As far as we know, this is the first study that investigates the prognostic value and the relationship between GLS and microvascular resistances in TTS patients. The main findings of our study were: 1) the presence of a more impaired coronary microvascular resistance (MR) together with a worse GLS were associated with a higher rate of MACE at 1-year of follow-up, 2) LS was globally impaired in patients with TTS with worse values in apical segments, and 3) NT-proBNP at admission and the recovery of LVEF, but not MR and hs-cTnT, were correlated with GLS values.
First, a reduced LVEF on admission has been shown to have prognostic implications in patients with TTS (9,26,27). Assessment of the myocardial function of the left ventricle using GLS is a more accurate evaluation of the recovery of the myocardial abnormalities in these patients. Alashi et al (18) reported that GLS could have prognostic value incremental to LVEF in the long-term prognosis in TTS patients, while Dias et al (17) showed the prognostic value of GLS for in-hospital mortality in these patients. In our study, we found that patients who had simultaneously NH-IMRangio and GLS values above the median population values developed a higher rate of MACE during the 1-year follow-up than those with one or both values below the median value. Thus, in our cohort GLS provides incremental prognostic value to the degree of impaired MR in TTS patients.
As we have commented in the introduction, myocardial dysfunction in TTS could be not only secondary to catecholaminergic toxicity and CMD but also a "protective mechanism" to avoid further damage by the catecholaminergic surge. It has been hypothesized that in the myocardium, the switch from β2-adrenergic receptor Gs coupling to β2-adrenergic receptor Gi coupling in response to the catecholamine surge could limit the induction of apoptotic pathways but causing a negative inotropic effect (28,29). Interestingly, we found a trend towards a mild negative correlation between LAD NH-IMRangio and GLS that would support the hypothesis that part of the ventricular dysfunction in TTS patients could be a mechanism to minimize myocardial damage during the acute phase of the disease. Nevertheless, these data are only hypothesis generating and would require a multicenter, prospective validation.
Furthermore, we found an alteration of the LS longitudinal strain in the three LV slices (basal, mid ventricular and apical) with the apical region showing the worst LS values. Our results are aligned with previous studies that reported a global LV involvement despite the visual appearance of basal hypercontractility in TTS patients, being the apical GLS the most severely affected (30–32).
Finally, in our study, NT-proBNP levels at admission were positively correlated with GLS values while we found a trend to a mild positive correlation between hs-cTnT levels and GLS values. The release of NT-proBNP is associated with the degree of LV wall stress while hs-cTnT is a marker of myocardial injury. Thus, a worse myocardial contractility during the acute phase of TTS would favor a higher release of both cardiac biomarkers (33–35). On the other hand, although we did not find a significant correlation between NH-IMRangio and GLS values, we observed a trend towards worse GLS values in those patients with less impaired MR, suggesting that ventricular dysfunction in TTS patients may not be only due to myocardial damage. However, as mentioned, these data are of hypothesis-generating value at this stage.