Key result
Higher myocardial T2 values linked to ~40% higher MACE risk per 5-ms increase in Takotsubo syndrome.
Why the study?
The prognostic value of cardiac magnetic resonance global T2 mapping in patients with Takotsubo syndrome was unclear.
Does CMR-derived global myocardial T2 mapping predict MACE in patients with Takotsubo syndrome?
Cohort (n=110)
Blinded to clinical data
Does CMR-derived global myocardial T2 mapping predict MACE in patients with Takotsubo syndrome?
Hazard Ratio: 1.4 (95% CI 1.06–1.87)
p-value: p=0.020
CMR-derived global myocardial T2 mapping provides incremental prognostic value for predicting adverse events in patients with Takotsubo syndrome.
May inform TTS prognosis via T2 mapping; hypothesis-generating in small observational data, needs prospective validation.
BACKGROUND: Myocardial oedema is a hallmark of Takotsubo syndrome (TTS). Cardiac magnetic resonance (CMR) T2 mapping quantifies myocardial oedema, but its prognostic value in TTS is unclear. We evaluated the association between CMR-derived global myocardial T2 and major adverse cardiovascular and cerebrovascular events (MACE). METHODS: : We retrospectively identified consecutive TTS patients undergoing CMR with tissue mapping within 30 days of admission. Imaging was re-analysed blinded to clinical data. The primary endpoint was MACE (all-cause death, heart failure hospitalisation, recurrent TTS, stroke, or transient ischaemic attack). Time-dependent ROC analysis derived a T2 threshold. Prespecified covariates were summarised by ridge-penalised Cox into a single linear predictor for adjustment. A Firth-penalised Cox model tested robustness. RESULTS: Among 110 patients (median age 68 years; 91% women), median global T2 was 56 ms (IQR 53-60), and 17 (15.5%) experienced MACE over a median follow-up of 763 days (IQR 525-1357). T2 ≥63 ms predicted 1-year MACE (AUC 0.671, sensitivity 56%, specificity 89%) and separated Kaplan-Meier curves (log-rank p=0.003). In ridge-penalised Cox models, each 5-ms increase in global T2 was associated with MACE (HR 1.40, 95% CI 1.06-1.87; p=0.020). This association was also observed after adjustment in the Firth-penalised model (HR 1.70, 95% CI 1.20-2.40; p=0.004). An internally derived threshold of T2 ≥63 ms was also associated with MACE but showed modest 1-year discrimination (AUC 0.671). CONCLUSIONS: Global myocardial T2 may provide incremental prognostic information beyond prespecified clinical and imaging indices in TTS and refine risk stratification.
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Kadoya et al. (2026) conducted a cohort in Takotsubo syndrome (n=110). Global myocardial T2 vs. Lower global myocardial T2 was evaluated on MACE (all-cause death, heart failure hospitalisation, recurrent TTS, stroke, or transient ischaemic attack) (HR 1.40, 95% CI 1.06-1.87, p=0.020). Higher global myocardial T2 values on CMR were associated with an increased risk of MACE in patients with Takotsubo syndrome (HR 1.40 per 5-ms increase; 95% CI 1.06-1.87; P=0.020).
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