/- 11% and 41 +/- 14%, p <0.01). This wa s associated with an increase in periinfarct I-123 paraphenylpentadeca noic acid activity (40 +/- 11% and 48 +/- 9%, p <0.05), but not Tc-99m sestamibi activity (48 +/- 10% and 48 +/- 11%). in conclusion, we did not observe sympathetic reinnervation in the infarct zone between 3 a nd 12 months after myocardial infarction. However, MIBG activity of th e periinfarct zone increased, suggesting partial reinnervation, and th is was associated with a recovery of myocardial metabolic activity of the periinfarct zone.