Correlation between mean pulmonary arterial pressure measurement by echocardiography and right ventricular function

2018 ◽  
Vol 6 (1) ◽  
pp. 11
Author(s):  
Nakisa Khansary ◽  
Shahram Homayounfar
Vascular ◽  
2017 ◽  
Vol 26 (2) ◽  
pp. 183-188
Author(s):  
Mustafa Aldemir ◽  
Sadık Volkan Emren ◽  
Çınar Balçık ◽  
Ersel Onrat ◽  
Merve Gürsoy

Objectives Pulmonary hypertension with heart failure is related to venous insufficiency. However, there is no clear data whether pulmonary arterial hypertension with preserved right ventricular function cause venous insufficiency. In this study, we aim to investigate the relation between pulmonary arterial pressure with venous insufficiency in pulmonary arterial hypertension patients with preserved right ventricular function. Methods Between January 2012 and October 2014, 38 patients with a diagnosis of pulmonary arterial hypertension and 47 control group patients were included. Venous disability score and venous segmental disease score of both groups were calculated in order to measure venous insufficiency. The relationship between venous disability score and venous segmental disease scores and mean pulmonary arterial pressure and World Heart Organization functional capacity was examined. Results Total venous segmental disease score (5 ± 3.9 vs. 2 ± 1.8 p < 0.001), right venous segmental disease score (2.6 ± 2.2 vs. 1 ± 0.9 p < 0.001), left venous segmental disease score (2.4 ± 2.2 vs. 1 ± 0.9 p < 0.001), and venous disability scores (2.2 ±1 vs. 1.6 ± 0.7 p < 0.001) of patients with pulmonary arterial hypertension were higher than the control group. While the total venous segmental disease score was highly related to mean pulmonary arterial pressure (r = 0.829, p < 0.001), the venous disability score was only weakly related (r = 0.343, p = 0.037). Total venous segmental disease score (r = 0.606, p < 0.001) and venous disability scores (r = 0.601, p < 0.001) were moderately related with World Health Organization functional capacity intensity. Conclusions The degree of venous insufficiency increase in accordance with the mean pulmonary arterial pressure even in patients with preserved right ventricular function.


2016 ◽  
Vol 38 (1) ◽  
pp. 44-49
Author(s):  
Yong-Hee Park ◽  
Da-Hye Yoo ◽  
Eun-Hee Kim ◽  
In-Kyung Song ◽  
Ji-Hyun Lee ◽  
...  

2020 ◽  
pp. 204887262092525 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Gammelgaard Schultz ◽  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism ( n = 6) or sham ( n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased ( P < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( P < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( P < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( P = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo–arterial coupling was reduced ( P < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( P < 0.01) suggesting right ventricular failure. Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.


2020 ◽  
Author(s):  
Adrienne K Conger ◽  
Steven J Halliday ◽  
Meredith E Pugh ◽  
Ivan M Robbins ◽  
Anna R Hemnes

Abstract BackgroundParenteral prostacyclins are the only therapy proven to extend survival in pulmonary arterial hypertension (PAH), yet at the bedside clinicians have no tools to predict which patients are most likely to benefit from this medication class. MethodsWe retrospectively analyzed all PAH patients treated with IV epoprostenol therapy at our center from 1/1/1996 to 12/31/2016. We analyzed survival in patients and defined the 90 th percentile of survival. Patients were divided into those who survived past this point (super responders) and those who had had an event prior to this time point after initiation of iv epoprostenol (usual responders).ResultsThe median survival after IV epoprostenol initiation was 4.32 years, and the 90 th percentile of event-free survival was 11.09 years. Fourteen patients met criteria for super responder and 45 had a survival <90 th percentile, comprising the usual responder group. Super responders tended to be younger, have longer six-minute walk distances and higher mean pulmonary arterial pressure (p<0.05 for all). In follow up, super responders continued to have a higher six-minute walk distance and were more likely to have achieved normal or only mildly impaired right ventricular function, though no differences in hemodynamics were observed.ConclusionsThere may be a super responder phenotype that can be defined in patients with PAH by >90 th percentile of survival. Super responders were more likely that usual responders to be younger and were more likely to have achieved favorable right ventricular function at follow up, however, differences in hemodynamics were not observed.


2021 ◽  
Author(s):  
Adrienne K Conger ◽  
Steven J Halliday ◽  
Meredith E Pugh ◽  
Ivan M Robbins ◽  
Anna R Hemnes

Abstract Background: Parenteral prostacyclins are the only therapy proven to extend survival in pulmonary arterial hypertension (PAH), yet at the bedside clinicians have no tools to predict which patients are most likely to benefit from this medication class. Methods: We retrospectively analyzed all PAH patients treated with IV epoprostenol therapy at our center from 1/1/1996 to 12/31/2016. We analyzed survival in patients and defined the 90 th percentile of survival. Patients were divided into those who survived past this point (super responders) and those who had had an event prior to this time point after initiation of iv epoprostenol (usual responders). Results: The median survival after IV epoprostenol initiation was 4.32 years, and the 90 th percentile of event-free survival was 11.09 years. Fourteen patients met criteria for super responder and 45 had a survival <90 th percentile, comprising the usual responder group. Super responders tended to be younger, have longer six-minute walk distances and higher mean pulmonary arterial pressure (p<0.05 for all). In follow up, super responders continued to have a higher six-minute walk distance and were more likely to have achieved normal or only mildly impaired right ventricular function, though no differences in hemodynamics were observed. Conclusions: There may be a super responder phenotype that can be defined in patients with PAH by >90 th percentile of survival. Super responders were more likely that usual responders to be younger and were more likely to have achieved favorable right ventricular function at follow up, however, differences in hemodynamics were not observed.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Seyeon Oh ◽  
Albert Y. Jang ◽  
Sehyun Chae ◽  
Seungbum Choi ◽  
Jeongsik Moon ◽  
...  

AbstractDespite the advancement of targeted therapy for pulmonary arterial hypertension (PAH), poor prognosis remains a reality. Mesenchymal stem cells (MSCs) are one of the most clinically feasible alternative treatment options. We compared the treatment effects of adipose tissue (AD)-, bone marrow (BD)-, and umbilical cord blood (UCB)-derived MSCs in the rat monocrotaline-induced pulmonary hypertension (PH) model. The greatest improvement in the right ventricular function was observed in the UCB-MSCs treated group. The UCB-MSCs treated group also exhibited the greatest improvement in terms of the largest decrease in the medial wall thickness, perivascular fibrosis, and vascular cell proliferation, as well as the lowest levels of recruitment of innate and adaptive immune cells and associated inflammatory cytokines. Gene expression profiling of lung tissue confirmed that the UCB-MSCs treated group had the most notably attenuated immune and inflammatory profiles. Network analysis further revealed that the UCB-MSCs group had the greatest therapeutic effect in terms of the normalization of all three classical PAH pathways. The intravenous injection of the UCB-MSCs, compared with those of other MSCs, showed superior therapeutic effects in the PH model for the (1) right ventricular function, (2) vascular remodeling, (3) immune/inflammatory profiles, and (4) classical PAH pathways.


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