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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Plasma adiponectin: a contributing factor for cardiac changes in visceral obesity-associated hypertension
Tiziana Di Chiara1, Anna Licata, Christiano Argano
1Dipartimento Biomedico di Medicina Interna e Specialistica, University of Palermo , Palermo , Italy.
Insights
Adiponectin levels are lower in individuals with visceral obesity and hypertension. Lower adiponectin is linked to increased left ventricular mass, suggesting a key role in cardiac damage, especially in hypertensive patients.
Area of Science:
- Cardiology
- Endocrinology
- Obesity Research
Background:
- Visceral obesity is associated with hypertension and cardiac remodeling.
- Adiponectin, an adipokine, plays a role in metabolic and cardiovascular health.
- The specific impact of adiponectin on left ventricular geometry in obesity-associated hypertension requires further elucidation.
Purpose of the Study:
- To evaluate the relationship between adiponectin levels and left ventricular geometry and function.
- To investigate this relationship in subjects with visceral obesity-associated hypertension compared to lean controls.
Main Methods:
- Study included 94 subjects (53 hypertensive, 41 normotensive), aged ≤65 years, stratified by visceral obesity.
- Adiponectin levels were measured using radioimmunoassay.
- Echocardiography and Doppler assessed left ventricular dimensions, mass (LVM/h(2.7)), and diastolic function.
Main Results:
- Adiponectin levels were significantly lower in visceral obesity-associated hypertensives compared to lean hypertensives and normotensives.
- Left ventricular mass (LVM/h(2.7)) was significantly higher in both hypertensive groups and in visceral obesity-associated normotensives.
- Adiponectin inversely correlated with LVM/h(2.7) in visceral obese normotensive and hypertensive subjects, independent of other risk factors.
Conclusions:
- Adiponectin plays a significant role in the increased left ventricular mass observed in visceral obesity, in both normotensive and hypertensive individuals.
- In hypertensive subjects with visceral obesity, adiponectin levels may be a more critical determinant of cardiac damage than blood pressure itself.
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.
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