Insulin resistance and glycemic abnormalities are associated with deterioration of left ventricular diastolic function: a cross-sectional study

Abstract

BackgroundLeft ventricular diastolic dysfunction (LVDD) is considered a precursor of diabetic cardiomyopathy, while insulin resistance (IR) is a precursor of type 2 diabetes mellitus (T2DM) and independently predicts heart failure (HF). We assessed whether IR and abnormalities of the glucose metabolism are related to LVDD.MethodsWe included 208 patients with normal ejection fraction, 57 (27%) of whom had T2DM before inclusion. In subjects without T2DM, an oral glucose tolerance test (oGTT) was performed. IR was assessed using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). The lower limit of the top quartile of the HOMA-IR distribution (3.217) was chosen as threshold for IR. LVDD was verified according to current guidelines.ResultsIR was diagnosed in 38 (18%) patients without a history of diabetes. The prevalence of LVDD was 92% in subjects with IR vs. 72% in patients without IR (n = 113), respectively (p = 0.013). In the IR group, the early diastolic mitral inflow velocity (E) in relation to the early diastolic tissue Doppler velocity (averaged from the septal and lateral mitral annulus, E'av) ratio (E/E'av) was significantly higher compared to those without IR (9.8 [8.3-11.5] vs. 8.1 [6.6-11.0], p = 0.011). This finding remains significant when patients with IR and concomitant T2DM based on oGTT results were excluded (E/E'av ratio 9.8 [8.2-11.1)] in IR vs. 7.9 [6.5-10.5] in those without both IR and T2DM, p = 0.014). There were significant differences among patients with and without LVDD regarding the HOMA-IR (1.71 [1.04-3.88] vs. 1.09 [0.43-2.2], p = 0.003). The HOMA-IR was independently associated with LVDD on multivariate logistic regression analysis, a 1-unit increase in HOMA-IR value was associated with an odds ratio for prevalent LVDD of 2.1 (95% CI 1.3-3.1, p = 0.001). Furthermore, the E/E'av ratio increases along the glucose metabolism status from normal glucose metabolism (7.6 [6.2-10.1]) to impaired glucose tolerance (8.8 [7.4-11.0]) and T2DM (10.5 [8.1-13.2]), respectively (p < 0.001).ConclusionsInsulin resistance is independently associated with LVDD in subjects without overt T2DM. Patients with IR and glucose metabolism disorders might represent a target population to prevent the development of HF. Screening programs for glucose metabolism disturbances should address the assessment of diastolic function and probably IR.

Relationship between Aortic Stiffness and the Left Ventricular Function in Patients with Prediabetes

“…Our results are consistent with those of a recently published study in patients without overt type 2 diabetes (21). In this study, diastolic changes were also found to be associated with an unaltered geometric pattern and insignificantly depressed systolic function in the prediabetic group.…”

Doppler Echocardiography Evaluation of the Relationship between Insulin Resistance and Early Diastolic Dysfunction in Prediabetes Patients

“…This demonstrates that, with increase in insulin resistance, progression of the left ventricle disorder could develop. The results which support these findings could be encountered in two similar studies in patients with prediabetes [7]. Moreover, studies that have been done with patients who have diabetes, obesity and metabolic syndrome provided similar findings; and, insulin resistance in three of the groups seemed to be the main cause [8][9][10].…”

Speckle tracking echocardiography in hypertensive males with glucose metabolism disorders

“…Hyperinsulinemia exerts cardioprotective effects via glucose-dependent and independent mechanisms, including aversion of glucose toxicity, positive inotropy, modulation of apoptosis, infl ammation and coronary fl ow [7]. W. Dinh et al registrated that ranges of global LS didn't differ between IR and non-IR patients in a cross-sectional study [8]. According to Framingham Heart Study, IR was associated with increased LVMI and wall thickness in women but not in men [9].…”