Correlations of Serum Lipid Parameters and Atherogenic Indices With Left Ventricular Diastolic Dysfunction Among Apparently Healthy Patients With Type 2 Diabetes Mellitus: A Multicenter In-Hospital Cross-Sectional Study.

Background: In adolescents with Type 1 diabetes, lipid ratios are predictors of left ventricular diastolic dysfunction (LVDD). However, whether this also applies to adults with Type 2 Diabetes Mellitus (T2DM) is unclear. This study is aimed at assessing the correlations of serum lipid parameters and atherogenic indices with LVDD in patients with T2DM. Methods: This cross-sectional study included 203 patients with T2DM aged 59.9 ± 13.6 years (111 males, sex ratio: 1 : 2 in favor of males) from eight randomly selected urban hospitals. Demographic information was collected, an anthropometric assessment was performed, and blood pressure was measured. Fasting blood samples were obtained to assess total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), glucose, and glycated hemoglobin. The atherogenic index of plasma (AIP), Castelli Risk Index I (CRI-I), Castelli Risk Index II (CRI-II), atherogenic coefficient, and non-HDL-C were determined using specific formulas. Diastolic function was assessed using echocardiography as per the 2016 updated guidelines of the American Society of Echocardiography (ASE) and the European Association of Cardiovascular Imaging (EACVI). Results: Approximately 47.8% of the participants had LVDD. Compared with participants with normal diastolic function, those with LVDD were more likely to be older than 55 years (p < 0.001), tended to have obesity (p = 0.045), had a higher risk of developing dyslipidemia (p = 0.041), and higher AIP and CRI-II (p < 0.05) levels while having similar low HDL-C and hypertriglyceridemia frequencies. In the multivariate model adjusting for age, high AIP (adjusted odds ratio [aOR], 3.37; 95% confidence interval [CI], 1.22-5.34) and high CRI-II (aOR: 3.80; 95% CI: 2.25-6.35) were independent determinants of LVDD. Conclusions: These results highlight the importance of considering atherogenic indices, primarily AIP and CRI-II in the management of T2DM patients. High AIP and high CRI-II could serve as surrogate markers of LVDD, an early cardiovascular manifestation in patients with T2DM.

Effect of insulin resistance on left ventricular remodelling in essential hypertensives: a cross-sectional study.

BACKGROUND: In clinical practice, left ventricular hypertrophy (LVH) is defined by physical findings and electrocardiographic criteria, which are useful but imperfect tools, echocardiographic criteria and cardiac magnetic resonance imaging. In echocardiography, LVH is defined not by left ventricular wall thicknesses but by left ventricular mass. The latter is calculated according to Devereux's formula, and is increased by insulin resistance/hyperinsulinaemia. It is however unclear whether insulin resistance, hyperinsulinaemia, or both, is actually causative and what their collective or individual influence is on the components of Devereux's formula and parameters of left ventricular diastolic function. This study evaluated the associations of the homeostatic model assessment for insulin resistance (HOMAIR) and fasting plasma insulin levels with components of Devereux's formula and parameters of left ventricular diastolic function. METHODS: Relevant clinical data were collected from 220 hypertensive patients recruited between January and December 2019. The associations of components of Devereux's formula and parameters of diastolic function with insulin resistance were tested using binary ordinal, conditional and classical logistic regression models. RESULTS: Thirty-two (14.5%) patients (43.9 ± 9.1 years), 99 (45%) patients (52.4 ± 8.7 years) and 89 (40.5%) patients (53.1 ± 9.8 years) had normal left ventricular geometry, concentric left ventricular remodelling and concentric left ventricular hypertrophy, respectively. In multivariable adjusted analysis, 46.8% of variation in interventricular septum diameter (R² = 0.468; overall p = 0.001) and 30.9% of E-wave deceleration time (R² = 0.309; overall p = 0.003) were explained by insulin level and HOMAIR, 30.1% of variation in left ventricular end-diastolic diameter (R² = 0.301; p = 0.013) by HOMAIR alone, and 46.3% of posterior wall thickness (R² = 0.463; p = 0.002) and 29.4% of relative wall thickness (R² = 0.294; p = 0.007) by insulin level alone. CONCLUSIONS: Insulin resistance and hyperinsulinaemia did not have the same influence on the components of Devereux's formula. Insulin resistance appeared to act on left ventricular end-diastolic diameter, while hyperinsulinaemia affected the posterior wall thickness. Both abnormalities acted on the interventricular septum and contributed to diastolic dysfunction via the E-wave deceleration time.