Endothelial function in patients with COPD: an updated systematic review of studies using flow-mediated dilatation

Vaes, Anouk W.; Boever, Patrick De; Franssen, Frits M.E.; Uszko-Lencer, Nicole H.M.K.; Vanfleteren, Lowie E.G.W.; Spruit, Martijn A.

doi:10.1080/17476348.2023.2176845

Cited by 1 publication

(2 citation statements)

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“…Therefore, the relatively low severity of the model could explain the disparity between our findings and the published data for humans. Our observed increase in endothelium-dependent vasorelaxation may appear contradictory to previous results of meta-analyses of COPD, which have shown a significant decrease in endothelial-dependent vasorelaxation [ 5 , 6 , 14 ]. However, studies assessing invasive (acetylcholine-induced) or non-invasive (flow-mediated) vasorelaxation in COPD patients have not consistently demonstrated its impairment [ 52 , 53 ].…”

Section: Discussioncontrasting

confidence: 99%

“…Of these, high blood pressure (BP) is the most common, being present in approximately 50% of COPD patients [ 3 , 4 ] and having a 33% increased mortality risk [ 1 ]. Vascular remodeling and dysfunction have been observed in COPD patients, including in particular peripheral endothelial dysfunction [ 5 , 6 ] and also increased arterial stiffness [ 7 , 8 ], arterial wall thickening [ 9 ], enlargement of the conductive arteries [ 10 ] and capillary rarefaction in the skeletal muscle [ 11 , 12 ]. Endothelial dysfunction, often described as a common feature of COPD, is defined as a state of imbalance between endothelium-derived relaxing and constrictive factors (generally related to an impaired NO bioavailability) that favors vasoconstriction [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

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Elevated Blood Pressure Occurs without Endothelial Dysfunction in a Rat Model of Pulmonary Emphysema

Desplanche,

Grillet,

Wynands

et al. 2023

IJMS

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Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease involving airway closure and parenchyma destruction (emphysema). Cardiovascular diseases are the main causes of morbi-mortality in COPD and, in particular, hypertension and heart failure with preserved ejection fraction (HFpEF). However, no mechanistic link has currently been established between the onset of COPD, elevated blood pressure (BP) and systemic vascular impairment (endothelial dysfunction). Thus, we aimed to characterize BP and vascular function and remodeling in a rat model of exacerbated emphysema focusing on the role of sympathetic hyperactivity. Emphysema was induced in male Wistar rats by four weekly pulmonary instillations of elastase (4UI) and exacerbation by a single dose of lipopolysaccharides (LPS). Five weeks following the last instillation, in vivo and ex vivo cardiac and vascular functions were investigated. Exacerbated emphysema induced cardiac dysfunction (HFpEF) and a BP increase in this COPD model. We observed vasomotor changes and hypotrophic remodeling of the aorta without endothelial dysfunction. Indeed, changes in contractile and vasorelaxant properties, though endothelium-dependent, were pro-relaxant and NO-independent. A β1-receptor antagonist (bisoprolol) prevented HFpEF and vascular adaptations, while the effect on BP increase was partial. Endothelial dysfunction would not trigger hypertension and HFpEF in COPD. Vascular changes appeared as an adaptation to the increased BP. The preventing effect of bisoprolol revealed a pivotal role of sympathetic hyperactivation in BP elevation. The mechanistic link between HFpEF, cardiac sympathetic activation and BP deserves further studies in this exacerbated-emphysema model, as well as in COPD patients.

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