Cardiac Troponin release, myocardial function and inflammation in patients with takotsubo syndrome: a cardiac magnetic resonance study.

Abstract

Background Takotsubo syndrome (TTS) is an acute heart failure phenotype characterized by transient left ventricular dysfunction and modest Troponin release. Mechanisms of myocardial injury remain unclear. We aimed to investigate relationships between Troponin T release, myocardial edema by cardiac magnetic resonance (CMR) T2 mapping, and systemic inflammatory biomarkers in TTS. Methods N = 94 patients with acute TTS underwent CMR (median 4 days after admission) and serial blood sampling during the index hospitalization. Patients were stratified by a previously defined prognostic relevant peak high-sensitivity Troponin T cut-off (≥ 28.8× upper limit of normal [ULN] vs. <28.8× ULN). Full blood count was obtained at admission and on the day of CMR. Results Mean age of the study population was 74 years, 7% male. Patients with higher Troponin release presented with more severe left ventricular systolic dysfunction (admission LVEF 36% vs. 41%, p = 0.005) and higher T2 mapping values (60 vs. 57 ms, p < 0.05). On the CMR day, higher NLR (3.7 ± 2.4 vs. 2.7 ± 1.4, p = 0.020) and lymphocyte-to-monocyte ratio (LMR) (3.2 ± 1.0 vs. 3.9 ± 1.6, p = 0.020) were observed in the high-Troponin release subgroup. Multivariable linear regression analysis identified admission LVEF (β=-0.524, p < 0.001), T2 mapping (β = 0.171, p = 0.045), NLR (β = 0.262, p = 0.032), and LMR (β=-0.282, p = 0.033) as independent correlates of Troponin release as a continuous variable. Conclusions Troponin release in TTS reflects an interplay between ventricular dysfunction, myocardial edema, and systemic inflammatory activation, supporting a non-ischemic pattern of myocardial injury. Troponin may serve as a simple surrogate marker of myocardial and systemic inflammation.