Scintigraphically assessed cardiac sympathetic dysinnervation in poorly controlled type 1 diabetes mellitus: One-year follow-up with improved metabolic control

Diabetic neuropathy is thought to comprise a reversible metabolic and an irreversible structural component of neuronal abnormality. To study whether cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 Diabetes Mellitus (DM) without myocardial perfusion abnormalities is partially reversible with improved metabolic control, 123-I-metaiodobenzylguanidine (123-I-MIBG) scintigraphy (myocardial uptake score 1-6) was performed in 11 Type 1 DM patients (HbAlc 12.0 ± 1.8%, duration of diabetes 10 ± 4 yrs) one year after initial assessment. During follow-up, all patients had been treated with intensive insulin therapy and at one year, HbAlc had fallen to 8.4 ± 1.4% (p < 0.01). The global myocardial 123-I-MIBG uptake score had improved in 5 patients at one year, remained unchanged in 5 patients, and deteriorated in 1 patient. Cardiac sympathetic dysinnervation (123-I-MIBG myocardial uptake (MU) score > 2), initially observed in 10 patients, was detectable in 8 patients at follow-up. Myocardial uptake scores of the anterior, lateral, posterior, septal and apical region had improved in 6, 6, 6, 7 and 6 patients, but the mean changes of these scores did not reach significance. In patients with substantial improvement of metabolic control (HbAlc 7.3 ± 0.6% at one year, mean HbAlc of months 2-12: 7.8%, n = 6), global myocardial uptake had improved from 4.3 ± 1.0 to 3.2 ± 1.0 (p < 0.05). Respectively, myocardial uptake score of the anterior, posterior and septal region had ameliorated: 3.8 ± 1.3 vs 2.3 ± 0.8 (p < 0.05), 4.0 ± 1.7 vs 2.5 ± 1.0 (p < 0.05), 4.3 ± 1.2 vs 3.2 ± 1.5 (p < 0.05). In conclusion, cardiac sympathetic dysinnervation in poorly controlled longer-term Type 1 DM patients is dominated by irreversible neuronal abnormalities. Substantial metabolic improvement, however, partially restores cardiac sympathetic dysinnervation, indicating the presence of a reversible component of cardiac sympathetic dysfunction in longer-term Type 1 DM.