SA JOURNAL OF DIABETES & VASCULAR DISEASE RESEARCH ARTICLE VOLUME 20 NUMBER 1 • JUNE 2023 9 Effect of insulin resistance on left ventricular remodelling in essential hypertensives: a cross-sectional study BERNARD KIANU PHANZU, ALIOCHA NKODILA NATUHOYILA, ELEUTHÈRE KINTOKI VITA, BENJAMIN LONGO-MBENZA, JEAN-RENÉ M’BUYAMBA KABANGU Correspondence to: Bernard Kianu Phanzu Department of Internal Medicine, Division of Cardiology, University of Kinshasa Hospital, and Centre Médical de Kinshasa, Kinshasa, Democratic Republic of the Congo e-mail: doctorkianu@gmail.com Eleuthère Kintoki Vita, Benjamin Longo-Mbenza, Jean-René M’Buyamba Kabangu Department of Internal Medicine, Division of Cardiology, University of Kinshasa Hospital, Kinshasa, Democratic Republic of the Congo Aliocha Nkodila Natuhoyila Department of Biostatistics, School of Public Health, Kinshasa, Democratic Republic of the Congo Published online in Cardiovasc J Afr; 21 June 2023 S Afr J Diabetes Vasc Dis 2023; 20: 9–16 Abstract Background: In clinical practice, left ventricular hypertrophy (LVH) is definedbyphysical findings andelectrocardiographic 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. Keywords: hyperinsulinaemia, insulin resistance, left ventricular remodelling, diastolic dysfunction, hypertension Hypertensive patients with insulin resistance (IR) are at increased cardiovascular risk compared to hypertensive patients without IR.1 Likewise, the presence of target-organ damage, including left ventricular hypertrophy (LVH), is associated with a poor prognosis in hypertensive patients.2 International guidelines therefore recommend considering hypertensive patients with target-organ damage, including LVH, as being at high cardiovascular risk.3-5 Hypertension-induced LVH is a known corollary not only of barometric overload secondary to high blood pressure, but also of various metabolic abnormalities induced by IR6,7 and hyperinsulinaemia.8,9 LVH represents a phenotype of the formidable capacity of the heart to adapt to various constraints in order to maintain a cardiac output sufficient to meet the metabolic needs of the whole organism. This left ventricular (LV) remodelling is defined as the set of changes in the size, shape and function of the left ventricle.10 LVH has a poor prognosis.2,10-12 It is defined not by the ventricular wall thickness, but by the left ventricular mass (LVM), calculated according to the formula of Devereux, also known as Penn’s formula,13 as: LVM (g) = 0.8 × 1.04 [(LVED + IVS + PWT)3 – LVED3] + 0.6 g, where LVED indicates left ventricular end-diastolic diameter, IVS indicates interventricular septal thickness and PWT indicates posterior wall thickness. Therefore, any factor that increases LVM might affect at least one of the following components: LVED and/or IVS and/or PWT. Because IR and hyperinsulinaemia increase LVM, the purpose of this study was to assess the collective and isolated influence of IR/ hyperinsulinaemia on each component of the Devereux formula and on diastolic functional parameters. Methods This was a cross-sectional study conducted in the Centre Médical de Kinshasa (CMK) between January and December 2019. The CMK is a reference clinic with a cardiology centre named Pôle de
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