Abstract 15399: Cardiac Sympathetic Nerve Activity in Women With a History of Takotsubo Syndrome: A Novel Stress Myocardial Radionuclide Imaging Strategy

Abstract

Introduction: Takotsubo syndrome (TTS) is characterized by transient left ventricular (LV) systolic dysfunction, triggered by physical or emotional stress, and associated with increased long-term cardiovascular morbidity. Cardiac iodine-123-meta-iodobenzylguanidine (mIBG) imaging has previously demonstrated sympathetic hyperactivity in the TTS subacute state which improves at follow-up during rest imaging. Cardiac neuronal dysfunction in response to stress has not been evaluated in recovered TTS. Hypothesis: Sympathetic hyperactivity, as measured by stress mIBG, is abnormal in TTS after recovery of LV ejection fraction (LVEF). Methods: To elicit a sympathetic challenge, women with history of TTS with recovered LVEF (n=19) and asymptomatic age- and sex-matched reference controls (n=10) underwent treadmill (6 minutes) with simultaneous mental-stress testing (public speaking with anger recall). mIBG (10 mCi) was injected during exercise, and planar and SPECT imaging were performed at 15 min (early) and 240 min (late), followed by Tc-99m tetrofosmin myocardial perfusion imaging. Early and late heart-to-mediastinal ratio (HMR) and washout rate (WR) corrected for background were calculated. Results: Median time from last TTS event was 23 months (range 4-56). Overall mean age was 60± 12 years, body mass index 25 ± 4kg/m 2 , resting LVEF 70 ± 7%, 41% hypertension and 0% diabetes with no difference between TTS and controls. TTS had higher resting (140 ± 22 vs 123 ± 19 mmHg, p=0.049) and peak (187 ± 17 vs 171 ± 15 mmHg, p= 0.018) systolic blood pressure. While the early HMR and WR were similar, the late HMR was significantly lower in the TTS group (Figure). Conclusions: Women with a history of TTS have lower late HMR but similar WR, suggesting neuronal dysfunction in response to sympathetic challenge persists long after recovery from TTS event. Further analysis of catecholamine levels and central nervous system neural pathways will explore the mechanism of dysregulation.