The association of left ventricular mass index with metabolic syndrome in comparison to hypertensive patients

Abstract

Background and Objectives:The metabolic syndrome (MS) is a condition associated with the clustering of risk factors including high blood pressure (BP), abdominal obesity, glucose intolerance, and dyslipidemia; which increases cardiovascular morbidity and mortality. High burden of subclinical disease component of MS contributes to the increased risk by causing left ventricular (LV) hypertrophy, thereby affecting long-term prognosis. This cross-sectional study uncovers the role of LV hypertrophy (LVH) and LV mass index (LVMI) in patients with MS in comparison to hypertensive patients.Subjects and Methods:A total of fifty North Indians, out of which 25 subjects were cases with the MS (obesity, dyslipidemia, glucose intolerance/diabetes with hypertension) and rest of the 25 subjects were control with hypertensive patients were included in the study and assessed for LVH and LVMI by two-dimensional echocardiography. Data were analyzed by SPSS version 21.0 based program.Results:MS cases had a significantly higher mean LVMI (49.60 ± 21.23 g/m2.7) (P < 0.05), also higher exposure rate of LVH with 11 cases (44%) and relative risk of 1.38 (odds ratio 1.67, 95% confidence interval 0.53–5.29) than controls with hypertensive patients. Among LVH patients, mean LVMI was highest in MS cases with males (50.31 ± 26.03 g/m2.7), high body mass index >30 kg/m2 (51.14 ± 22.08 g/m2.7), FBS ≤ 140 mg/dl (53.72 ± 27.91 g/m2.7), high TG > 150 mg/dl (50.00 ± 22.09 g/m2.7), and low HDL (male <40, female <50 mg/dl) (57.22 ± 27.23 g/m2.7) than controls with hypertension; respectively (P > 0.05, not significant).Conclusion:MS, as a clustering of cardiovascular risk factors, is associated with higher LVM and prevalence of LVH. Therefore, high BP, increased waist circumference, dyslipidemia, and hyperglycemia separately and additively contributes to LVH suggesting that optimal BP control along with weight loss, lipid lowering agents, and euglycemic state may contribute to regression of LVH and LVM.

Prevalence of cardiac abnormalities and heart failure in unselected out-patients with type 2 diabetes mellitus and associated clinical factors: Real-world evidence from an Indian registry

“…In a case–control study, North Indian patients with metabolic syndrome were reported to have a higher exposure rate of LV hypertrophy (44 % vs 32 %; relative risk: 1.38; odds ratio: 1.67 [95 % CI 0.53, 5.29]) compared to hypertensive patients without T2DM. 45 De Simone also showed that the hazard of HF is increased by 1 % for each 1 % increase in excessive LV mass (HR: 1.01; 95 % CI 1.02, 1.04; p = 0.0001) after adjusting for age, sex, obesity, diabetes, arterial hypertension, and antihypertensive treatment and accounting for incident myocardial infarction. 43 However, none of the Indian studies including ours have evaluated the risk of adverse CV events associated with LV GLS values and LV mass as per our knowledge.…”

Left Ventricular Geometrical Changes in Severely Obese Adolescents: Prevalence, Determinants, and Clinical Implications

“…The association between anthropometric measures, in particular BMI and abdominal circumference, with metabolic syndrome is well established [28]. Similarly, several anthropometric variables, including BMI, waist circumference, waist-hip ratio, and waist-length ratios are associated with LVM in adults [29][30][31][32][33][34]. The pediatric literature relating et al raise the question whether further increases in BMI are associated with an increased severity of left ventricular hypertrophy [4].…”

Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure

“…Metabolic syndrome, central obesity, and diabetes substantially increase risk for VH/HF, independent of their common association with hypertension [ 447 , 448 , 449 , 450 , 451 , 452 , 453 , 454 , 455 , 456 , 457 ]. These disorders are characterized by high tissue exposure to free fatty acids, and there is reason to suspect that increased exposure to long-chain saturated fatty acids is a mediator of this increased risk.…”