scholarly journals In situ Pulmonary Artery Thrombosis: A Previously Overlooked Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Yunshan Cao ◽  
Chao Geng ◽  
Yahong Li ◽  
Yan Zhang
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
De Novo ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Systemic Circulation ◽  
Artery Thrombosis ◽  
Thromboembolic Pulmonary Hypertension ◽  
Thrombotic Diseases

Pulmonary thromboembolism (PTE) is the third leading cause of death in cardiovascular diseases. PTE is believed to be caused by thrombi detached from deep veins of lower extremities. The thrombi travel with systemic circulation to the lung and block pulmonary arteries, leading to sudden disruption of hemodynamics and blood gas exchange. However, this concept has recently been challenged by accumulating evidence demonstrating that de novo thrombosis may be formed in pulmonary arteries without deep venous thrombosis. On the other hand, chronic thromboembolic pulmonary hypertension (CTEPH), a subtype of pulmonary hypertension, could have different pathogenesis than traditional PTE. Therefore, this article summarized and compared the risk factors, the common and specific pathogenic mechanisms underlying PTE, in situ pulmonary artery thrombosis, and CTEPH at molecular and cellular levels, and suggested the therapeutic strategies to these diseases, aiming to facilitate understanding of pathogenesis, differential diagnosis, and precision therapeutics of the three pulmonary artery thrombotic diseases.

Pulmonary Endarterectomy: Assessment of Operability, Surgical Description, and Post-op Care

2014 ◽  
Vol 12 (4) ◽  
pp. 186-192 ◽  
Author(s):  
David Poch ◽  
Victor Pretorius
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Endarterectomy ◽  
Pulmonary Thromboendarterectomy ◽  
Thromboembolic Pulmonary Hypertension ◽  
Wedge Pressure

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.

scholarly journals Chronic Thromboembolic Pulmonary Hypertension

2018 ◽  
Vol 35 (02) ◽  
pp. 136-142 ◽  
Author(s):  
G. Pretorius ◽  
Stuart Jamieson
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Scar Tissue ◽  
Right Heart ◽  
Fibrotic Scar ◽  
Thromboembolic Pulmonary Hypertension

AbstractChronic thromboembolic pulmonary hypertension occurs when acute thromboemboli fail to dissolve completely. The resulting fibrotic scar tissue within the pulmonary arteries is obstructive and eventually leads to right heart failure. Medical therapy for this condition is supportive, but surgery with pulmonary artery endarterectomy is curative, and carries a low mortality at experienced centers.

scholarly journals Parameters of acute vasoreactivity testing after balloon pulmonary angioplasty in patients with chronic thromboembolic pulmonary hypertension

2020 ◽  
Vol 17 (3) ◽  
pp. 53-58
Author(s):  
Sergey Y. Yarovoy ◽  
Irina E. Chazova ◽  
Yuri G. Matchin ◽  
Nikolay M. Danilov
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Structural Parameters ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Hemodynamic Parameters ◽  
Artery Pressure ◽  
Balloon Pulmonary Angioplasty ◽  
Thromboembolic Pulmonary Hypertension

Aim.To study the effect of balloon pulmonary angioplasty (BPA) on the changes of pulmonary artery pressure, cardiac output and structural parameters of pulmonary arteries after acute vasoreactivity testing (AVT) in inoperable patients with chronic thromboembolic pulmonary hypertension (CTEPH). Materials and methods.The prospective study included 22 patients with inoperable CTEPH. 11 patients underwent intravascular ultrasound (IVUS) of the pulmonary arteries. The assessment of clinical and hemodynamic parameters, vasoreactivity, structural parameters of the pulmonary arteries according to IVUS data was performed at 2 visits before the first BPA and after a series of BPA. Results.The patients underwent 2.31.4 stages of BPA. The follow up was 160 (85; 248) days. Positive changes after a series of BPA were revealed in clinical (functional class, distance in the 6-minute walk test, level of brain natriuretic peptide) and hemodynamic (systolic and mean pulmonary artery pressure, right atrium pressure, etc.) parameters. The results of the AVT after BPA demonstrated a decrease in the portion of non-responders from 63.6 to 55.5%, and a group of responders (16.7%) has appeared. According to IVUS before and after AVT, the response to iloprost administration was observed basically in branches of subsegmental pulmonary arteries and initially corresponded to the process of vasodilation. However, after a series of BPA there was noted a paradoxical reaction in the middle section after the AVT a decrease in the vessel lumen and an increase in the thickness and area of the vessel wall. This effect is probably associated with the response to the test at the level of the microvasculature, as in pulmonary arterial hypertension before the onset of its pronounced structural changes. The data obtained confirm the reverse remodeling of the pulmonary vessels and the restoration of vasoreactivity after a series of BPA. Conclusion.BPA improves clinical and hemodynamic parameters, as well as pulmonary vasoreactivity, in inoperable patients with CTEPH. AVT may be included in the recommendations for the examination of patients with CTEPH to assess the effectiveness of BPA and determine the disease prognosis.

In situ central pulmonary artery thrombosis in primary pulmonary hypertension

2005 ◽  
Vol 46 (7) ◽  
pp. 696-700 ◽  
Author(s):  
P. P. Agarwal ◽  
A. L. Wolfsohn ◽  
F. R. Matzinger ◽  
J. M. Seely ◽  
R. A. Peterson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Bronchial Arteries ◽  
Artery Thrombosis ◽  
Central Pulmonary Artery ◽  
Pulmonary Arterial ◽  
Segmental Arteries

A rare case of extensive in situ central pulmonary artery thrombosis in primary pulmonary hypertension (PPH) is presented. The differentiation from chronic thromboembolic pulmonary arterial hypertension (CTEPH) is of paramount importance because of different therapeutic strategies. In this case, the presence of mural thrombus in the central pulmonary arteries on computed tomography made the distinction difficult. However, the possibility of in situ thrombosis was suggested on the basis of absence of other findings of CTEPH (abrupt narrowing/truncation of segmental arteries, variation in size of segmental vessels, arterial webs, mosaic attenuation, pulmonary infarcts, and dilated bronchial arteries), and this was confirmed on final pathology.

scholarly journals Mimickers of chronic thromboembolic pulmonary hypertension on imaging tests: a review

2020 ◽  
Vol 10 (1) ◽  
pp. 204589401988262
Author(s):  
Shraddha Narechania ◽  
Rahul Renapurkar ◽  
Gustavo A. Heresi
Keyword(s):  
Pulmonary Hypertension ◽  
Imaging Techniques ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Artery Sarcoma ◽  
Radiological Features ◽  
Thromboembolic Pulmonary Hypertension ◽  
Perfusion Defects ◽  
Perfusion Scan

Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by mechanical obstruction of large pulmonary arteries secondary to one or more episodes of pulmonary embolism. Ventilation perfusion scan is the recommended initial screening test for this condition and typically shows multiple large mismatched perfusion defects. However, not all patients with an abnormal ventilation perfusion scan have CTEPH since there are other conditions that be associated with a positive ventilation perfusion scan. These conditions include in situ thrombosis, pulmonary artery sarcoma, fibrosing mediastinitis, pulmonary vasculitis and sarcoidosis, among others. Although these conditions cannot be distinguished from CTEPH using a ventilation perfusion scan, they have certain characteristic radiological features that can be demonstrated on other imaging techniques such as computed tomography scan and can help in differentiation of these conditions. In this review, we have summarized some key clinical and radiological features that can help differentiate CTEPH from the CTEPH mimics.

Chronic Thromboembolic Pulmonary Hypertension

2010 ◽  
pp. 224-227
Author(s):  
Edward C. Rosenow
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Lower Lobe ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Progressive Dyspnea ◽  
Thromboembolic Pulmonary Hypertension ◽  
Hilar Adenopathy

Enlarged central pulmonary arteries mimic hilar adenopathy, which does not explain dyspnea on exertion. Enlarged right lower lobe pulmonary artery is 20 mm in width (normal, 〈14 mm) (arrow) • 15-year-old girl • Progressive dyspnea on exertion • CXR findings were interpreted as normal

scholarly journals EXPRESS: Chronic thromboembolic pulmonary hypertension following pulmonary embolism with a right ventricular thrombus: A report of two cases

2021 ◽  
pp. 204589402110136
Author(s):  
Tailong Zhang ◽  
Weitao Liang ◽  
Longrong Bian ◽  
Zhong Wu
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Imaging Features ◽  
Pulmonary Endarterectomy ◽  
Right Heart ◽  
Thromboembolic Pulmonary Hypertension ◽  
The Right ◽  
Cardiac Masses

Right heart thrombus (RHT) accompanied by chronic thromboembolic pulmonary hypertension (CTEPH) is a rare entity. RHT may develop in the peripheral veins or in situ within the right heart chambers. The diagnosis of RHT is challenging, since its symptoms are typically non-specific and its imaging features resemble those of cardiac masses. Here, we report two cases of RHT with CTEPH that presented as right ventricular masses initially. Both patients underwent simultaneous pulmonary endarterectomy (PEA) and resection of the ventricular thrombi. Thus, when mass-like features are confirmed by imaging, RHT should be suspected in patients with CTEPH, and simultaneous RHT resection is required along with PEA.

scholarly journals The soluble guanylate cyclase stimulator riociguat is the first-line therapy for chronic thromboembolic pulmonary hypertension patients

Kardiologiia ◽  
2020 ◽  
Vol 60 (8) ◽  
pp. 115-123
Author(s):  
Z. S. Valieva ◽  
S. E. Gratsianskaya ◽  
T. V. Martynyuk
Keyword(s):  
Pulmonary Hypertension ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
First Line ◽  
Pulmonary Thromboendarterectomy ◽  
First Line Therapy ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Microcirculation

Chronic thromboembolic pulmonary hypertension (CTEPH) is a precapillary type of pulmonary hypertension with chronic obstruction of large and medium branches of pulmonary arteries along with secondary alterations in pulmonary microcirculation, which cause progressive increases in pulmonary vascular resistance and pulmonary arterial pressure and ensuing severe right heart dysfunction and heart failure. Pulmonary thromboendarterectomy (PTE) is the treatment of choice for CTEPH; however, this procedure is available not for all patients. Although the surgery performed in the conditions of centers with advanced experience generally shows good results, up to 40% of patients are technically inoperable or PTE is associated with a high risk of complications. At present, riociguat, the only officially approved drug from the class of soluble guanylate cyclase stimulators, is considered as a first-line treatment for inoperable and residual forms of STEPH. Introduction of riociguat to clinical practice can be called a real breakthrough in the treatment of patients with STEPH who cannot undergo PTE or those with relapse or persistent STEPH after the surgery.

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