Abstract 563: Cardiac Washout Rate of Iodine-123 Metaiodobenzylguanidine is High in Chronic Heart Failure Patients With Central Sleep Apnea
Background: Cardiac iodine-123 metaiodobenzylguanidine (123I-MIBG) imaging is useful to estimate cardiac sympathetic nervous activity and predict poor clinical outcomes in patients with chronic heart failure (CHF). However, the relationship between sleep-disordered breathing (SDB) assessed by polysomnography and cardiac sympathetic nervous activity assessed by 123I-MIBG imaging has not been investigated in patients with CHF. In this study, we sought to clarify this relationship in those patients.
Methods: We prospectively performed cardiac 123I-MIBG scintigraphy and overnight polysomnography in 70 patients with stable CHF (New York Heart Association functional class II/III and LV ejection fraction <50%). The patients were classified into the following 3 groups: patients with central sleep apnea (CSA) (apnea-hypopnea index [AHI] ≥10 and dominant central apneic events) (n = 22), those with obstructive sleep apnea (OSA) (AHI ≥10 and dominant obstructive apneic events) (n = 29); and those without SDB (AHI ≥ 10) (n = 19). The cardiac washout rate (WR) of 123I-MIBG, a useful index of cardiac sympathetic nervous activity, was obtained from initial (15 min) and delayed (4 h) planar 123I-MIBG images.
Results: The WR was significantly higher in patients with CSA (52.6±13.3%) than in those with OSA (37.6±8.6%, p < 0.05) and without SDB (38.5±5.7%, p < 0.05), and it did not differ between those with OSA and without SDB. The WR correlated positively with central apnea index (ρ = 0.35, p = 0.004) but did not with obstructive apnea index. After adjusting for age, gender, diabetes, log brain natriuretic peptide, angiotensin-conzerting enzyme inhibitor/angiotensin receptor blocker use, beta blocker use, and spirono-lactone use, CSA was associated with the WR.
Conclusions: The cardiac WR of 123I-MIBG is significantly higher in CHF patients with CSA than in those without it, indicating highly activated cardiac sympathetic nervous system in those with CSA. This suggests that highly activated sympathetic nervous system, which can enhance central chemosensitivity to CO2, contributes to the genesis of CSA in CHF and supports adverse clinical outcomes of CHF patients with CSA.