Key result
Post-sepsis status linked to ~74 ms higher septal native T1 values and lower LVEF.
Why the study?
Post-sepsis cardiomyopathy increases the risk of adverse cardiovascular outcomes but remains poorly understood, limiting therapeutic development.
Does acute sepsis cause persistent myocardial structural and functional changes detectable by CMR in survivors with suspected cardiac injury?
Case-Control (n=38)
Single-blind (CMR maps analyzed blinded to clinical data)
No
Does acute sepsis cause persistent myocardial structural and functional changes detectable by CMR in survivors with suspected cardiac injury?
Absolute Event Rate: 1071% vs 997%
p-value: p=<0.001
CMR evaluation of sepsis survivors identifies prevalent non-ischemic cardiomyopathy patterns characterized by LV dilatation, systolic dysfunction, and myocardial fibrosis, extending evidence of sepsis-induced chronic cardiac sequelae.
May support CMR evaluation in symptomatic post-sepsis survivors; extends evidence of chronic sequelae but remains hypothesis-generating.
Background: Post-sepsis cardiomyopathy is associated with an increased risk of adverse cardiovascular outcomes. It remains poorly understood, which limits therapeutic development. This study characterised post-sepsis cardiomyopathy using cardiovascular magnetic resonance (CMR) imaging. Methods: Patients admitted with acute sepsis and suspected cardiac injury or heart failure who subsequently (47 days [IQR: 22–122]) underwent CMR at a UK tertiary cardiac centre were included. Age- and gender-matched controls (n = 16) were also included. Subjects underwent CMR at 1.5 Tesla with cines, native T1- and T2-mapping, and late gadolinium enhancement (LGE) imaging. Results: Of the 22 post-sepsis patients (age 50 ± 13 years; 64% males), 13 patients (59%) had left ventricular (LV) dilatation. Patients had significantly elevated left ventricular (LV) end-diastolic and end-systolic volume indices compared to controls (p = 0.011 and p = 0.013, respectively). Eleven patients (50%) had LV systolic dysfunction (ejection fraction < 50%), most of whom (8/11) had non-ischaemic patterns of LGE (n = 7 mid-wall; n = 1 mid-wall/patchy). In the eleven patients with preserved LV systolic function (ejection fraction ≥ 50%), three patients (27%) had significant LGE (n = 1 mid-wall; n = 1 subepicardial/mid-wall; n = 1 patchy). Compared to controls, patients had elevated septal native myocardial T1 values (p < 0.001) but similar septal native myocardial T2 values (p = 0.090), suggesting the presence of myocardial fibrosis without significant oedema. Conclusions: Post-sepsis cardiomyopathy is characterised by LV dilatation, systolic dysfunction, and myocardial fibrosis in a non-ischaemic distribution. Significant myocardial oedema is not prominent several weeks post-recovery. Further work is needed to test these findings on a multi-centre basis and to develop novel therapies for post-sepsis cardiomyopathy.
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Malomo et al. (2025) conducted a case-control in Acute sepsis with suspected cardiac injury or heart failure (n=38). Acute sepsis vs. Matched controls without recent sepsis was evaluated on Septal native myocardial T1 values (surrogate for diffuse myocardial fibrosis) (p=<0.001). Post-sepsis patients demonstrated significantly elevated septal native myocardial T1 values compared to controls (1071 ms vs 997 ms, p<0.001) and lower LV ejection fraction (49% vs 61%, p=0.038).
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