Abstract
AIMS/HYPOTHESIS: Hyperglycaemia and insulin resistance have been linked to diastolic dysfunction experimentally. We investigated the association between glucose metabolism and diastolic function along the whole spectrum of glucose metabolism states. METHODS: In the observational Diagnostic Trial on Prevalence and Clinical Course of Diastolic Dysfunction and Diastolic Heart Failure (DIAST-CHF) study, patients with risk factors for heart failure were included. We analysed data including comprehensive echocardiography from a subgroup of patients classified by OGTT and history as normal (n = 343), prediabetic (n = 229) and non-insulin treated (n = 335) or insulin-treated (n = 178) type 2 diabetic. RESULTS: While ejection fraction did not differ, markers of diastolic function significantly worsened across groups. Prediabetes represented an intermediate between normal glucose metabolism and diabetes with regard to echocardiography changes. Prevalence and severity of diastolic dysfunction increased significantly (p < 0.001) along the diabetic continuum. Glucose metabolism status was significantly associated with prevalence of diastolic dysfunction on multivariate logistic regression analysis. In the whole cohort, HbA(1c) correlated with early diastolic mitral inflow velocity (E):early diastolic tissue Doppler velocity at mitral annulus (e') ratio (E:e') (r = 0.20, p < 0.001). HbA(1c) was significantly associated with E:e' on multivariate analysis. Similarly, glucose metabolism status was significantly associated with E:e' on multivariate analysis. The distance walked in 6 min decreased along the diabetic spectrum and was significantly correlated with E:e' and grade of diastolic dysfunction. CONCLUSIONS/INTERPRETATION: Glucose metabolism is associated with diastolic dysfunction across the whole spectrum. Our data extend previous observations into the prediabetic and normal range, and may be relevant to preventive approaches, as no effective treatment has been identified for diastolic heart failure once established.