Strategies for Imaging Metabolic Remodeling of the Heart in Obesity and Heart Failure

Haidar, Amier; Taegtmeyer, Heinrich

doi:10.1007/s11886-022-01650-3

Cited by 5 publications

(11 citation statements)

References 72 publications

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“…A host of pathophysiologic cardiovascular changes occurs in response to excess body mass in obesity [ 8 ]. The cardiac remodeling that occurs is multi-factorial and involves a combination of changes in hemodynamics, neurohormonal signaling, and/or myocardial metabolism [ 23 ]. Metabolically, obesity induces myocardial cellular mechanisms such as ectopic cardiac fat deposition, toxic lipid metabolite accumulation, mitochondrial dysfunction, and inflammation that lead to metabolic adaptations [ 23 ].…”

Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

“…The cardiac remodeling that occurs is multi-factorial and involves a combination of changes in hemodynamics, neurohormonal signaling, and/or myocardial metabolism [ 23 ]. Metabolically, obesity induces myocardial cellular mechanisms such as ectopic cardiac fat deposition, toxic lipid metabolite accumulation, mitochondrial dysfunction, and inflammation that lead to metabolic adaptations [ 23 ]. Hemodynamically, the metabolic demand of obesity is associated an increase in intravascular blood volume and cardiac output through an increase in stroke volume and heart rate [ 8 ].…”

Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

“…Obesity is a significant risk factor for heart failure with both preserved and reduced ejection fraction [ 6 •, 42 ]. Obesity leads to heart failure through hemodynamic and metabolic changes that affect the myocardium [ 7 , 9 , 23 ]. Both the renin-angiotensin-aldosterone system and the sympathetic nervous system are upregulated in obesity [ 7 ].…”

Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

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Obesity, Cardiorespiratory Fitness, and Cardiovascular Disease

Haidar,

Horwich

2023

Curr Cardiol Rep

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Purpose of Review Obesity, generally defined by body mass index (BMI), is an established risk factor for the development of cardiovascular disease (CVD), while cardiorespiratory fitness (CRF) decreases risk. In chronic CVD, an obesity survival paradox in which higher BMI is associated with improved prognosis has been reported. This paper will examine the effect of obesity on CVD risk, explore obesity as a risk factor in patients with established CVD, and investigate the relationship between CRF, obesity, and CVD. Recent Findings Through metabolic and hemodynamic changes, obesity increases the risk for CVD and contributes to the development of other cardiovascular risk factors such as diabetes, dyslipidemia, and hypertension. Obesity is associated with metabolic, hormonal, and inflammatory changes that leads to atherosclerosis increasing the risk for coronary artery disease, and myocardial remodeling increasing the risk for heart failure. However, it has also been observed that overweight/obese patients with established CVD have a better prognosis when compared to non-obese individuals termed the obesity paradox. CRF is a vital component of health associated with improved cardiovascular outcomes and furthermore has been shown to markedly attenuate or nullify the relationship between obesity and CVD risk/prognosis. Summary Increasing CRF mitigates CVD risk factors and improves overall prognosis in CVD regardless of obesity status.

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Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

Section: Obesity and Cardiovascular Disease Riskmentioning

confidence: 99%

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Obesity, Cardiorespiratory Fitness, and Cardiovascular Disease

Haidar,

Horwich

2023

Curr Cardiol Rep

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“…Metabolic reprogramming occurs as an adaptive event in both cancer (35) and cardiac cells (36) in response to pathophysiological insult and stress, indicating that both cells share the same metabolic pathways. In HF and cancer, glucose oxidation and glycolysis are central metabolic pathways to generate energy in the form of adenosine triphosphate (ATP) (37,38).…”

Section: Metabolic Remodelingmentioning

confidence: 99%

Evidence for reciprocal network interactions between injured hearts and cancer

Guler

Tscheiller

Sabater-Molina

et al. 2022

Front. Cardiovasc. Med.

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Heart failure (HF) and cancer are responsible for 50% of all deaths in middle-aged people. These diseases are tightly linked, which is supported by recent epidemiological studies and case control studies, demonstrating that HF patients have a higher risk to develop cancer such as lung and breast cancer. For HF patients, a one-size-fits-all clinical management strategy is not effective and patient management represents a major economical and clinical burden. Anti-cancer treatments-mediated cardiotoxicity, leading to HF have been extensively studied. However, recent studies showed that even before the initiation of cancer therapy, cancer patients presented impairments in the cardiovascular functions and exercise capacity. Thus, the optimal cardioprotective and surveillance strategies should be applied to cancer patients with pre-existing HF. Recently, preclinical studies addressed the hypothesis that there is bilateral interaction between cardiac injury and cancer development. Understanding of molecular mechanisms of HF-cancer interaction can define the profiles of bilateral signaling networks, and identify the disease-specific biomarkers and possibly therapeutic targets. Here we discuss the shared pathological events, and some treatments of cancer- and HF-mediated risk incidence. Finally, we address the evidences on bilateral connection between cardiac injury (HF and early cardiac remodeling) and cancer through secreted factors (secretoms).

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“…We highlight how congruent are the derangements of HFpEF and obesity on the cardiovascular system, functional capacity, immune system, and renal function. The effects of obesity on cardiac metabolism and obesity-related conditions (hypertension [HT] and type 2 diabetes [T2D]) on HFpEF were recently reviewed and thus not discussed [38][39][40][41][42]. We then examine the effect of MBS on left ventricular mass (LVM) assessed by cardiac magnetic resonance imaging (CMR) and the effect of MBS on the incidence of heart failure (HF) in patients with obesity.…”

Section: Introductionmentioning

confidence: 99%

Obesity, Preserved Ejection Fraction Heart Failure, and Left Ventricular Remodeling

Stencel

Alai

Dhorepatil

et al. 2023

JCM

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Owing to the overwhelming obesity epidemic, preserved ejection fraction heart failure commonly ensues in patients with severe obesity and the obese phenotype of preserved ejection fraction heart failure is now commonplace in clinical practice. Severe obesity and preserved ejection fraction heart failure share congruent cardiovascular, immune, and renal derangements that make it difficult to ascertain whether the obese phenotype of preserved ejection fraction heart failure is the convergence of two highly prevalent conditions or severe obesity enables the development and progression of the syndrome of preserved ejection fraction heart failure. Nevertheless, the obese phenotype of preserved ejection fraction heart failure provides a unique opportunity to assess whether sustained and sizeable loss of excess body weight via metabolic bariatric surgery reverses the concentric left ventricular remodeling that patients with preserved ejection fraction heart failure commonly display.

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Strategies for Imaging Metabolic Remodeling of the Heart in Obesity and Heart Failure

Cited by 5 publications

References 72 publications

Obesity, Cardiorespiratory Fitness, and Cardiovascular Disease

Obesity, Cardiorespiratory Fitness, and Cardiovascular Disease

Evidence for reciprocal network interactions between injured hearts and cancer

Obesity, Preserved Ejection Fraction Heart Failure, and Left Ventricular Remodeling

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