The pathogenesis of pulmonary hypertension — vessel wall ischemia as the driving force in disease initiation and progression

Heise, E; Чурилов, Леонид Павлович; Novitskaya, Tatiana; Yablonsky, Piotr; Haverich, Axel

doi:10.21638/spbu11.2021.103

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…Atherosclerosis and hypertension progressing are accelerated in patients with systemic autoimmune disorders accompanied by vasculitis syndrome [ 10 ]. There is a concept which regards vasculitis of vasa vasorum or small periadventitial vessels as a key link of atherogenesis and related cardiovascular disorders [ 11 , 12 , 13 , 14 ]. Excessive systemic action of proinflammatory autacoids may cause the development of CHF, based on the paradigm of systemic non-infectious low-intensity inflammation.…”

Section: Introductionmentioning

confidence: 99%

Heart Dysfunction in Essential Hypertension Depends on Systemic Proinflammatory Influences: A Retrospective Clinical Pathophysiological Study

et al. 2022

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Low-intensity systemic inflammation is an important element of heart failure pathogenesis. The aim of this study is to assess proinflammatory status serum indicators (C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6)) in middle-aged males (M) and females (F) with essential hypertension (HTN) depending on left ventricular (LV) diastolic dysfunction (LVDD). The main group comprised 55 M and 49 F with the first- to second-severity grade HTN with mild heart failure and a preserved LV ejection fraction ≥50%. Patients had sinus rhythm, first or second-severity degree LVDD, LV hypertrophy, left atrium dilatation, and NT-proBNP > 125 pg/mL. Comparison group: 30 hypertensives without cardiac dysfunction; control group: 31 normotensives. Quantitative features were compared using the Mann–Whitney test, median χ2, ANOVA module. Spearman’s rank correlation coefficients were determined to identify the relationship between the proinflammatory pattern and exercise tolerance. Hypertensive M had markedly higher CRP, TNF-α, and IL-6 levels compared to F. All mean values corresponded to reference range. In patients with second-degree LVDD, CRP, TNF-α, and IL-6 levels were significantly greater than in subjects with first-degree LVDD (both within M and within F samples). Significant negative associations between CRP, IL-6, and TNF-α levels and the 6 min walk test existed in hypertensive M and F. The study demonstrated a close relationship between the proinflammatory pattern and LVDD and exercise tolerance indicators, regardless of the hypertensive patient’s sex.

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Section: Introductionmentioning

confidence: 99%

Heart Dysfunction in Essential Hypertension Depends on Systemic Proinflammatory Influences: A Retrospective Clinical Pathophysiological Study

et al. 2022

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Hypoxic perfusion of pulmonary arterial vasa vasorum increases pulmonary arterial pressure

Heise,

Salman,

Webs

et al. 2024

American Journal of Physiology-Lung Cellular and Molecular Phys

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The pathophysiology of pulmonary hypertension (PH) is not fully understood. Here, we tested the hypothesis that hypoxic perfusion of the vasa vasorum of the pulmonary arterial (PA) wall causes PH. Young adult pig lungs were explanted and placed into a modified ex vivo lung perfusion unit (Organ care system, OCS) allowing the separate adjustment of parameters for mechanical ventilation, as well as PA perfusion and bronchial arterial (BA) perfusion. PA vasa vasorum are branches of the BA. The lungs were used either as control (n=3) or intervention group (n=8). The protocol of the intervention group was as follows: normoxic ventilation and perfusion (steady state) -hypoxic BA perfusion -steady state -hypoxic BA perfusion. During hypoxic BA perfusion, ventilation and PA perfusion maintained normal. Control lungs were kept under steady state conditions for 105 minutes. During the experiments, PA pressure (PAP) and blood gas analysis was frequently monitored. Hypoxic perfusion of the BA resulted in an increase in systolic and mean PAP, a reaction that was reversible upon normoxic BA perfusion. The PAP increase was reproducible in the second hypoxic BA perfusion. Under control conditions the PAP stayed constant until about 80 minutes of the experiment. In conclusion, the results of the current study prove that hypoxic perfusion of the vasa vasorum of the PA directly increases PAP in an ex situ lung perfusion setup suggesting that PA vasa vasorum function and wall ischemia may contribute to the development of PH.

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The pathogenesis of pulmonary hypertension — vessel wall ischemia as the driving force in disease initiation and progression

Cited by 2 publications

References 33 publications

Heart Dysfunction in Essential Hypertension Depends on Systemic Proinflammatory Influences: A Retrospective Clinical Pathophysiological Study

Heart Dysfunction in Essential Hypertension Depends on Systemic Proinflammatory Influences: A Retrospective Clinical Pathophysiological Study

Hypoxic perfusion of pulmonary arterial vasa vasorum increases pulmonary arterial pressure

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