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

Abstract

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 (R^² = 0.468; overall p = 0.001) and 30.9% of E-wave deceleration time (R^² = 0.309; overall p = 0.003) were explained by insulin level and HOMAIR, 30.1% of variation in left ventricular end-diastolic diameter (R^² = 0.301; p = 0.013) by HOMAIR alone, and 46.3% of posterior wall thickness (R^² = 0.463; p = 0.002) and 29.4% of relative wall thickness (R^² = 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.