Noradrenaline depletion in patients with coronary artery disease before and after percutaneous transluminal coronary angioplasty with iodine-123 metaiodobenzylguanidine and single-photon emission tomography

Scintigraphic evidence for cardiac sympathetic dysinnervation in long-term IDDM patients with and without ECG-based autonomic neuropathy

“…Sympathetic denervation has been described in infarcted myocardium with a subsequent potential for arrythmogenicity [33,34]. In coronary artery disease a reduction of 123I-MIBG uptake has been observed, which emphasises the high sensitivity of the sympathetic nervous system to ischaemia [35]. In the present study, however, myocardial perfusion abnormalities in the diabetic patients were excluded by means of 99mTc-MIBI-scintigraphy, although there is evidence that microvascular factors such as impaired nerve blood flow play an important role in the pathogenesis of diabetic neuropathy [36].…”

11C-meta-hydroxyephedrine defects persist despite functional improvement in hibernating myocardium

“…Since regional norepinephrine uptake is only moderately reduced in hibernating myocardium6,7 as compared to infarction11,12 or cardiac transplantation,13,14 we have hypothesized that the partially dysinnervated myocardium may reflect a functional abnormality of the nerves rather than denervation 8. Although previous studies of patients with chronic coronary artery disease have shown very limited potential for improvement in regional dysinnervation,11,15,16 this could have been the result of denervation associated with unrecognized infarction. In contrast, we hypothesized that the sympathetic dysinnervation associated with the reversible ischemia in hibernating myocardium6,7 may result from a functional, ischemically mediated inhibition of the norepinephrine reuptake mechanism.…”

Impaired Cardiac Sympathetic Nerve Function in Patients with Kawasaki Disease: Comparison with Myocardial Perfusion

“…Myocardial ischemia could promote denervation in the area surrounding ischemic lesions, and sympathetic nerve is thought to be more susceptible than cardiac muscle cell to permanent ischemic damage (31). In CAD patients after percutaneous transluminal coronary angioplasty, although partial re-innervation could be seen sometimes in the area with well patent coronary artery, 123 I-MIBG defect remained wider than the ischemia-induced or scar-associated perfusion defect (37). Considering the finding of more 123 I-MIBG defects than perfusion defects and the histories of the patients in group B, the impairment of CSNF in KD patients, likely sharing the same mechanism as that in the adult patients with CAD, is subsequent to the ischemia caused by the formation of coronary artery stenosis.…”