Obesity and heart failure: epidemiology, pathophysiology, clinical manifestations, and management

doi:10.1016/j.trsl.2014.04.010

Translational Research

Volume 164, Issue 4, October 2014, Pages 345-356

https://doi.org/10.1016/j.trsl.2014.04.010 Get rights and content

Obesity is a risk factor for heart failure (HF) in both men and women. The mortality risk of overweight and class I and II obese adults with HF is lower than that of normal weight or underweight adults with HF of comparable severity, a phenomenon referred to as the obesity paradox. Severe obesity produces hemodynamic alterations that predispose to changes in cardiac morphology and ventricular function, which may lead to the development of HF. The presence of systemic hypertension, sleep apnea, and hypoventilation, comorbidities that occur commonly with severe obesity, may contribute to HF in such patients. The resultant syndrome is known as obesity cardiomyopathy. Substantial weight loss in severely obese persons is capable of reversing most obesity-related abnormalities of cardiac performance and morphology and improving the clinical manifestations of obesity cardiomyopathy.

Introduction

Obesity is both a risk factor for and a direct cause of heart failure (HF) and is associated with a variety of adverse hemodynamic changes that predispose to cardiac remodeling and ventricular dysfunction.1, 2, 3 These alterations are most pronounced in severely obese persons and may predispose to the development of HF, even in the absence of comorbidities such as coronary artery disease (CAD), valvular heart disease, pericardial disease, and congenital heart disease.1, 2 Recently, a variety of neurohormonal and metabolic abnormalities associated with obesity have been identified that may contribute to cardiac remodeling, ventricular dysfunction, and subsequent HF.1, 3 In this review, we describe the epidemiology, pathophysiology, and clinical manifestations of HF as they relate to obesity in adults. We also discuss the management of HF attributable to severe obesity with special emphasis on the role of purposeful weight loss.

Section snippets

Definitions

The World Health Organization (WHO) classifies obesity in terms of body mass index (BMI).⁴ The WHO classification is as follows: underweight (BMI < 18.5 kg/m²), normal weight (BMI: 18.5–24.9 kg/m²), overweight (BMI: 25.0–29.9 kg/m²), class I obesity (BMI: 30.0–34.9 kg/m²), class II obesity (BMI: 35.0–39.9 kg/m²), and class III obesity (BMI ≥ 40 kg/m²).⁴ In recent years the term “superobesity” has been used to characterize those whose BMI is ≥50 kg/m².5, 6 For the purpose of this review, the

Epidemiology

HF afflicts 23 million persons worldwide and 5.8 million persons in the United States.8, 10, 11 Reportedly, 40%–71% (mean: 56%) of those with HF have a normal or near normal left ventricular or left ventricle (LV) ejection fraction (LVEF).9, 10 In a study of 6076 patients hospitalized and discharged with a diagnosis of HF reported by Owan et al,¹² the incidence of obesity was 41.4% in subjects with a preserved LVEF and 35.5% in those with a reduced LVEF. It has been estimated that obesity is

Hemodynamic alterations with obesity

An early hemodynamic study by Alexander et al²³ showed a positive correlation between the amount overweight and both total blood volume and cardiac output (CO). In a subsequent study of 50 extremely obese patients, Alexander²⁴ confirmed that CO increased in proportion to the excess in body weight. In this study, heart rate did not differ from that predicted for ideal body weight. Stroke volume (SV) increased in proportion to the excess in body weight. Arteriovenous oxygen difference was normal

Clinical Manifestations of Obesity Cardiomyopathy

Obesity serves as a risk factor for HF. In such patients, clinical manifestations of HF are similar to those of HF from other causes. Severe obesity, however, is capable of causing HF in the absence of other forms of organic heart disease.⁸⁷ When this occurs, the clinical syndrome that results is termed “obesity cardiomyopathy.”⁸⁷ Most people who develop obesity cardiomyopathy have a body weight ≥135 kg, a relative weight of 175%–200%, or a BMI ≥40 kg/m².⁸⁷ Most have been severely obese for at

Management of Obesity Cardiomyopathy

The management of obesity cardiomyopathy is similar in many respects to management of HF from other causes.⁸⁷ A thorough search for and treatment of precipitating factors, particularly HTN and atrial fibrillation, is indicated in all cases. Moderate salt restriction and loop diuretics are key components of management regardless of LV systolic function. Angiotensin converting enzyme inhibitors or angiotensin receptor blockers should be administered in patients with severe LV systolic

Conclusions

Obesity is both a risk factor for and a direct cause of HF. Severe obesity in particular is capable of producing hemodynamic alterations that may cause cardiac remodeling and changes in ventricular function that may lead to LV and RV failure (Fig 1). Certain neurohormonal and metabolic abnormalities associated with obesity may contribute to this process. Purposeful weight loss is the most effective long-term measure for reversing abnormalities of cardiac performance and morphology associated

Acknowledgments

Conflict of interests: None.

Editorial support: None.

The manuscript has been reviewed and approved by all named authors.

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Obesity is an independent risk factor for heart failure (HF). Substantial weight loss has been shown to reverse obesity-related cardiomyopathy. This study aimed to report our institution’s experience with laparoscopic sleeve gastrectomy (LSG) in patients with morbid obesity and end-stage HF.
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The LSG and non-LSG cohorts had comparable ages (P = .088) and starting BMI score (P = .918), and a proportion of patients had a ventricular assist device (P = .191). Patients who underwent LSG lost significantly more weight than the patients who did not, with an average decrease in BMI score of 8.9 kg/m² (SD, ±6.13) and 1.1 kg/m² (SD, ±4.10), respectively (P = .040). Of note, 6 patients (37.5%) who underwent LSG eventually underwent transplantation, compared with 2 patients (20.0%) from the matched cohort (P = .884). Of the 26 patients, there were 6 deaths: 2 (12.5%) in the LSG cohort and 4 (40.0%) in the non-LSG cohort (P = .525).
LSG may be safe and effective for weight loss in patients with HF. This operation may provide patients affected by obesity with end-stage HF the lifesaving opportunity to achieve transplant candidacy.
Effects evaluation of different exercises on subclinical left ventricular dysfunction in obese rats by speckle-tracking echocardiography
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To identify subclinical left ventricle dysfunction (LVD) in obese rats by speckle-tracking echocardiography, and to evaluate the effects of 12-week Moderate-Intensity Continuous Training (MICT) or High-Intensity Interval Training (HIIT) on LV geometry, histology and function in obese rats.
Eighteen male standard or obese Sprague-Dawley rats were randomly divided into the Control group, the MICT group, and the HIIT group. Exercise interventions were conducted for 12 weeks, with equal total load and increased intensity gradient. Using dual-energy X-ray, two-dimensional speckle-tracking echocardiography, pulse Doppler, and HE staining to evalucate body shape, LV morphology, structure, and myocardial mechanics function.
(1) Both MICT and HIIT have good weight loss shaping effect. (2) The LV of obese rats underwent pathological remodeling, with decreased longitudinal contractility and synchrony, and increased circumferential contractility and synchrony. (3) Exercise can inhibit LV pathological remodeling, improve myocardial mechanical function. HIIT is superior to MICT. (4) The global longitudinal strain of obese rats in the HIIT group showed a significant correlation with Fat% and Lean%.
Obesity can induce LV pathological remodeling and subclinical dysfunction. Compared with MICT, 12-week HIIT can effectively inhibit the pathological remodeling of LV and promote the benign development of myocardial mechanical function in obese rats.
Update on obesity, the obesity paradox, and obesity management in heart failure
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Obesity is a major public health challenge worldwide. It is costly, predisposes to many cardiovascular (CV) diseases (CVD), is increasing at an alarming rate, and disproportionately affects people of low-socioeconomic status. It has a myriad of deleterious effects on the body, particularly on the CV system. Obesity is a major risk factor for heart failure (HF) and highly prevalent in this population, particularly in those with HF with preserved ejection fraction (HFpEF), to the extent that an obesity HFpEF phenotype has been proposed in the literature. However, once HF is developed, an obesity paradox exists where those with obesity have better short- and mid-term survival than normal or underweight individuals, despite a greater risk for hospitalizations. It may be argued that excess energy reserve, younger patient population, higher tolerability of HF therapy and better nutritional status may account for at least part of the obesity paradox on survival. Furthermore, body mass index (BMI) may not be an accurate measure of body composition, especially in HF, where there is an excess volume status. BMI also fails to delineate fat-free mass and its components, which is a better predictor of functional capacity and cardiorespiratory fitness (CRF), which particularly is increasingly being recognized as a risk modifier in both healthy individuals and in persons with comorbidities, particularly in HF. Notably, when CRF is accounted for, the obesity paradox disappears, suggesting that improving CRF might represent a therapeutic target with greater importance than changes in body weight in the setting of HF.
In this narrative review, we discuss the current trends in obesity, the causal link between obesity and HF, an update on the obesity paradox, and a description of the major flaws of BMI in this population. We also present an overview of the latest in HF therapy, weight loss, CRF, and the application of these therapeutic approaches in patients with HF and concomitant obesity.
A novel double GLA gene mutation of W24R and N419D in a patient with cardiac Fabry disease
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Fabry disease (FD) is an X-linked lysosomal storage disorder caused by insufficient activity of α-galactosidase A (α-Gal A) encoded by GLA. The enzymatic defect causes the progressive accumulation of sphingolipids in various tissues and body fluids, causing systemic disorders. We report a rare familial case of inherited cardiac FD associated with a novel double mutation in the GLA gene: W24R and N419D.
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Obesity has become a worldwide public health issue. Many obese patients concomitantly suffer with heart failure with reduced ejection fraction. There have been reports of improvement in left ventricular systolic function following significant weight loss after bariatric surgery. We sought to investigate this phenomenon within our institution. This was a retrospective single-center analysis of patients conducted between 2010 and 2019. The study included patients with morbid obesity (body mass index >35 kg/m² and an obesity-related comorbid condition, or a body mass index >40 kg/m²) and left ventricular systolic dysfunction. Analysis was performed based on systolic function recovery after bariatric surgery and advanced heart failure therapy. Of the 190 patients identified, 57 patients had a left ventricular ejection fraction of <40%. Twenty-two patients underwent bariatric surgery, of which at least 54.5% had systolic function recovery. Patients who had systolic function recovery after bariatric surgery were significantly older (51.58 years ± 10.48 vs 32.3 years ± 5.03, P = 0.001). Older age and female sex were predictors of systolic function recovery. In patients with obesity and heart failure with reduced ejection fraction, weight loss following bariatric surgery was shown to be correlated with significant improvement in left ventricular systolic function.

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In-Depth Review: Excess Adiposity and DiseaseReview ArticleObesity and heart failure: epidemiology, pathophysiology, clinical manifestations, and management

Introduction

Section snippets

Definitions

Epidemiology

Hemodynamic alterations with obesity

Clinical Manifestations of Obesity Cardiomyopathy

Management of Obesity Cardiomyopathy

Conclusions

Acknowledgments

J Am Coll Cardiol Heart Failure

J Am Coll Cardiol

Prog Cardiovasc Dis

Lancet

Am J Med Sci

Am J Cardiol

Am Heart J

Am J Cardiol

Am Heart J

J Card Fail

Am J Cardiol

Am J Cardiol

Am J Med

Am J Med Sci

Dis Chest

Am J Med Sci

Am J Cardiol

Am J Cardiol

JACC Cardiovasc Imaging

Chest

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

Arch Med Res

Am Heart J

Mayo Clin Proc

Transplant Proc

World Health Organization Technical Report 894. Obesity: preventing and managing the global epidemic

Bariatric surgery and cardiovascular risk factors: a scientific statement from the American Heart Association

Circulation

Cardiovascular evaluation and management of severely-obese patients undergoing surgery: a science advisory from the American Heart Association

Circulation

2009 Update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults

Circulation

The natural history of congestive heart failure: the Framingham study

N Engl J Med

Epidemiology and risk profile in heart failure

Nat Rev Cardiol

Epidemiology of heart failure

Circ Res

Trends in prevalence and outcome of heart failure with preserved ejection fraction

N Engl J Med

Obesity and the risk of heart failure

N Engl J Med

Obesity as an independent risk factor for heart failure: Zona Franco Cohort Study

Clin Cardiol

Abdominal obesity is an independent risk factor for heart failure in older people

J Am Geriatr Soc

The obesity paradox in patients with preserved versus reduced ejection fraction: a meta-analysis of individual patient data

Int J Obes

Blood volume, cardiac output and distribution of systemic blood flow in extreme obesity

Cardiovasc Res Cent Bull

Obesity and cardiac function

Circulation

Hemodynamic alterations with obesity in man

Assessment of cardiac function in patients who were morbidly obese

Surgery

Relation of regional fat distribution to left ventricular structure and function

Circ Cardiovasc Imaging

Cardiovascular function in extreme obesity

Acta Med Scand

Hemodynamic adaptation in severe obesity with or without arterial hypertension

Cardiologia

Adiposity of the heart

Arch Intern Med

The cardiac pathology of obesity

Circulation

In-Depth Review: Excess Adiposity and Disease
Review Article
Obesity and heart failure: epidemiology, pathophysiology, clinical manifestations, and management