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Published on: July 14, 2021
Obesity and Cardiac Remodeling in Adults: Mechanisms and Clinical Implications
Martin A Alpert1, Kamalesh Karthikeyan1, Obai Abdullah1
1Division of Cardiovascular Medicine, University of Missouri School of Medicine, Columbia, MO, USA.
Insights
Severe obesity causes hemodynamic changes and cardiac alterations, potentially leading to heart failure. Neurohormonal and metabolic factors common in obesity significantly impact heart structure and function.
Area of Science:
- Cardiology
- Metabolic Disorders
- Obesity Research
Background:
- Severe obesity induces significant hemodynamic alterations.
- Cardiac changes include high output state, left ventricular hypertrophy, and diastolic dysfunction.
- Right heart issues can arise from left ventricular failure, hypercirculation, and sleep-disordered breathing.
Purpose of the Study:
- To review the mechanisms linking obesity-related neurohormonal and metabolic changes to cardiac structure and function.
- To elucidate how these factors contribute to heart failure development in obese individuals.
Main Methods:
- Review of experimental and human studies.
- Analysis of neurohormonal pathways (renin-angiotensin-aldosterone, sympathetic nervous system).
- Examination of metabolic factors (leptin resistance, adiponectin, insulin resistance, lipotoxicity).
Main Results:
- Obesity commonly involves activated renin-angiotensin-aldosterone and sympathetic nervous systems.
- Leptin resistance, low adiponectin, insulin resistance, and potential cardiac lipotoxicity are prevalent.
- These factors contribute to cardiac adaptations and maladaptations.
Conclusions:
- Neurohormonal and metabolic alterations in obesity play a crucial role in cardiac structural and functional changes.
- These obesity-associated factors promote the development of heart failure.
Abstract:
Obesity, particularly severe obesity is capable of producing hemodynamic alterations that contribute to changes in cardiac morphology which may predispose to impairment of ventricular function and heart failure. These include a high cardiac output state in most, left ventricular (LV) hypertrophy, and LV diastolic dysfunction. Right heart involvement may result from LV failure, the hypercirculatory state, and sleep disordered breathing. In recent years experimental studies and some studies in humans suggest that certain neurohormonal and metabolic alterations that occur commonly in obesity may contribute to alterations in cardiac structure and function. These include activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, hyperleptinemia due to leptin resistance, low circulating adiponectin levels, insulin resistance with hyperinsulinemia, and possibly cardiac lipotoxicity. This review will describe the ways in which these factors weave together to promote adaptations and maladaptations that result in alterations in cardiac structure and function which may contribute to the development of heart failure.
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