Plasma adiponectin: A contributing factor for cardiac changes in visceral obesity-associated hypertension

Abstract

This study has been designed to evaluate the impact of adiponectin levels on left ventricular geometry and function in visceral obesity-associated hypertension. 94 consecutive subjects, 53 of them were hypertensives and 41 normotensives with age ≤ 65 years, subgrouped according to the presence or absence of visceral obesity, were studied. Total adiponectin levels were measured by a validated competitive radioimmunoassay. Left ventricular telediastolic internal diameter, interventricular septum, posterior wall thickness, total left ventricular mass (LVM) and normalized for height to the 2.7 power (LVM/h(2.7)), relative wall thickness, left ventricular ejection fraction by echocardiography and isovolumic relaxation time, E/A ratio and deceleration time of E velocity, by pulsed-wave Doppler, were calculated. Plasma adiponectin levels were significantly lower in visceral obesity-associated hypertensives than lean hypertensives (p < 0.001) and in lean normotensives (p < 0.001). LVM and LVM/h(2.7) were significantly (p < 0.05) higher in both hypertensive groups, and in visceral obesity-associated normotensives in comparison with lean normotensives. Adiponectin levels correlated inversely with LVM/h(2.7) but only in normotensives (adjusted R squared 0.77, p < 0.0001) and hypertensives (0.67, p < 0.0001) subjects with visceral obesity. Multiple regression analysis indicated that adiponectin levels remain significantly associated (p < 0.001) to LVM/h(2.7) also when adjusted for age, gender, body mass index, waist to hip ratio and mean blood pressure. Our data suggest an important role of adiponectin in increased LVM/h(2.7) in visceral obesity-associated normotensive and hypertensive subjects. In this last group, adiponectin, more than blood pressure, may be able to explain the development of cardiac damage.

"May Adiponectin be considered as a Novel Cardiometabolic Biomarker?"

“…However, plasma adiponectin levels are low in subjects with visceral fat accumulation and it seems to play an important role in the pathogenesis of visceral fat syndrome [1][2][3]. Our previous data [4] and some clinical studies reported an inverse association between ADPN and left ventricular mass (LVM) [1,5]. Moreover, increased ADPN expression can attenuate left ventricular hypertrophy (LVH) induced by pathological stimuli and it is able to protect the ischemic heart from injury, through the activation of independent pathways [1,2,4,5].…”

“…The concentration of ADPN was obtained by a radioimmunoassay using a human ADPN RIA kit (LINCO Research, Inc., Billerica, MA, USA) as previously described [4]. Patients with and without MetS were further subdivided in four groups, according to level of ADPN, higher than or equal to 6 µg/mL (normal ADPN groups) and less than 6 µg/mL (low ADPN groups) ( Table 1).…”

“…Our previous data [4] and some clinical studies reported an inverse association between ADPN and left ventricular mass (LVM) [1,5]. Moreover, increased ADPN expression can attenuate left ventricular hypertrophy (LVH) induced by pathological stimuli and it is able to protect the ischemic heart from injury, through the activation of independent pathways [1,2,4,5].…”

“…Accumulation of intra-abdominal visceral fat stands upstream of various risk factors and dysfunction of adipocyte is considered the cellular basis of metabolic syndrome (MetS) [1][2][3][4]. Adiponectin (ADPN) is an adipocyte-specific protein abundantly present in the plasma.…”

“…), LVM and pharmacological treatment. Body height, weight and waist circumference were all taken in a standardized manner [1,4]. Body mass index was calculated as weight divided by squared height and expressed as kg/m 2 and WHR by waist/hip ratio [4].…”