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, remained elusive. In this study, we investigated
whether cardiac sympathetic reinnervation occurs in men recovering from myocardial
infarction. 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 < or = 30% of the maximal myocardial
activity. The size of the MIBG defect was not significantly 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 myocardium
at 3 and 12 months (average 9 +/- 6% and 10 +/- 5%, respectively). MIBG activity of
the infarct zone (expressed as a percentage of MIBG activity of the myocardium with
normal perfusion) did not change (17 +/- 13% and 20 +/- 16%), whereas MIBG activity
of the periinfarct zone increased during follow-up (32 +/- 11% and 41 +/- 14%, p <
0.01). This was associated with an increase in periinfarct I-123 paraphenylpentadecanoic
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 and 12 months after myocardial infarction. However,
MIBG activity of the periinfarct zone increased, suggesting partial reinnervation,
and this was associated with a recovery of myocardial metabolic activity of the periinfarct
zone.