Abstract
BackgroundConflicting information exists regarding the association between insulin resistance (IR) and left ventricular hypertrophy (LVH). We described the associations between obesity, fasting insulinemia, homeostasis model assessment of insulin resistance (HOMA-IR), and LVH in Black patients with essential hypertension.MethodsA case–control study was conducted at the Centre Médical de Kinshasa (CMK), the Democratic Republic of the Congo, between January and December 2019. Cases and controls were hypertensive patients with and without LVH, respectively. The relationships between obesity indices, physical inactivity, glucose metabolism and lipid disorder parameters, and LVH were assessed using linear and logistic regression analyses in simple and univariate exploratory analyses, respectively. When differences were observed between LVH and independent variables, the effects of potential confounders were studied through the use of multiple linear regression and in conditional logistic regression in multivariate analyses. The coefficients of determination (R2), adjusted odds ratios (aORs), and their 95% confidence intervals (95% CIs) were calculated to determine associations between LVH and the independent variables.ResultsEighty-eight LVH cases (52 men) were compared against 132 controls (81 men). Variation in left ventricular mass (LVM) could be predicted by the following variables: age (19%), duration of hypertension (31.3%), body mass index (BMI, 44.4%), waist circumference (WC, 42.5%), glycemia (20%), insulinemia (44.8%), and HOMA-IR (43.7%). Hypertension duration, BMI, insulinemia, and HOMA-IR explained 68.3% of LVM variability in the multiple linear regression analysis. In the logistic regression model, obesity increased the risk of LVH by threefold [aOR 2.8; 95% CI (1.06–7.4); p = 0.038], and IR increased the risk of LVH by eightfold [aOR 8.4; 95 (3.7–15.7); p < 0.001].ConclusionObesity and IR appear to be the primary predictors of LVH in Black sub-Saharan African hypertensive patients. The comprehensive management of cardiovascular risk factors should be emphasized, with particular attention paid to obesity and IR. A prospective population-based study of Black sub-Saharan individuals that includes the use of serial imaging remains essential to better understand subclinical LV deterioration over time and to confirm the role played by IR in Black sub-Saharan individuals with hypertension.
Highlights
Conflicting information exists regarding the association between insulin resistance (IR) and left ven‐ tricular hypertrophy (LVH)
A significantly larger proportion of sedentary persons was identified among patients with LVH (Table 1), with significantly increased measurements for Relative wall thickness (RWT), E-wave deceleration time, E/e’ ratio, triglyceridemia, atherogenicity index (AI), glycemia, HbA1c, insulinemia, homeostasis model assessment of insulin resistance (HOMA-IR), IR, and hyperuricemia, compared with those in patients without LVH (Table 2)
In the present study, compared with patients without LVH, we found that hypertensive participants with LVH had a lower E/A ratio and a longer deceleration time, which indicated abnormalities in relaxation [41, 42, 64], associated with normal left ventricular filling pressure (LVFP), as evidenced by a normal E/e’ ratio (˂8) [43], with an almost-normal Left atrium area (LAA)
Summary
Conflicting information exists regarding the association between insulin resistance (IR) and left ven‐ tricular hypertrophy (LVH). Reaven is fondly remembered as the father of IR due to his contributions to our current understanding of the central role played by IR in cardiovascular disease, including the development of the insulin suppression test, which was the first quantitative method introduced to assess insulin-mediated glucose uptake in humans [4]. Using this test, Reaven established the important contributions of IR to human disease, type 2 diabetes [5, 6]. In a non-diabetic patient population, he illustrated the roles played by IR in the development of essential HTN [7]; osmotic balance [8]; sympathetic nervous system stimulation [9]; hypercoagulability [10]; decreased urinary uric acid clearance, with resultant hyperuricemia [11]; increased postprandial lipemia and the accumulation of residual lipoproteins [12]; the occurrence of lipid abnormalities, such as hypertriglyceridemia [13]; low levels of high-density lipoprotein cholesterol (HDL-c) [14]; and a decrease in the diameter of low-density lipoprotein cholesterol (LDL-c) particles [15]
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