Why the study?
Attempts to characterize cardiac structure in HFpEF in people with T2D have yielded inconsistent findings.
Does the presence of type 2 diabetes alter cardiac remodelling, biomarker profiles, and clinical outcomes in patients with HFpEF compared to those without diabetes?
Does the presence of type 2 diabetes alter cardiac remodelling, biomarker profiles, and clinical outcomes in patients with HFpEF compared to those without diabetes?
In patients with HFpEF, the presence of type 2 diabetes is associated with distinct cardiac remodelling and increased systemic inflammation, suggesting a different underlying pathophysiology despite similar mid-term clinical outcomes.
BACKGROUND: Attempts to characterize cardiac structure in heart failure with preserved ejection fraction (HFpEF) in people with type 2 diabetes (T2D) have yielded inconsistent findings. We aimed to determine whether patients with HFpEF and T2D have a distinct pattern of cardiac remodelling compared with those without diabetes and whether remodelling was related to circulating markers of inflammation and fibrosis and clinical outcomes. METHODS: We recruited 140 patients with HFpEF (75 with T2D and 65 without). Participants underwent comprehensive cardiovascular phenotyping, including echocardiography, cardiac magnetic resonance imaging and plasma biomarker profiling. RESULTS: = 0.004) than those without diabetes. Plasma biomarkers of inflammation and extracellular matrix remodelling were elevated in those with T2D. Overall, there were 45 hospitalizations for HF and 22 deaths over a median follow-up period of 47 months [interquartile range (IQR) 38-54]. There was no difference in the primary composite endpoint of hospitalization for HF and mortality between groups. On multivariable Cox regression analysis, age, prior HF hospitalization, history of pulmonary disease and LV mass/volume were independent predictors of the primary endpoint. CONCLUSIONS: Patients with HFpEF and T2D have increased concentric LV remodelling, smaller LA volumes and evidence of increased systemic inflammation compared with those without diabetes. This suggests the underlying pathophysiology for the development of HFpEF is different in patients with and without T2D. CLINICALTRIALSGOV IDENTIFIER: NCT03050593.
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Gulsin et al. (2019) studied this question.
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