4094Microvascular dysfunction in takotsubo syndrome visualized at stress and rest using 82-rubidium PET imaging

Abstract

Abstract Introduction Takotsubo Syndrome (TTS) is recognized as the acute onset of reversible heart failure, often mimicking acute coronary syndrome with ECG changes and rise in cardiac biomarkers, but with no apparent coronary obstruction. The pathophysiological mechanisms of TTS are not yet fully understood, but it is well established that microvascular dysfunction and constriction plays a crucial role in the pathogenesis of TTS. Positron emission tomography (PET) using the radioactive tracer Rubidium-82 (Rb-82) is routinely used to asses myocardial perfusion and microvascular function in a wide array of cardiological conditions. Purpose The purpose of this study was to evaluate myocardial perfusion and flow reserve in patients with TTS using Rb-82 positron emission tomography (PET) molecular imaging during rest and pharmacologically induced stress, in the acute phase and after 3 months of follow-up. Methods A total of 8 patients were diagnosed with TTS due to acute onset of symptoms, rise in cardiac biomarkers, absence of significant coronary obstruction and apical ballooning of the left ventricle. Subsequently the patients underwent Rb-82 PET scan in the acute phase (1–4 days after onset), and again at 3 months of follow-up. Rb-82 PET scans were performed both during resting conditions and during pharmacologically induced stress with infusion of adenosine. Myocardial blood flow (MBF) and total perfusion defect (TPD) were quantified during rest and stress, and the coronary flow reserve (CFR) was calculated. The AHA-17 segment model was used to determine summed rest scores (SRS) and summed stress scores (SSS). Data are presented as means ± SEM Results MBF during stress was significantly lower in the acute phase than at 3 months follow-up (2.99±0.35 vs. 3.82±0.19 ml/g/min, P=0.016) as opposed to resting MBF, which did not differ significantly (1.33±0.14 vs. 1.45±0.09 ml/g/min, P=0.309). The CFR of the patients was not significantly different in the acute phase compared to 3 months follow-up (2.33±0.25 vs 2.65±0.12, P=0.11), though 4 of the patients had a CFR <2.0 in the acute phase, which was normalized at follow-up. TPD was significantly lower at follow-up compared to the acute phase at both rest (21.6±5.86 vs. 0.75±0.61%, P=0.009) and stress (25.3±6.01 vs. 1.25±0.31%, P=0.006). SRS (12.6±3.24 vs. 0.75±0.59, P=0.01) and SSS (19.9±3.39 vs. 1.38±0.59, P=0.001) was significantly higher in the acute phase compared to follow-up. At follow up, all values were normalized. Figure 1 Conclusion These results supports the evidence that TTS is partly caused by microvascular dysfunction and constriction during the acute phase. Further studies are needed to uncover the exact mechanisms behind.