Serial phase-contrast MRI for prediction of pulmonary hemodynamic changes in patients with pulmonary arterial hypertension

2012 ◽  
Vol 157 (1) ◽  
pp. 140-142 ◽  
Author(s):  
Santo Dellegrottaglie ◽  
Pasquale Perrone-Filardi ◽  
Ana García-Alvarez ◽  
Sergio Moral ◽  
Gerin R. Stevens ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Phase Contrast ◽  
Hemodynamic Changes ◽  
Phase Contrast Mri ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Arterial

Assessment of hemodynamic changes in the systemic and pulmonary arterial circulation in patients with cystic fibrosis using phase-contrast MRI

2005 ◽  
Vol 15 (8) ◽  
pp. 1575-1580 ◽  
Author(s):  
Sebastian Ley ◽  
Michael Puderbach ◽  
Christian Fink ◽  
Monika Eichinger ◽  
Christian Plathow ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Phase Contrast ◽  
Hemodynamic Changes ◽  
Phase Contrast Mri ◽  
Arterial Circulation ◽  
Pulmonary Arterial

scholarly journals Iloprost for acute tests in patients with pulmonary arterial hypertension

2012 ◽  
Vol 9 (4) ◽  
pp. 54-57
Author(s):  
E A Belyatko ◽  
N M Danilov ◽  
Y G Matchin ◽  
T V Martynyuk ◽  
I E Chazova
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Intima Media Thickness ◽  
Vascular Wall ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Hemodynamic Changes ◽  
Pulmonary Arterial ◽  
Inner Diameter

Objective: in our study, iloprost was used as a drug for acute tests in patients with pulmonary arterial hypertension (PAH). Design and Method. We included 7 pts with pulmonary arterial hypertension (PAH): 5 females and 2 males, average age 32,0±12,0 years. All patients underwent right heart catheterization including acute tests with both nitric oxide and Iloprost. In addition to hemodynamic changes the intravascular ultrasound (IVUS) parameters were analyzed. We used parameters such as: intima-media thickness, the pulsatility index (PI), the outer and inner diameter of the vessel, the area of the vascular wall. Results. Compared with the action of nitric oxide, the degree of reduction of medium pulmonary arterial pressure (mPAP) after Iloprost was 17,2±5 and 25,37±9 mm Hg respectively, and pulmonary vascular resistance (PVR) 251,4±120 and 276±129 dynes×c×cm-5 respectively (p

Astragalus Polysaccharides Attenuate Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats

2017 ◽  
Vol 45 (04) ◽  
pp. 773-789 ◽  
Author(s):  
Lin-Bo Yuan ◽  
Chun-Yan Hua ◽  
Sheng Gao ◽  
Ya-Ling Yin ◽  
Mao Dai ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Biological Activities ◽  
Right Ventricular Hypertrophy ◽  
Astragalus Polysaccharides ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Arterial

Astragalus polysaccharides (APS) have been shown to possess a variety of biological activities including anti-oxidant and anti-inflammation functions in a number of diseases. However, their function in pulmonary arterial hypertension (PAH) is still unknown. Rats received APS (200[Formula: see text]mg/kg once two days) for 2 weeks after being injected with monocrotaline (MCT; 60[Formula: see text]mg/kg). The pulmonary hemodynamic index, right ventricular hypertrophy, and lung morphological features of the rat models were examined, as well as the NO/eNOS ratio of wet lung and dry lung weight and MPO. A qRT-PCR and p-I[Formula: see text]B was used to assess IL-1[Formula: see text], IL-6 and TNF-[Formula: see text] and WB was used to detect the total I[Formula: see text]B. Based on these measurements, it was found that APS reversed the MCT-induced increase in mean pulmonary arterial pressure (mPAP) (from 32.731[Formula: see text]mmHg to 26.707[Formula: see text]mmHg), decreased pulmonary vascular resistance (PVR) (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text] min/L to 246.351[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L), and reduced right ventricular hypertrophy (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L to 246.351 mmHg[Formula: see text][Formula: see text][Formula: see text]min/L) ([Formula: see text]0.05). In terms of pulmonary artery remodeling, the WT% and WA% decreased with the addition of APS. In addition, it was found that APS promoted the synthesis of eNOS and the secretion of NO, promoting vasodilation and APS decreased the MCT-induced elevation of MPO, IL-1[Formula: see text], IL-6 and TNF-[Formula: see text], reducing inflammation. Furthermore, APS was able to inhibit the activation of pho-I[Formula: see text]B[Formula: see text]. In couclusion, APS ameliorates MCT-induced pulmonary artery hypertension by inhibiting pulmonary arterial remodeling partially via eNOS/NO and NF-[Formula: see text]B signaling pathways.

scholarly journals High Right Ventricular Afterload during Exercise in Patients with Pulmonary Arterial Hypertension

2021 ◽  
Vol 10 (9) ◽  
pp. 2024
Author(s):  
Mari Nishizaki ◽  
Aiko Ogawa ◽  
Hiromi Matsubara
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Exercise Training ◽  
Arterial Hypertension ◽  
Hemodynamic Response ◽  
Pulmonary Vasculature ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Arterial ◽  
Response To Exercise

The right ventricle (RV) is more sensitive to an increase in afterload than the left ventricle (LV), and RV afterload during exercise increases more easily than LV afterload. Pulmonary arterial hypertension (PAH)-specific therapy has improved pulmonary hemodynamics at rest; however, the pulmonary hemodynamic response to exercise is still abnormal in most patients with PAH. In these patients, RV afterload during exercise could be higher, resulting in a greater increase in RV wall stress. Recently, an increasing number of studies have indicated the short-term efficacy of exercise training. However, considering the potential risk of promoting myocardial maladaptive remodeling, even low-intensity repetitive exercise training could lead to long-term clinical deterioration. Further studies investigating the long-term effects on the RV and pulmonary vasculature are warranted. Although the indications for exercise training for patients with PAH have been expanding, exercise training may be associated with various risks. Training programs along with risk stratification based on the pulmonary hemodynamic response to exercise may enhance the safety of patients with PAH.

scholarly journals Distinct Types of Plexiform Lesions Identified by Synchrotron-Based Phase Contrast Micro-CT

2021 ◽  
Author(s):  
Christian Westöö ◽  
Christian Carl Norvik ◽  
Niccolò Peruzzi ◽  
Oscar van der Have ◽  
Goran Lovric ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Phase Contrast ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Vasa Vasorum ◽  
Dimensional Structure ◽  
Micro Ct ◽  
Plexiform Lesions ◽  
Pulmonary Arterial

In pulmonary arterial hypertension, plexiform lesions are associated with severe arterial obstruction and right ventricular failure. Exploring their structure and position is crucial for understanding the interplay between hemodynamics and vascular remodeling. The aim of this research was to use synchrotron-based phase contrast micro-CT to study the three-dimensional structure of plexiform lesions. Archived paraffin-embedded tissue-samples from 14 patients with pulmonary arterial hypertension (13 idiopathic, 1 with known BMPR2-mutation) were imaged. Clinical data showed high median PVR (12,5 WU) and mPAP (68 mmHg). Vascular lesions with more than one lumen were defined as plexiform. Prior radiopaque dye injection in some samples facilitated 3D-rendering. Four distinct types of plexiform lesions were identified: (1) localized within or derived from monopodial branches (supernumerary arteries), often with connection to the vasa vasorum; (2) localized between pulmonary arteries and larger airways as a tortuous transformation of intrapulmonary bronchopulmonary anastomoses; (3) as spherical structures at unexpected abrupt ends of distal pulmonary arteries; and (4) as occluded pulmonary arteries with re-canalization. By appearance and localization, types 1-2 potentially relieve pressure via the bronchial circulation, as pulmonary arteries in these patients were almost invariably occluded distally. In addition, types 1-3 were often surrounded by dilated thin-walled vessels, often connected to pulmonary veins, peri-bronchial vessels or the vasa vasorum. Collaterals, by-passing completely occluded pulmonary arteries, were also observed to originate within plexiform lesions. In conclusion, synchrotron-based imaging revealed significant plexiform lesion heterogeneity, resulting in a novel classification. The four types likely have different effects on hemodynamics and disease progression.

scholarly journals Caffeic Acid Phenethyl Ester Rescues Pulmonary Arterial Hypertension through the Inhibition of AKT/ERK-Dependent PDGF/HIF-1α In Vitro and In Vivo

2019 ◽  
Vol 20 (6) ◽  
pp. 1468 ◽  
Author(s):  
Chin-Chang Cheng ◽  
Pei-Ling Chi ◽  
Min-Ci Shen ◽  
Chih-Wen Shu ◽  
Shue-Ren Wann ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Caffeic Acid ◽  
Systolic Pressure ◽  
Caffeic Acid Phenethyl Ester ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial proliferation and remodeling, resulting in a specific increase in right ventricle systolic pressure (RVSP) and, ultimately right ventricular failure. Recent studies have demonstrated that caffeic acid phenethyl ester (CAPE) exerts a protective role in NF-κB-mediated inflammatory diseases. However, the effect of CAPE on PAH remains to be elucidated. In this study, monocrotaline (MCT) was used to establish PAH in rats. Two weeks after the induction of PAH by MCT, CAPE was administrated by intraperitoneal injection once a day for two weeks. Pulmonary hemodynamic measurements and pulmonary artery morphological assessments were examined. Our results showed that administration of CAPE significantly suppressed MCT-induced vascular remodeling by decreasing the HIF-1α expression and PDGF-BB production, and improved in vivo RV systolic performance in rats. Furthermore, CAPE inhibits hypoxia- and PDGF-BB-induced HIF-1α expression by decreasing the activation of the AKT/ERK pathway, which results in the inhibition of human pulmonary artery smooth muscle cells (hPASMCs) proliferation and prevention of cells resistant to apoptosis. Overall, our data suggest that HIF-1α is regarded as an alternative target for CAPE in addition to NF-κB, and may represent a promising therapeutic agent for the treatment of PAH diseases.

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