Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Citation
S. Simula et al., Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction, CLIN PHYSL, 20(5), 2000, pp. 366-373
Citations number
37
Language
INGLESE
art.tipo
Article
Categorie Soggetti
General & Internal Medicine",Physiology
Journal title
CLINICAL PHYSIOLOGY
ISSN journal
0144-5979 → ACNP
Volume
20
Issue
5
Year of publication
2000
Pages
366 - 373
Database
ISI
SICI code
0144-5979(200009)20:5<366:CAIWTF>2.0.ZU;2-S
Abstract
It is widely accepted that myocardial infarction results in adrenergic dene rvation of the infarcted and peri-infarcted myocardium. On the contrary, th e concept of re-innervation of adrenergic nerve fibres is less well establi shed. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innerv ation are only poorly known. In this study we investigated changes in cardi ac adrenergic innervation and myocardial perfusion during the early convale scence period (the first 3 months) after an acute myocardial infarction. Si ngle-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I-123-metaiodo bentzylguanidine (MIBG) and Tc-99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake less than or equal to 30% of maximal myocardial activity. The size of the MIBG defect calculated as a p ercentage of left ventricular mass remained unchanged between 1 week and 3 months after myocardial infarction (31.1 +/- 17.3% vs. 30.5 +/- 16.8%, resp ectively). Accordingly, MIBG activity of the infarct and peri-infarct zones (expressed as a percentage of MIBG activity of the myocardium with normal perfusion) showed no significant change (23.7 +/- 10.0% vs. 25.3 +/- 11.0% and 39.0 +/- 11.3% vs. 40.8 +/- 12.8%, respectively) during the follow-up. On the other hand, the size of MIBI defect decreased significantly during t he follow-up (14.2 +/- 11.5% vs. 11.4 +/- 9.7%, P < 0.05, respectively) ind icating improved myocardial perfusion. The results demonstrate that cardiac adrenergic re-innervation is a slow process; despite a significant increas e in myocardial perfusion we found no evidence of adrenergic re-innervation during the first 3 months after acute myocardial infarction.