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Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
Published on: October 28, 2020
Left ventricular geometry in obesity: Is it what we expect?
G de Simone1, R Izzo, N De Luca
1The Hypertension Center, Department of Translational Medical Sciences, Federico II University Hospital, via S. Pansini 5 bld 1, 80131 Naples, Italy.
Nutrition, Metabolism, and Cardiovascular Diseases : NMCD
|October 8, 2013
Summary
Obesity causes left ventricular (LV) hypertrophy through both cardiac workload and non-hemodynamic factors like body composition. Addressing only cardiac load is insufficient for reducing LV hypertrophy in obese individuals.
Area of Science:
- Cardiology
- Obesity Medicine
- Physiology
Background:
- Obesity involves disproportionate growth in adipose and lean mass.
- Left ventricular (LV) hypertrophy is common in obesity, driven by hemodynamic and non-hemodynamic factors.
- Visceral fat activity and body composition contribute to cardiac workload.
Purpose of the Study:
- To review the pathophysiology and prevalence of LV hypertrophy in obesity.
- To examine LV geometric abnormalities associated with obesity.
- To explore the relationship between body size and LV hypertrophy.
Main Methods:
- Review of existing literature on obesity and cardiac function.
- Analysis of studies focusing on LV geometry in obese populations.
- Examination of the interplay between body composition, visceral fat, and myocardial structure.
Main Results:
- Cardiomyocyte hypertrophy results from hemodynamic load via sarcomeric replication.
- Non-muscular myocardial components, including interstitial fat and triglycerides, also increase.
- These non-muscular changes influence LV geometric patterns and hypertrophy.
Conclusions:
- LV hypertrophy in obesity is multifactorial, involving both muscle and non-muscle components.
- Interventions targeting only hemodynamic load may not effectively reduce LV hypertrophy.
- Understanding body composition and fat distribution is crucial for managing LV hypertrophy in obesity.
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