scholarly journals Circular Sympathetic Pulmonary Artery Denervation in Cardiac Surgery Patients With Mitral Valve Defect, Atrial Fibrillation and High Pulmonary Hypertension

Kardiologiia ◽  
2020 ◽  
Vol 60 (1) ◽  
pp. 35-42 ◽  
Author(s):  
N. A. Trofimov ◽  
A. P. Medvedev ◽  
V. Y. Babokin ◽  
I. P. Efimova ◽  
V. A. Kichigin ◽  
...  

Objective Investigate the influence of the sympathetic denervation of the pulmonary trunk and the orifices of the pulmonary arteries on the degree of pulmonary hypertension (PH) and outcomes of the surgical treatment of atrial fibrillation (AF) in patients with mitral valve defects, complicated AF, and high PH.Material and methods We analyzed the surgical treatment of 140 patients with mitral valve defect, concomitant AF, and high PH – pulmonary artery systolic pressure (PASP) gradient more than 40 mm Hg. The group of interest included 51 patients (46 patients with severe mitral stenosis and five patients with grade 4 mitral valve regurgitation). All patients underwent mitral valve correction (47 valve replacement surgeries and 4 valve-sparing interventions), biatrial Maze IV procedure, and additionally, denervation of the pulmonary trunk and the orifices of the pulmonary arteries. The control group included 89 patients diagnosed with mitral valve defect, AF, and PH with PASP > 40 mm Hg. However, unlike in patients of interest, denervation of the pulmonary arteries was not performed.Results Circular radiofrequency denervation of the pulmonary trunk and the orifices of the pulmonary arteries using a clamp-destructor is an effective and safe method, significantly reduces secondary PH (p=0.018), promotes reverse remodeling of the heart chambers, left atrium in particular (p=0.01), and improves outcomes of the Maze IV procedure (p=0.022) by restoring sinus rhythm in patients with mitral valve defects, complicated AF, and high PH.Conclusion This technique must be studied further involving a more significant number of patients, analyzing long-term results, and using this technique in patients with non-valvular causes of secondary PH.

2019 ◽  
Vol 34 (3) ◽  
pp. 129-143
Author(s):  
N. A. Trofimov ◽  
A. P. Medvedev ◽  
V. E. Babokin ◽  
A. G. Dragunov ◽  
V. A. Kichigin ◽  
...  

Aim. To analyze the dynamics of echocardiographic parameters after surgical treatment of severe pulmonary hypertension in patients with mitral valve disease and atrial fibrillation.Material and Methods. Data of surgical treatment in 202 patients with mitral valve disease complicated by severe pulmonary hypertension with blood pressure more than 40 mm Hg and atrial fibrillation were analyzed. Surgical intervention in these patients consisted in surgical correction of mitral dysfunction with artificial prosthetic valve or valve-preserving intervention (group 1, n = 62). In patients of group 2 (n = 89), correction of mitral valve defect was also performed as well as the Maze IV procedure for concomitant atrial fibrillation using bipolar radiofrequency ablator AtriCure. Patients of group 3 (n = 51) underwent integrated surgery, which consisted in the elimination of mitral valve defect, surgical correction of atrial fibrillation by Maze IV procedure, as well as circular radiofrequency denervation of the trunk and mouth of the pulmonary arteries (pulmonary artery denervation (PADN)).Conclusions. The circular PADN procedure was effective and safe, significantly reduced the level of pulmonary hypertension in the postoperative period (p = 0.018), and promoted reverse remodeling of the heart cavities. Integrated surgical correction in patients with mitral dysfunction, atrial fibrillation, and severe pulmonary hypertension may significantly reduce the phenomenon of heart failure (p = 0.023). Further analysis of the effectiveness of radiofrequency denervation of pulmonary arteries with the study of a larger number of patients, analysis of long-term results, as well as determining the possibility of this technique in patients with non-valvular forms of pulmonary hypertension are required. 


2019 ◽  
Vol 11 (4) ◽  
pp. 95
Author(s):  
N.A. Trofimov ◽  
A.P. Medvedev ◽  
A.V. Nikolsky ◽  
V.A. Kichigin ◽  
S.S. Zhamlikhanova ◽  
...  

2021 ◽  
Author(s):  
Koichi Sugimoto ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Takashi Kaneshiro ◽  
Akiomi Yoshihisa ◽  
...  

Abstract Background: It has been widely recognized that metabolic disorder is associated with pulmonary hypertension. It is known that elevated pulmonary artery pressure induced by hypoxia in mice returns to normal pressure under reoxygenation. However, it is still unclear how metabolic disorder affects the reverse remodeling of pulmonary arteries. In this study, we investigated the effects of a high-fat diet (HFD) on the decrease of pulmonary artery pressure and reverse remodeling of pulmonary arteries in mice with hypoxia-induced pulmonary hypertension.Methods: We used female C57/Bl6 mice aged 8 weeks. After the mice were exposed to hypoxia (10% oxygen for 4 weeks) for induction of pulmonary hypertension. Then, they were returned to normoxic conditions and randomized into a normal diet (ND) group and a HFD group. Both groups were fed their respective diets for 12 weeks.Results: The right ventricular systolic pressure measured by a micro-manometer catheter and the Fulton index were significantly higher in the HFD group than in the ND group at 12 weeks after reoxygenation. The medial smooth muscle area was larger in the HFD group. Caspase 3 activity in lung tissue of the HFD group was decreased, and an apoptosis of pulmonary smooth muscle cells was suppressed after reoxygenation. Moreover, the expression levels of peroxisome proliferator-activated receptor-γ and apelin were lower in the HFD group than in the LFD group.Conclusion: Our results suggest the metabolic disorder may suppress pulmonary artery reverse remodeling in mice with hypoxia-induced pulmonary hypertension under reoxygenation.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Koichi Sugimoto ◽  
Tetsuro Yokokawa ◽  
Tomofumi Misaka ◽  
Takashi Kaneshiro ◽  
Akiomi Yoshihisa ◽  
...  

Abstract Background It is widely recognized that metabolic disorder is associated with pulmonary hypertension (PH). It is known that hypoxia-induced elevated pulmonary artery pressure in mice returns to normal pressure during reoxygenation. However, it is still unclear how metabolic disorder affects the reverse remodeling of pulmonary arteries. In this study, we investigated the effects of high-fat diet (HFD) on the decrease in pulmonary artery pressure and reverse remodeling of pulmonary arteries in mice with hypoxia-induced PH. Methods We used female C57BL/6 mice aged 8 weeks. After being exposed to hypoxia (10% oxygen for four weeks) to induce PH, the mice were returned to normoxic conditions and randomized into a normal diet (ND) group and HFD group. Both groups were fed with their respective diets for 12 weeks. Results The Fulton index and right ventricular systolic pressure measured by a micro-manometer catheter were significantly higher in the HFD group than in the ND group at 12 weeks after reoxygenation. The medial smooth muscle area was larger in the HFD group. Caspase-3 activity in the lung tissue of the HFD group was decreased, and the apoptosis of pulmonary smooth muscle cells was suppressed after reoxygenation. Moreover, the expression levels of peroxisome proliferator-activated receptor-γ and apelin were lower in the HFD group than in the ND group. Conclusions The results suggest that metabolic disorder may suppress pulmonary artery reverse remodeling in mice with hypoxia-induced PH during reoxygenation.


2014 ◽  
Vol 12 (4) ◽  
pp. 186-192 ◽  
Author(s):  
David Poch ◽  
Victor Pretorius

Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as a mean pulmonary artery pressure ≥25 mm Hg and pulmonary artery wedge pressure ≤15 mm Hg in the presence of occlusive thrombi within the pulmonary arteries. Surgical pulmonary thromboendarterectomy (PTE) is considered the best treatment option for CTEPH.


2021 ◽  
Vol 22 (9) ◽  
pp. 4980
Author(s):  
Inés Roger ◽  
Javier Milara ◽  
Paula Montero ◽  
Julio Cortijo

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular, and cellular processes involved in PH. Chronic inflammation contributes to pulmonary artery remodeling and PH, among other vascular disorders, and many inflammatory mediators signal through the JAK/STAT pathway. Recent evidence indicates that the JAK/STAT pathway is overactivated in the pulmonary arteries of patients with PH of different types. In addition, different profibrotic cytokines such as IL-6, IL-13, and IL-11 and growth factors such as PDGF, VEGF, and TGFβ1 are activators of the JAK/STAT pathway and inducers of pulmonary remodeling, thus participating in the development of PH. The understanding of the participation and modulation of the JAK/STAT pathway in PH could be an attractive strategy for developing future treatments. There have been no studies to date focused on the JAK/STAT pathway and PH. In this review, we focus on the analysis of the expression and distribution of different JAK/STAT isoforms in the pulmonary arteries of patients with different types of PH. Furthermore, molecular canonical and noncanonical JAK/STAT pathway transactivation will be discussed in the context of vascular remodeling and PH. The consequences of JAK/STAT activation for endothelial cells and pulmonary artery smooth muscle cells’ proliferation, migration, senescence, and transformation into mesenchymal/myofibroblast cells will be described and discussed, together with different promising drugs targeting the JAK/STAT pathway in vitro and in vivo.


2021 ◽  
Author(s):  
Siriwan Sakarin ◽  
Anudep Rungsipipat ◽  
Sirilak Disatian Surachetpong

Abstract Background: Degenerative mitral valve disease (DMVD) is the most common cause of pulmonary hypertension (PH) in dogs. Medial thickening of the pulmonary artery is a major histopathological change in PH. A decrease in apoptosis of pulmonary arterial smooth muscle cells (SMCs) may be the cause of medial thickening. This study aimed to demonstrate the expression of apoptosis molecules in the pulmonary artery of dogs affected with PH secondary to DMVD (DMVD+PH) compared to DMVD without PH (DMVD) and healthy dogs (control). Lung samples were collected from three groups including control (n=5), DMVD (n=7) and DMVD+PH (n=7) groups. Masson trichrome and apoptotic proteins including Bax, Bcl2 and caspase-3 and -8, were stained. Results: The medial thickness in the DMVD and DMVD+PH groups was greater than in the control group and it was greatest in the DMVD+PH group. Bax, Bcl2 and caspase-3 and -8 were expressed mainly in the medial layer of the pulmonary artery. The percentages of Bax and caspase-3 and -8 positive cells were higher in the DMVD group compared to the DMVD+PH group, whereas the percentage of Bcl2-positive cells was increased in the DMVD and DMVD+PH groups. These findings suggested that apoptosis of pulmonary arterial SMCs occurred mainly in the DMVD group and decreased dramatically in the DMVD+PH group. Conclusions: An increase in the medial thickness in dogs affected with PH secondary to DMVD may occur due to a decrease in apoptosis of pulmonary arterial SMCs.


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