Impact of Adiponectin on Left Ventricular Mass Index in Non-complicated Obese Subjects

Abstract

Abstract. To evaluate the relationship between the adiponectin levels and left ventricular mass index (LVMI) in uncomplicated obese subjects. Fifty-nine subjects were assigned to the obese (BMI≥30 kg/m 2 ) and 58 to the lean (BMI<30 kg/m 2 ) group. Plasma glucose, insulin, serum total cholesterol and high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides and adiponectin were measured. Insulin resistance was determined by the Homeostasis Assessment Model (HOMA-IR). The left ventricular functions of all subjects were determined by 2D and pulse wave Doppler echocardiography. LVMI was calculated as left ventricular mass (LVM) normalized for height in m 2.7 . The obese group displayed significantly higher LVMI and late mitral inflow velocity. Thirty-three obese subjects met the criteria for left ventricular hypertrophy (LVH) and had lower serum adiponectin levels compared with obese subjects without LVH and lean subjects (p<0.05). Adiponectin was negatively correlated with LVMI (R: -0.277, p: 0.002). Furthermore, during the partial correlation analysis where HOMA-IR was controlled, the negative correlation between adiponectin and LVMI progressed (r: -0.283, p: 0.002). The linear regression analysis showed an independent relationship between LVMI and adiponectin. (β: -0.214, p: 0.01) Obesity is associated with LVH. This study showed direct influence of adiponectin on LVMI. OBESITY leads to serious changes in cardiac structure and functions [1]. These changes are characterized by an increase in left ventricular mass index (LVMI), diastolic dysfunction, and in advanced stages of the condition, systolic dysfunction [2]. It is currently believed that hemodynamic factors alone do not account for obesity-related cardiac structure abnormality. An investigation of possible metabolic inflammatory causes of left ventricular hypertrophy (LVH) in obesity may help the prevention and treatment of these changes [3].Recent studies have shown that adipose tissue acts like an endocrine organ and synthesizes various hormones. One of these hormones is adiponectin, which is believed to possess anti-atherogenic and anti-diabetic qualities [4]. Obesity or other obesity related complications are associated with decreased adiponectin levels [4], and thus is believed to play a role in the etiology of a number of diseases such as obesity, insulin resistance, hypertension, dyslipidemia, and atherosclerotic heart disease. Therefore, hypoadiponectinemia may be a factor in obesity-related LVH [5], which may be an independent effect or result of complications, such as obesity or obesity-related insulin resistance and hypertension [5]. Thus, an improvement in adiponectin levels can be expected to lower obesity-related morbidity and mortality [6]. However, there are few studies in

Relationship Between Adiponectin and Left Atrium Size in Uncomplicated Obese Patients: Adiponectin, a Link Between Fat and Heart

“…On the other hand, the inverse correlation of LV mass with adiponectin has been recently reported [42,50] including its persistence after HOMA adjustment [50].…”

Adiponectin and Cardiovascular Disease

“…Hypo-adiponectinemia is associated with progression of left ventricular hypertrophy (LVH), which is accompanied by diastolic dysfunction. 33 In non-complicated obese subjects, adiponectin levels are negatively correlated with left ventricular mass index, 34 and are also inversely associated with LVH by electrocardiographic and echocardiographic analysis in healthy subjects. 35,36 Because hypoadiponectinemia is recognized as an independent risk factor for hypertension, 22 its contribution to the development of hypertrophic cardiomyopathy may be related, in part, to modulation of blood pressure.…”

Left-ventricular hypertrophy and obesity

“…According to criteria based on left-ventricular mass indexed to BSA, LVH prevalence ranged from 22.0 [27] to 67.0% [21]; the corresponding figures for left-ventricular mass indexed to height 2.7 were 20.0 [17] and 85.0% [32]. A meta-analysis aimed at comparing the prevalence of LVH in normotensive (six studies, 418 participants) [17][18][19]26,31,35] and hypertensive obese individuals (eight studies, 1976 participants) [15,16,21,22,28,29,32,33], and failed to find significant difference between the groups (54 versus 59%; P ¼ 0.44).…”