Patients without Myocardial Accumulation of ¹²³I-metaiodobenzylguanidine Does it always reflect cardiac adrenergic dysfunction?

Abstract

Since December 1992 to March 1994, we have performed myocardial imaging with ¹²³I metaiodobenzylguanidine (¹²³I-MIBG) in 110 patients to examine myocardial sympathetic integrity. Among them 11 patients (10%) showed no accumulation of ¹²³I-MIBG in the heart. So we have examined the mechanisms of no myocardial ¹²³I-MIBG accumulation.
¹²³I-MIBG imaging was obtained at 20 min and 3 h after intravenous injection of ¹²³I-MIBG (148 MBq) at rest. In addition to routine tomography, anterior planar imaging of the heart and the whole body imaging were performed. Eleven patients without myocardial ¹²³I-MIBG accumulation consisted of 5 patients with orthostatic hypotension (including 3 patients with diabetic neuropathy), four patients with hypertrophic cardiomyopathy (HCM), one patient with hypertension and one normal subject. In patients with orthostatic hypotension, standing test showed cardiac sympathetic dysfunction. In addition to no myocardial ¹²³I-MIBG accumulation, accumulation of ¹²³I-MIBG in the salivary glands was not found in all of them. These indicated that in patients with orthostatic hypotension, generalized sympathetic dysfunction caused no myocardial ¹²³I-MIBG accumulation. But in other 6 patients there was no evidence which suggested the cardiac sympathetic nerve dysfunction. Age, sex, serum norepinephrine level, myocardial perfusion and the medication were not different between the patients with and without myocardial ¹²³I-MIBG accumulation. So the mechanism of no myocardial ¹²³I-MIBG accumulation was not clear in these patients. But it was noteworthy that in patients with HCM, no myocardial ¹²³I-MIBG accumulation appeared in 17% (4/24), and the frequency of no myocardial ¹²³I-MIBG accumulation in HCM was significantly (p<0.05) higher than in other disease entities when patients with orthostatic hypotension were excluded.