Amera Halabi1, Hilda Yang2, Leah Wright3, Elizabeth Potter1, Quan Huynh1, Kazuaki Negishi4, Thomas H Marwick5. 1. Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia. 2. Menzies Institute for Medical Research, Imaging Research, Hobart, Tasmania, Australia. 3. Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; Menzies Institute for Medical Research, Imaging Research, Hobart, Tasmania, Australia. 4. Menzies Institute for Medical Research, Imaging Research, Hobart, Tasmania, Australia; Sydney Medical School Nepean, Charles Perkins Centre Nepean, Faculty of Medicine and Health, University of Sydney, Sydney, Australia. 5. Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia; School of Public Health and Preventive Medicine, Monash University, Melbourne, Victoria, Australia; Menzies Institute for Medical Research, Imaging Research, Hobart, Tasmania, Australia. Electronic address: tom.marwick@baker.edu.au.
Abstract
OBJECTIVES: The determinants of changes in systolic and diastolic parameters in patients age >65 years, at risk of heart failure (HF), and with and without asymptomatic type 2 diabetes mellitus (T2DM) was assessed by echocardiography. The association between metformin and myocardial function was also assessed. BACKGROUND: The increasing prevalence of T2DM will likely further fuel the epidemic of HF. Understanding the development or progression of left ventricular (LV) dysfunction may inform effective measures for HF prevention. METHODS: A total of 982 patients with at least one HF risk factor (hypertension, obesity, or T2DM) were recruited from 2 community-based populations and divided into 2 groups: T2DM (n = 431, age 71 ± 4 years) and non-T2DM (n = 551, age 71 ± 5 years). Associations of metformin therapy were evaluated in the T2DM group. All underwent a comprehensive echocardiogram, including global longitudinal strain (GLS) and diastolic function (transmitral flow [E], annular velocity [e']) at baseline and follow-up (median 19 months [interquartile range: 17 to 26 months]). Comparisons were facilitated by propensity matching. RESULTS: A reduction in GLS was observed in the T2DM group (baseline -17.8 ± 2.6% vs. follow-up -17.4 ± 2.8%; p = 0.003), but not in the non-T2DM group (-18.7 ± 2.7% vs. -18.6 ± 3.0%; p = 0.41). Estimated LV filling pressures increased in both the T2DM group (p = 0.001) and the non-T2DM group (p = 0.04). Metformin-treated patients with T2DM did not increase estimated LV filling pressure (E/e' baseline 8.9 ± 2.7 vs. follow-up 9.1 ± 2.7; p = 0.485) or change e' (7.6 ± 1.5 cm/s vs. 7.6 ± 1.8 cm/s; p = 0.88). After propensity matching, metformin was associated with a smaller change in e' (β = 0.58 [95% CI: 0.13 to 1.03]; p = 0.013) and E/e' (β = -0.96 [95% CI: -1.66 to -0.26]; p = 0.007) but was not associated with a change in GLS (p = 0.46). CONCLUSIONS: Over 2 years, there is a worsening of GLS and LV filling pressures in asymptomatic diabetic patients with HF risk factors. Metformin use is associated with less deterioration of LV filling pressures and myocardial relaxation but had no association with systolic function.
OBJECTIVES: The determinants of changes in systolic and diastolic parameters in patients age >65 years, at risk of heart failure (HF), and with and without asymptomatic type 2 diabetes mellitus (T2DM) was assessed by echocardiography. The association between metformin and myocardial function was also assessed. BACKGROUND: The increasing prevalence of T2DM will likely further fuel the epidemic of HF. Understanding the development or progression of left ventricular (LV) dysfunction may inform effective measures for HF prevention. METHODS: A total of 982 patients with at least one HF risk factor (hypertension, obesity, or T2DM) were recruited from 2 community-based populations and divided into 2 groups: T2DM (n = 431, age 71 ± 4 years) and non-T2DM (n = 551, age 71 ± 5 years). Associations of metformin therapy were evaluated in the T2DM group. All underwent a comprehensive echocardiogram, including global longitudinal strain (GLS) and diastolic function (transmitral flow [E], annular velocity [e']) at baseline and follow-up (median 19 months [interquartile range: 17 to 26 months]). Comparisons were facilitated by propensity matching. RESULTS: A reduction in GLS was observed in the T2DM group (baseline -17.8 ± 2.6% vs. follow-up -17.4 ± 2.8%; p = 0.003), but not in the non-T2DM group (-18.7 ± 2.7% vs. -18.6 ± 3.0%; p = 0.41). Estimated LV filling pressures increased in both the T2DM group (p = 0.001) and the non-T2DM group (p = 0.04). Metformin-treated patients with T2DM did not increase estimated LV filling pressure (E/e' baseline 8.9 ± 2.7 vs. follow-up 9.1 ± 2.7; p = 0.485) or change e' (7.6 ± 1.5 cm/s vs. 7.6 ± 1.8 cm/s; p = 0.88). After propensity matching, metformin was associated with a smaller change in e' (β = 0.58 [95% CI: 0.13 to 1.03]; p = 0.013) and E/e' (β = -0.96 [95% CI: -1.66 to -0.26]; p = 0.007) but was not associated with a change in GLS (p = 0.46). CONCLUSIONS: Over 2 years, there is a worsening of GLS and LV filling pressures in asymptomatic diabeticpatients with HF risk factors. Metformin use is associated with less deterioration of LV filling pressures and myocardial relaxation but had no association with systolic function.