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Published on: September 29, 2017
Effects of Obesity on Cardiovascular Hemodynamics, Cardiac Morphology, and Ventricular Function
Martin A Alpert1,2, Jad Omran3, Brian P Bostick3
1Division of Cardiovascular Medicine, School of Medicine, University of Missouri-Columbia, Columbia, MO, USA. alpertm@health.missouri.edu.
Insights
Obesity can cause heart problems like left and right ventricular dysfunction and even heart failure (obesity cardiomyopathy). Fortunately, significant weight loss can reverse many of these cardiovascular changes.
Area of Science:
- Cardiovascular Medicine
- Obesity Research
- Cardiology
Background:
- Obesity is linked to hemodynamic changes affecting cardiac morphology and function.
- Neurohormonal and metabolic issues in obesity contribute to cardiac abnormalities.
- Severe obesity can lead to heart failure (obesity cardiomyopathy) independent of other heart diseases.
Purpose of the Study:
- To examine the cardiovascular alterations associated with obesity.
- To understand the mechanisms leading to obesity cardiomyopathy.
- To identify reversible cardiac changes with weight loss.
Main Methods:
- Review of hemodynamic, morphological, and functional cardiac changes in obese patients.
- Analysis of contributing factors like sleep-disordered breathing and neurohormonal imbalances.
- Assessment of cardiac function in normotensive obese individuals.
Main Results:
- Obesity commonly causes elevated cardiac output, low peripheral vascular resistance, and increased left ventricular (LV) end-diastolic pressure.
- Sleep-disordered breathing can exacerbate right heart pressures.
- Obesity is associated with LV hypertrophy, impaired diastolic function, and sometimes systolic dysfunction.
Conclusions:
- Obesity-induced cardiovascular changes can lead to heart failure.
- Neurohormonal and metabolic factors play a significant role.
- Substantial voluntary weight loss can reverse many cardiac alterations.
Abstract:
Obesity produces a variety of hemodynamic alterations that may cause changes in cardiac morphology which predispose to left and right ventricular dysfunction. Various neurohormonal and metabolic alterations commonly associated with obesity may contribute to these abnormalities of cardiac structure and function. These changes in cardiovascular hemodynamics, cardiac morphology, and ventricular function may, in severely obese patients, predispose to heart failure, even in the absence of other forms of heart disease (obesity cardiomyopathy). In normotensive obese patients, cardiac involvement is commonly characterized by elevated cardiac output, low peripheral vascular resistance, and increased left ventricular (LV) end-diastolic pressure. Sleep-disordered breathing may lead to pulmonary arterial hypertension and, in association with left heart failure, may contribute to elevation of right heart pressures. These alterations, in association with various neurohormonal and metabolic abnormalities, may produce LV hypertrophy; impaired LV diastolic function; and less commonly, LV systolic dysfunction. Many of these alterations are reversible with substantial voluntary weight loss.
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