Vascular and Microvascular Endothelial Function in Heart Failure With Preserved Ejection Fraction

Maréchaux, Sylvestre; Samson, Rohan; Belle, Éric Van; Breyne, Joke; Monte, Juliette de; Dédrie, Céline; Chebai, Nassim; Menet, Aymeric; Banfı, Carlo; Bouabdallaoui, Nadia; Jemtel, Thierry H. Le; Ennezat, Pierre‐Vladimir

doi:10.1016/j.cardfail.2015.09.003

Cited by 78 publications

(88 citation statements)

References 31 publications

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“…The largest study to date reported no significant difference in FMD between HFpEF patients and healthy volunteers matched for age and gender [61]. In contrast, in almost all studies assessing microvascular peripheral endothelial function through RHI measurement, HFpEF patients have evidence of microvascular ED [48, 62–65]. Also, prognostic significance for ED in HFpEF has only been proven for microvascular dysfunction [47].…”

Section: Various Vascular Beds Display Endothelial Dysfunction In mentioning

confidence: 99%

Targeting Endothelial Function to Treat Heart Failure with Preserved Ejection Fraction: The Promise of Exercise Training

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et al. 2017

Oxidative Medicine and Cellular Longevity

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Although the burden of heart failure with preserved ejection fraction (HFpEF) is increasing, there is no therapy available that improves prognosis. Clinical trials using beta blockers and angiotensin converting enzyme inhibitors, cardiac-targeting drugs that reduce mortality in heart failure with reduced ejection fraction (HFrEF), have had disappointing results in HFpEF patients. A new “whole-systems” approach has been proposed for designing future HFpEF therapies, moving focus from the cardiomyocyte to the endothelium. Indeed, dysfunction of endothelial cells throughout the entire cardiovascular system is suggested as a central mechanism in HFpEF pathophysiology. The objective of this review is to provide an overview of current knowledge regarding endothelial dysfunction in HFpEF. We discuss the molecular and cellular mechanisms leading to endothelial dysfunction and the extent, presence, and prognostic importance of clinical endothelial dysfunction in different vascular beds. We also consider implications towards exercise training, a promising therapy targeting system-wide endothelial dysfunction in HFpEF.

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Section: Various Vascular Beds Display Endothelial Dysfunction In mentioning

confidence: 99%

Targeting Endothelial Function to Treat Heart Failure with Preserved Ejection Fraction: The Promise of Exercise Training

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Lemmens

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et al. 2017

Oxidative Medicine and Cellular Longevity

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“…Stiffer aortas, which exhibit greater PWV, conduct forward and backward traveling waves at greater velocities and therefore promote an earlier arrival of wave reflections to the LV [6, 8, 12–14]. As a consequence of the aortic stiffening that occurs with aging and various disease states, the hemodynamic effects of wave reflections shift from diastole to systole, with prominent effects during mid-to-late systole in older adults [8, 12], particularly in women [3, 6, 7, 12, 15–17] and in patients with HFpEF [18–20]. In these conditions, wave reflections can have a substantial impact on the LV loading sequence (increasing mid/late relative to early systolic load).…”

Section: Arterial Load and The Left Ventricular Loading Sequence: Rolmentioning

confidence: 99%

Deep Phenotyping of Systemic Arterial Hemodynamics in HFpEF (Part 2): Clinical and Therapeutic Considerations

Chirinos

2017

J. of Cardiovasc. Trans. Res.

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Multiple phase III trials over the last few decades have failed to demonstrate a clear benefit of various pharmacologic interventions in heart failure with a preserved left ventricular (LV) ejection fraction (HFpEF). Therefore, a better understanding of its pathophysiology is important. An accompanying review describes key technical and physiologic aspects regarding the deep phenotyping of arterial hemodynamics in HFpEF. This review deals with the potential of this approach to enhance our clinical, translational, and therapeutic approach to HFpEF. Specifically, the role of arterial hemodynamics is discussed in relation to (1) the pathophysiology of left ventricular diastolic dysfunction, remodeling, and fibrosis, (2) impaired oxygen delivery to peripheral skeletal muscle, which affects peripheral oxygen extraction, (3) the frequent presence of comorbidities, such as renal failure and dementia in this population, and (4) the potential to enhance precision medicine approaches. A therapeutic approach to target arterial hemodynamic abnormalities that are prevalent in this population (particularly, with inorganic nitrate/nitrite) is also discussed.

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“…With HFpEF, in comparison to hypertensive patients without HF, there is a decrease in endothelial function as measured by cutaneous peak blood flow after arterial occlusion [57]. Microvascular blood flow was also assessed in a small study of HFpEF patients compared to healthy controls, which again found dysfunction in the periphery distinct from macrovascular disease [58].…”

Section: Introductionmentioning

confidence: 99%

Current Perspectives on Systemic Hypertension in Heart Failure with Preserved Ejection Fraction

et al. 2017

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Heart failure with preserved ejection fraction (HFpEF) is a prevalent but incompletely understood syndrome. Traditional models of HFpEF pathophysiology revolve around systemic HTN and other causes of increased left ventricular afterload leading to left ventricular hypertrophy (LVH) and diastolic dysfunction. However, emerging models attribute the development of HFpEF to systemic proinflammatory changes secondary to common comorbidities which include HTN. Alterations in passive ventricular stiffness, ventricular-arterial coupling, peripheral microvascular function, systolic reserve, and chronotropic response occur. As a result, HFpEF is heterogeneous in nature, making it difficult to prescribe uniform therapies to all patients. Nonetheless, treating systemic HTN remains a cornerstone of HFpEF management. Antihypertensive therapies have been linked to LVH regression and improvement in diastolic dysfunction. However, to date, no therapies have definitive mortality benefit in HFpEF. Non-pharmacologic management for HTN, including dietary modification, exercise, and treating sleep disordered breathing, may provide some morbidity benefit in the HFpEF population. Future research is need to identify effective treatments, perhaps in more specific subgroups, and focus may need to shift from reducing mortality to improving exercise capacity and symptoms. Tailoring antihypertensive therapies to specific phenotypes of HFpEF may be an important component of this strategy.

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Vascular and Microvascular Endothelial Function in Heart Failure With Preserved Ejection Fraction

Cited by 78 publications

References 31 publications

Targeting Endothelial Function to Treat Heart Failure with Preserved Ejection Fraction: The Promise of Exercise Training

Targeting Endothelial Function to Treat Heart Failure with Preserved Ejection Fraction: The Promise of Exercise Training

Deep Phenotyping of Systemic Arterial Hemodynamics in HFpEF (Part 2): Clinical and Therapeutic Considerations

Current Perspectives on Systemic Hypertension in Heart Failure with Preserved Ejection Fraction

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