Exercise Intolerance in Older Adults With Heart Failure With Preserved Ejection Fraction

Pandey, Ambarish; Shah, Sanjiv J.; Butler, Javed; Kellogg, Dean L.; Lewis, Gregory D.; Forman, Daniel E.; Mentz, Robert J.; Borlaug, Barry A.; Simon, Marc A.; Chirinos, Julio A.; Fielding, Roger A.; Volpi, Elena; Molina, Anthony J.A.; Haykowsky, Mark J.; Sam, Flora; Goodpaster, Bret H.; Bertoni, Alain G.; Justice, Jamie N.; White, James P.; Ding, Jingzhone; Hummel, Scott L.; LeBrasseur, Nathan K.; Taffet, George E.; Pipinos, Iraklis I.; Kitzman, Dalane W.

doi:10.1016/j.jacc.2021.07.014

Cited by 105 publications

(98 citation statements)

References 127 publications

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“…A common feature of both T2D and HFpEF is exercise intolerance (EI) ( Upadhya et al, 2015a ; Pandey et al, 2021 ). The cause of exercise training (ET) is multifactorial ( Pandey et al, 2021 ) in T2D and HFpEF with impairment in cardiac performance ( Pugliese et al, 2021a ) and skeletal muscle metabolism/perfusion ( Espino-Gonzalez et al, 2021 ). Obesity and T2D significantly contribute to EI in HFpEF.…”

Section: Effects Of Obesity On the Heartmentioning

confidence: 99%

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

et al. 2022

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Heart failure with preserved ejection fraction is a growing epidemic and accounts for half of all patients with heart failure. Increasing prevalence, morbidity, and clinical inertia have spurred a rethinking of the pathophysiology of heart failure with preserved ejection fraction. Unlike heart failure with reduced ejection fraction, heart failure with preserved ejection fraction has distinct clinical phenotypes. The obese-diabetic phenotype is the most often encountered phenotype in clinical practice and shares the greatest burden of morbidity and mortality. Left ventricular remodeling plays a major role in its pathophysiology. Understanding the interplay of obesity, diabetes mellitus, and inflammation in the pathophysiology of left ventricular remodeling may help in the discovery of new therapeutic targets to improve clinical outcomes in heart failure with preserved ejection fraction. Anti-diabetic agents like glucagon-like-peptide 1 analogs and sodium-glucose co-transporter 2 are promising therapeutic modalities for the obese-diabetic phenotype of heart failure with preserved ejection fraction and aggressive weight loss via lifestyle or bariatric surgery is still key to reverse adverse left ventricular remodeling. This review focuses on the obese-diabetic phenotype of heart failure with preserved ejection fraction highlighting the interaction between obesity, diabetes, and coronary microvascular dysfunction in the development and progression of left ventricular remodeling. Recent therapeutic advances are reviewed.

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Section: Effects Of Obesity On the Heartmentioning

confidence: 99%

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

et al. 2022

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“…In fact, large outcome trials and registries reveal that being overweight or obese is a major risk factor of HFpEF [ 7 ]. There are multiple mechanisms whereby obesity contributes to HFpEF, since adiposity increases systemic inflammation, insulin resistance, and dyslipidemia, and impairs arterial, skeletal muscle, and physical function [ 59 ], all of which are abnormal in HFpEF [ 60 ] ( Figure 1 ). In contrast, weight loss after bariatric surgery in the human decreases LV hypertrophy, and LV filling pressures and reduces diastolic dysfunction [ 61 ].…”

Section: The Dilemma Of Hfpef Definitionmentioning

confidence: 99%

The Cardiomyocyte in Heart Failure with Preserved Ejection Fraction—Victim of Its Environment?

Rocca

Heeswijk

Richiardi

et al. 2022

Cells

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Heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) is becoming the predominant form of HF. However, medical therapy that improves cardiovascular outcome in HF patients with almost normal and normal systolic left ventricular function, but diastolic dysfunction is missing. The cause of this unmet need is incomplete understanding of HFpEF pathophysiology, the heterogeneity of the patient population, and poor matching of therapeutic mechanisms and primary pathophysiological processes. Recently, animal models improved understanding of the pathophysiological role of highly prevalent and often concomitantly presenting comorbidity in HFpEF patients. Evidence from these animal models provide first insight into cellular pathophysiology not considered so far in HFpEF disease, promising that improved understanding may provide new therapeutical targets. This review merges observation from animal models and human HFpEF disease with the intention to converge cardiomyocytes pathophysiological aspects and clinical knowledge.

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“…In contrast, one of the major causes of post-capillary PH is left heart disease with elevated left-sided filling pressure. Both HFpEF (heart failure with preserved ejection fraction) and HFrEF (heart failure with reduced ejection fraction) can cause PH ( 13 – 16 ), however, recent studies suggest that PH is more common in patients with HFpEF (38% in HFpEF vs. 22.6% in HFrEF) ( 17 , 18 ).…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Arterial Hypertension and Consecutive Right Heart Failure Lead to Liver Fibrosis

Hamberger

Legchenko

Chouvarine

et al. 2022

Front. Cardiovasc. Med.

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Hepatic congestion occurs in patients with right heart failure and can ultimately lead to liver fibrosis or cardiac cirrhosis. Elevated pulmonary arterial pressure is found in patients with hepatic congestion. However, whether pulmonary arterial hypertension (PAH) can be a cause of liver fibrosis is unknown. The aim of this study was to investigate whether rats in the SuHx model with severe PAH develop liver fibrosis and to explore the mechanisms of congestive hepatic fibrosis both in rats and humans. To achieve this, PAH was induced in six to eight-week old male Sprague Dawley rats by a single subcutaneous injection of the VEGFR 2 inhibitor SU5416 and subsequent hypoxia for 3 weeks, followed by a 6-week period in room air. SuHx-exposed rats developed severe PAH, right ventricular hypertrophy (RVH), and consecutive right ventricular failure. Cardiac magnetic resonance imaging (MRI) and histological analysis revealed that PAH rats developed both hepatic congestion and liver fibrosis. Gene set enrichment analysis (GSEA) of whole liver RNA sequencing data identified a hepatic stellate cell specific gene signature in PAH rats. Consistently, tissue microarray from liver of patients with histological evidence of hepatic congestion and underlying heart disease revealed similar fibrogenic gene expression patterns and signaling pathways. In conclusion, severe PAH with concomitant right heart failure leads to hepatic congestion and liver fibrosis in the SU5416/hypoxia rat PAH model. Patients with PAH should therefore be screened for unrecognized liver fibrosis.

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Exercise Intolerance in Older Adults With Heart Failure With Preserved Ejection Fraction

Cited by 105 publications

References 127 publications

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

The Cardiomyocyte in Heart Failure with Preserved Ejection Fraction—Victim of Its Environment?

Pulmonary Arterial Hypertension and Consecutive Right Heart Failure Lead to Liver Fibrosis

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