medwireNews: Diabetes is associated with poor prognosis among patients with heart failure and preserved ejection fraction (HFpEF), study results suggest.
John McMurray (University of Glasgow, UK) and colleagues conducted a secondary analysis of the I-Preserve trial of irbesartan in patients with HFpEF, in which 27% of 4128 participants had diabetes.
After adjustment for known predictors of cardiovascular outcomes, patients with diabetes were 1.75 times more likely to experience cardiovascular death or hospitalization for HF compared with nondiabetic patients over a median follow-up of 4.1 years, with rates of 34% versus 22%.
Furthermore, 28% of patients with diabetes died, compared with 19% of patients without diabetes, translating into a 1.59-fold increased risk for mortality among those with diabetes.
“The study underlines the need for further investigation of which treatment approaches to both heart failure and diabetes might improve outcomes in patients with both conditions,” write the researchers in Circulation.
At baseline, patients with diabetes were significantly more likely to have a higher body mass index (31 vs 29 kg/m2), history of myocardial infarction (28 vs 22%), worse quality of life (as indicated by a higher Minnesota Living with HF score: 48 vs 40), and higher levels of N-terminal pro B-type natriuretic peptide (NT-proBNP; 403 vs 320 pg/mL), as well as more signs of congestion than participants without diabetes.
The authors conducted an additional echocardiographic substudy using data from 745 participants of the I-Preserve trial, of whom 25% had diabetes. Although they note that these data were “incomplete,” patients with diabetes had larger left ventricular (LV) dimensions (end-diastolic: 4.9 vs 4.8 cm, end-systolic: 3.3 vs 3.2 cm) and greater LV mass (173 vs 161 g) than nondiabetic patients.
“The finding of more signs of congestion, higher NT proBNP levels and echocardiographic evidence of higher filling pressures in patients with diabetes, compared to those without, raises the possibility that more intensive diuretic therapy might be therapeutically helpful,” say the researchers. However, they admit that “this hypothesis needs to be tested, prospectively, in a clinical trial.”
The author of an accompanying editorial, Brian Lindman (Washington University School of Medicine, St Louis, Missouri, USA) believes that further mechanistic studies involving control patients are needed “to clarify whether HFpEF patients with diabetes represent a more severe form of HFpEF along a disease spectrum or whether there is a differentiated underlying pathophysiology.”
He suggests that improving metabolic abnormalities and reducing systemic inflammation may be more effective than targeting cardiac remodeling and dysfunction among patients with HFpEF and diabetes, noting that “in short, the line between ‘cardiovascular’ and ‘metabolic/diabetes’ drugs may begin to fade in the treatment of HFpEF.”
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