Higher septal native T1 values trended higher in patients with adverse outcomes (1047.5 vs 1031.5 ms; p=0.065) but were not independently associated with the composite endpoint.
Cohort (n=45)
No
Does septal native T1 mapping predict adverse clinical outcomes in patients with non-ischemic dilated cardiomyopathy?
Septal native T1 mapping shows a trend toward predicting adverse outcomes in non-ischemic dilated cardiomyopathy but lacked independent prognostic value in this small cohort.
valor p: p=0.065
Background: Risk stratification in non-ischemic dilated cardiomyopathy (DCM) remains challenging because left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) do not fully capture the underlying myocardial substrate. Septal native T1 mapping provides a quantitative assessment of diffuse myocardial abnormalities and may contribute to myocardial tissue characterization within a multiparametric CMR framework. Methods: This retrospective single-center study included 45 consecutive patients with non-ischemic DCM referred for clinically indicated CMR at Perrino Hospital, Brindisi, Italy, between November 2023 and November 2025. All examinations were performed using a standardized CMR protocol including cine imaging, LGE, and native T1 mapping on a 1.5-T Siemens Healthineers scanner. Septal native T1 was used as the primary mapping parameter because of its established reproducibility and robustness for myocardial tissue characterization. Patients were followed for a composite endpoint including all-cause mortality, major ventricular arrhythmic events, appropriate ICD therapy, and hospitalization for heart failure. Endpoint coding was verified, and all analyses were performed using the final validated dataset. Results: During a median follow-up of 15 months, 14 patients (31.1%) experienced the composite endpoint. Patients with events had lower LVEF (27.1 ± 7.8% vs. 48.3 ± 10.5%; p < 0.001), higher LVEDVi (142.6 ± 28.5 vs. 110.6 ± 23.4 mL/m2; p = 0.001), and higher septal native T1 values among patients with available T1 measurements (1047.5 ± 25.0 vs. 1031.5 ± 24.3 ms; p = 0.065). ROC analysis identified a septal native T1 threshold of 1042 ms for prediction of the composite endpoint, with an exploratory AUC of 0.70. Event-free survival was lower in patients with septal native T1 ≥ 1042 ms. Given the limited number of events, all regression and hierarchical analyses should be interpreted as exploratory and hypothesis-generating. Conclusions: Higher septal native T1 values were observed in patients experiencing adverse clinical outcomes; however, native T1 was not independently associated with the composite endpoint in exploratory Cox regression analyses.
Montatore et al. (Fri,) conducted a cohort in Non-ischemic dilated cardiomyopathy (n=45). Higher septal native T1 values vs. Lower septal native T1 values was evaluated on Composite of all-cause mortality, major ventricular arrhythmic events, appropriate ICD therapy, and hospitalization for heart failure (p=0.065). Higher septal native T1 values trended higher in patients with adverse outcomes (1047.5 vs 1031.5 ms; p=0.065) but were not independently associated with the composite endpoint.
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