Clinical application of pulmonary vascular resistance in patients with pulmonary arterial hypertension

Deng, Jianying

doi:10.1186/s13019-021-01696-4

Cited by 6 publications

(5 citation statements)

References 71 publications

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“…Cells were seeded at a density of 3 × 10 3 cells per well in 96 well tissue culture plates. After serum starvation for 24 h, cells were treated with different concentrations of BTZ to detect the toxicity of BTZ to PASMCs.…”

Section: Methodsmentioning

confidence: 99%

“…1,2 The main cause of increased PVR in most patients with PAH is due to fixed vascular obstruction with loss of the cross-sectional area, which leads to reduced cardiac output, right heart failure, and premature death. 3 Vasodilators are the mainstay of treatment for PAH; however, vasodilators treatment does not directly improve vascular obstruction nor resolve right ventricular hypertrophy caused by fibrosis, ischemia, and microvascular rarefaction. 4,5 A new treatment paradigm for PAH is crucially needed to address the severe disease caused by dysfunction of the right ventricle and pulmonary vasculature.…”

Section: Introductionmentioning

confidence: 99%

“…Pulmonary arterial hypertension (PAH), a severe progressive disorder with high morbidity and mortality, is mainly caused by the increase of pulmonary vascular resistance (PVR) 1,2 . The main cause of increased PVR in most patients with PAH is due to fixed vascular obstruction with loss of the cross‐sectional area, which leads to reduced cardiac output, right heart failure, and premature death 3 . Vasodilators are the mainstay of treatment for PAH; however, vasodilators treatment does not directly improve vascular obstruction nor resolve right ventricular hypertrophy caused by fibrosis, ischemia, and microvascular rarefaction 4,5 .…”

Section: Introductionmentioning

confidence: 99%

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Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells

Liu,

Tseng,

Kuan

et al. 2024

The Kaohsiung J of Med Scie

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Pulmonary vascular remodeling is a key pathological process of pulmonary arterial hypertension (PAH), characterized by uncontrolled proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). Bortezomib (BTZ) is the first Food and Drug Administration (FDA)‐approved proteasome inhibitor for multiple myeloma treatment. Recently, there is emerging evidence showing its effect on reversing PAH, although its mechanisms are not well understood. In this study, anti‐proliferative and anti‐migratory effects of BTZ on PASMCs were first examined by different inducers such as fetal bovine serum (FBS), angiotensin II (Ang II) and platelet‐derived growth factor (PDGF)‐BB, while potential mechanisms including cellular reactive oxygen species (ROS) and mitochondrial ROS were then investigated; finally, signal transduction of ERK and Akt was examined. Our results showed that BTZ attenuated FBS‐, Ang II‐ and PDGF‐BB‐induced proliferation and migration, with associated decreased cellular ROS production and mitochondrial ROS production. In addition, the phosphorylation of ERK and Akt induced by Ang II and PDGF‐BB was also inhibited by BTZ treatment. This study indicates that BTZ can prevent proliferation and migration of PASMCs, which are possibly mediated by decreased ROS production and down‐regulation of ERK and Akt. Thus, proteasome inhibition can be a novel pharmacological target in the management of PAH.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells

Liu,

Tseng,

Kuan

et al. 2024

The Kaohsiung J of Med Scie

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“…Velocity-time integral of right ventricular outflow tract (VTI RVOT ) was obtained from aortic short-axis view using pulse wave Doppler. R/LVEDA ≥ 0.6, TAPSE < 1.7 cm, S' < 9.5 cm/s, FAC < 35%, and PVR > 3 wood units were considered abnormal [6,[18][19][20].…”

Section: Echocardiographymentioning

confidence: 99%

Echocardiographic features of right ventricle in septic patients with elevated central venous pressure

Zhang,

Lian

et al. 2024

BMC Anesthesiol

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Background Elevated central venous pressure (CVP) is deemed as a sign of right ventricular (RV) dysfunction. We aimed to characterize the echocardiographic features of RV in septic patients with elevated CVP, and quantify associations between RV function parameters and 30-day mortality. Methods We retrospectively reviewed a cohort of septic patients with CVP ≥ 8 mmHg in a tertiary hospital intensive care unit. General characteristics and echocardiographic parameters including tricuspid annular plane systolic excursion (TAPSE), pulmonary vascular resistance (PVR) as well as prognostic data were collected. Associations between RV function parameters and 30-day mortality were assessed using Cox regression models. Results Echocardiography was performed in 244 septic patients with CVP ≥ 8 mmHg. Echocardiographic findings revealed that various types of abnormal RV function can occur individually or collectively. Prevalence of RV systolic dysfunction was 46%, prevalence of RV enlargement was 34%, and prevalence of PVR increase was 14%. In addition, we collected haemodynamic consequences and found that prevalence of systemic venous congestion was 16%, prevalence of RV-pulmonary artery decoupling was 34%, and prevalence of low cardiac index (CI) was 23%. The 30-day mortality of the enrolled population was 24.2%. In a Cox regression analysis, TAPSE (HR:0.542, 95% CI:0.302–0.972, p = 0.040) and PVR (HR:1.384, 95% CI:1.007–1.903, p = 0.045) were independently associated with 30-day mortality. Conclusions Echocardiographic findings demonstrated a high prevalence of RV-related abnormalities (RV enlargement, RV systolic dysfunction and PVR increase) in septic patients with elevated CVP. Among those echocardiographic parameters, TAPSE and PVR were independently associated with 30-day mortality in these patients.

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“…Pulmonary hypertension (PH) is a progressive and refractory vascular disease characterized by a persistent increase in the pulmonary artery (PA) pressure (PAP). PAP elevation is caused by abnormal hemodynamic states, including increased pulmonary vascular resistance (PVR), increased blood flow, and elevated PA wedge pressure (PAWP) [ 1 , 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of a Soluble Guanylate Cyclase Stimulator Riociguat on Contractility of Isolated Pulmonary Artery and Hemodynamics of U46619-Induced Pulmonary Hypertension in Dogs

Kameshima

Nakamura

Uehara

et al. 2023

Veterinary Sciences

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Soluble guanylate cyclase (sGC) stimulator riociguat is a relatively novel therapeutic agent for pulmonary hypertension (PH) in human medicine. Riociguat induces endothelium-independent pulmonary artery (PA) relaxation by directly activating the sGC-cyclic guanosine-3′,5′-monophosphate (cGMP) pathway in muscle cells. Although riociguat may be effective in the treatment of dogs with refractory PH, basic studies on its clinical application in veterinary medicine are lacking. The present study aimed to explore the effects of riociguat on the contractility of an isolated canine PA and the hemodynamics of dogs with acute PH. In an isolated endothelium-denuded canine PA, the effects of riociguat on endothelin (ET)-1-induced contraction and cGMP levels were investigated using the Magnus method and ELISA, respectively. The effect of riociguat on the hemodynamics of the thromboxane A2 analog U46619-induced PH model dog was examined by invasive catheterization. Riociguat increased cGMP levels and reduced ET-1-induced contraction of the isolated PA. Riociguat inhibited the U46619-induced elevation of PA pressure and pulmonary vascular resistance and increased cardiac output, but it had no effect on basal systemic blood pressure. These results demonstrate for the first time that riociguat can inhibit the elevation of PA pressure through PA relaxation via an endothelium-independent increase in cGMP in dogs with PH.

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Clinical application of pulmonary vascular resistance in patients with pulmonary arterial hypertension

Cited by 6 publications

References 71 publications

Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells

Proteasome inhibitor bortezomib prevents proliferation and migration of pulmonary arterial smooth muscle cells

Echocardiographic features of right ventricle in septic patients with elevated central venous pressure

Effects of a Soluble Guanylate Cyclase Stimulator Riociguat on Contractility of Isolated Pulmonary Artery and Hemodynamics of U46619-Induced Pulmonary Hypertension in Dogs

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