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  • Title: Association of glycemic variability with left ventricular diastolic function in type 2 diabetes mellitus.
    Author: Yokota S, Tanaka H, Mochizuki Y, Soga F, Yamashita K, Tanaka Y, Shono A, Suzuki M, Sumimoto K, Mukai J, Suto M, Takada H, Matsumoto K, Hirota Y, Ogawa W, Hirata KI.
    Journal: Cardiovasc Diabetol; 2019 Dec 05; 18(1):166. PubMed ID: 31805945.
    Abstract:
    BACKGROUND: Type 2 diabetes mellitus (T2DM) is a major cause of heart failure (HF) with preserved ejection fraction (HFpEF), usually presenting as left ventricular (LV) diastolic dysfunction. Thus, LV diastolic function should be considered a crucial marker of a preclinical form of DM-related cardiac dysfunction. However, the impact of glycemic variability (GV) on LV diastolic function in such patients remains unclear. METHODS: We studied 100 asymptomatic T2DM patients with preserved LV ejection fraction (LVEF) without coronary artery disease (age: 60 ± 14 years, female: 45%). GV was evaluated as standard deviation of blood glucose level using continuous glucose monitoring system for at least 72 consecutive hours. LV diastolic function was defined as mitral inflow E and mitral e' annular velocities (E/e'), and > 14 was determined as abnormal. RESULTS: E/e' in patients with high GV (≥ 35.9 mg/dL) was significantly higher than that in patients with low GV (11.3 ± 3.9 vs. 9.8 ± 2.8, p = 0.03) despite similar age, gender-distribution, and hemoglobin A1c (HbA1c). Multivariate logistic regression analysis showed that GV ≥ 35.9 mg/dL (odds ratio: 3.67; 95% confidence interval: 1.02-13.22; p < 0.05) was an independently associated factor, as was age, of E/e' > 14. In sequential logistic models for the associations of LV diastolic dysfunction, one model based on clinical variables including age, gender and hypertension was not improved by addition of HbA1c (p = 0.67) but was improved by addition of high GV (p = 0.04). CONCLUSION: Since HFpEF is a syndrome caused by diverse agents, reducing GV may represent a potential new therapeutic strategy for the prevention of the development of HFpEF in T2DM patients.
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