Coronary microvascular dysfunction in takotsubo syndrome: an analysis using angiography-derived index of microcirculatory resistance

Abstract

Abstract Background Coronary microvascular dysfunction (CMD) has been proposed to be a major contributing factor in the pathophysiology of Takotsubo syndrome (TTS). To asses CMD, the angiography-derived index of microcirculatory resistance (caIMR) has been developed as a wire-free alternative to the conventional hyperemic wire-based index (IMR). This study aimed at evaluating the extent and transience of CMD and its implications on in-hospital outcome in TTS using caIMR. Methods Microcirculatory function of the three main coronary arteries of 96 TTS patients (48 with apical- and 48 with midventricular type) was assessed using caIMR. Measurements were compared with those of non-culprit vessels of 96 matched patients with ST-elevation myocardial infarction, as non-culprit vessels have previously been demonstrated to have an intact microcirculatory function [1]. In ten patients, follow-up caIMR was determined from angiographies without any cardiac event and was compared with event-caIMR. The prognostic role of caIMR on the in-hospital combined endpoint of death, cardiac arrest, ventricular arrhythmia, and vasopressor dependency was assessed via a binomial logistic regression analysis. Results CMD was present in all patients with TTS in at least one coronary vessel (caIMR>25), most frequently observed in the LCX (86 of 88 measurable LCXs [98%]). CaIMR in all three coronary arteries was significantly higher compared to the respective vessels of the control group. No significant difference in caIMR was observed comparing the apical and midventricular type of TTS. We could demonstrate normalization of caIMR in patients with follow-up angiographies performed at a median of 22 months (median [IQR] caIMR during event vs. follow-up: LCX 39.5 [33.9-52.0] vs. 25.1 [20.5-31.3]; LAD 34.2 [29.4-38.3] vs. 17.2 [15.9-23.9]; RCA: 31.7 [25.0-39.1] vs. 19.6 [17.1-24.0], Figure 1). The in-hospital combined endpoint correlated with the extent of CMD (p=0.036, Figure 2). Conclusion CMD was present during the acute TTS event and normalized during follow-up, suggesting that CMD is only a phenomenon of the acute phase of TTS and IMR values recover to normal dimensions. In addition, LAD caIMR was associated with the in-hospital end point of death, cardiac arrest, ventricular arrhythmia, and vasopressor dependence, however prospective validation will be necessary to further substantiate these findings.