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

Abstract

It is widely accepted that myocardial infarction results in adrenergic denervation of the infarcted and peri-infarcted myocardium. On the contrary, the concept of re-innervation of adrenergic nerve fibres is less well established. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innervation are only poorly known. In this study we investigated changes in cardiac adrenergic innervation and myocardial perfusion during the early convalescence period (the first 3 months) after an acute myocardial infarction. Single-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I123-metaiodobentzylguanidine (MIBG) and Tc99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake </=30% of maximal myocardial activity. The size of the MIBG defect calculated as a percentage of left ventricular mass remained unchanged between 1 week and 3 months after myocardial infarction (31.1 +/- 17.3% vs. 30. 5 +/- 16.8%, respectively). 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 the follow-up (14.2 +/- 11.5% vs. 11.4 +/- 9.7%, P<0.05, respectively) indicating improved myocardial perfusion. The results demonstrate that cardiac adrenergic re-innervation is a slow process; despite a significant increase in myocardial perfusion we found no evidence of adrenergic re-innervation during the first 3 months after acute myocardial infarction.

Dysinnervated but viable myocardium in ischemic heart disease

“…For example, in a study of patients with mild coronary artery disease and no exercise-induced perfusion abnormalities, initial MIBG uptake was regionally normal consistent with normal sympathetic nerve density 30. However, the subsequent rate of MIBG washout (after 4-5 hours) was increased, reflecting abnormal sympathetic nerve function.…”

Norepinephrine transporter function and human cardiovascular disease

“…In addition, NET dysfunction could limit the physiological adjustment in cardiac sympathetic through depletion of norepinephrine stores. Decreased tracer uptake has been observed in patients with myocardial infarction (68,120,121), stress-induced cardiomyopathy (17,23,56,88,100,101,110,127,135), and congestive heart failure (2,84). In a small study in patients with arrhythmogenic right ventricle cardiomyopathy cardiac uptake of […”

Targeting neuronal dysfunction and receptor imaging

“…Cardiac adrenergic re-innervation is a slow process after acute myocardial infarction. Simula et al [16] studied changes in cardiac adrenergic innervation and myocardial perfusion 1 week and 3 months after acute myocardial infarction. Despite a significant increase in myocardial perfusion, no evidence of cardiac re-innervation was found three months after acute myocardial infarction.…”