Pulmonary artery imaging

2019 ◽  
pp. 455-466
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vascular Malformations ◽  
Ct Scanning ◽  
Pulmonary Angiography ◽  
Pulmonary Artery Hypertension ◽  
Thromboembolic Disease ◽  
Chronic Pulmonary Hypertension ◽  
Patient Groups ◽  
Pulmonary Arterial

The main indications for pulmonary artery imaging are acute pulmonary thromboembolic disease and assessment of chronic pulmonary artery hypertension. Other indications, such as investigation of haemoptysis and pulmonary arterial vascular malformations are not addressed in this chapter. Although recurrent acute thromboembolic disease may eventually lead to pulmonary hypertension, the two are essentially separate patient groups for the purpose of CT scanning. This chapter covers CT pulmonary angiography, peripheral venous imaging, and chronic pulmonary hypertension.

scholarly journals Rare Presentation of Left Lower Lobe Pulmonary Artery Dissection

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
René Hako ◽  
Ján Fedačko ◽  
Štefan Tóth ◽  
Radoslav Morochovič ◽  
Pavol Kristian ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Lower Lobe ◽  
Pulmonary Angiography ◽  
Left Lower Lobe ◽  
Artery Dissection ◽  
Chronic Pulmonary Hypertension ◽  
Pulmonary Arterial

Background. Pulmonary arterial dissection with chronic pulmonary arterial hypertension as its major cause is a very rare but life-threatening condition. In most cases the main pulmonary trunk is the affected site usually without involvement of its branches. Segmental or lobar pulmonary artery dissection is extremely rare. Case Presentation. We report a unique case of left lower lobe pulmonary artery dissection in a 70-year-old male, with confirmed chronic pulmonary hypertension. To confirm dissection MDCT pulmonary angiography was used. Multiplanar reformation (MPR) images in sagittal, coronal, oblique sagittal, and curved projections were generated. This case report presents morphologic CT features of rare chronic left lobar pulmonary artery dissection associated with chronic pulmonary hypertension at a place of localised pulmonary artery calcification. CT pulmonary angiography excluded signs of thromboembolism and potential motion or flow artefacts. Conclusion. To the best of our knowledge, no case of lower lobe pulmonary artery dissection with flap calcification has been reported yet. CT imaging of the chest is a key diagnostic tool that is able to detect an intimal flap and a false lumen within the pulmonary arterial tree and is preferred in differential diagnosis of rare complications of sustained pulmonary arterial hypertension.

A Case of Extrinsic Compression of the Left Main Coronary Artery by Dilated Pulmonary Artery in Eisenmengers Syndrome

2021 ◽  
Vol 4 (1) ◽  
pp. 01-03
Author(s):  
Varshit Hathi ◽  
Nagamani Alur Chikkabasavaiah ◽  
Beeresh Puttegowda ◽  
Yeriswamy Yeriswamy ◽  
Ramesh Basavappa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Left Main Coronary Artery ◽  
Symptomatic Relief ◽  
Coronary Intervention ◽  
Pulmonary Artery Hypertension ◽  
Left Main ◽  
Extrinsic Compression ◽  
Pulmonary Arterial

The extrinsic compression of the left main coronary artery secondary to pulmonary artery trunk dilatation is a relatively rare syndrome. [1,2] It is mostly associated with congenital acyanotic heart disease, idiopathic pulmonary arterial dilatation or primary pulmonary hypertension. [3,4] Most cases of pulmonary artery hypertension with no atherosclerotic risk factors rarely undergo coronary angiography, and hence, diagnoses are seldom made and proper management is delayed.We describe a patient with Ostium secundum atrial septal defect with severe pulmonary hypertension who presented with clinical angina ,diagnosed to have left main coronary artery compression by CT angiography ,underwent successful percutaneous coronary intervention with good symptomatic relief.

Enhance Smooth Muscle Cells Apoptosis Associated With Pulmonary Arterial Remodeling in Dogs Affected With Pulmonary Hypertension Secondary to Degenerative Mitral Valve Disease

2021 ◽  
Author(s):  
Siriwan Sakarin ◽  
Anudep Rungsipipat ◽  
Sirilak Disatian Surachetpong
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Mitral Valve ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Mitral Valve Disease ◽  
Caspase 3 ◽  
Muscle Cells ◽  
Pulmonary Arterial ◽  
Medial Thickening

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.

scholarly journals Serotonin contributes to high pulmonary vascular tone in a sheep model of persistent pulmonary hypertension of the newborn

2013 ◽  
Vol 304 (12) ◽  
pp. L894-L901 ◽  
Author(s):  
Cassidy Delaney ◽  
Jason Gien ◽  
Gates Roe ◽  
Nicole Isenberg ◽  
Jenai Kailey ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Tryptophan Hydroxylase ◽  
Late Gestation ◽  
Persistent Pulmonary Hypertension ◽  
Sheep Model ◽  
Pulmonary Hemodynamics ◽  
Fetal Sheep ◽  
Pulmonary Arterial

Although past studies demonstrate that altered serotonin (5-HT) signaling is present in adults with idiopathic pulmonary arterial hypertension, whether serotonin contributes to the pathogenesis of persistent pulmonary hypertension of the newborn (PPHN) is unknown. We hypothesized that 5-HT contributes to increased pulmonary vascular resistance (PVR) in a sheep model of PPHN and that selective 5-HT reuptake inhibitor (SSRI) treatment increases PVR in this model. We studied the hemodynamic effects of 5-HT, ketanserin (5-HT2A receptor antagonist), and sertraline, an SSRI, on pulmonary hemodynamics of the late gestation fetal sheep with PPHN caused by prolonged constriction of the ductus arteriosis. Brief intrapulmonary infusions of 5-HT increased PVR from 1.0 ± 0.07 (baseline) to 1.4 ± 0.22 mmHg/ml per minute of treatment ( P < 0.05). Ketanserin decreased PVR from 1.1 ± 0.15 (baseline) to 0.82 ± 0.09 mmHg/ml per minute of treatment ( P < 0.05). Sertraline increased PVR from 1.1 ± 0.17 (baseline) to 1.4 ± 0.17 mmHg/ml per minute of treatment ( P = 0.01). In addition, we studied 5-HT production and activity in vitro in experimental PPHN. Compared with controls, pulmonary artery endothelial cells from fetal sheep with PPHN exhibited increased expression of tryptophan hydroxylase 1 and 5-HT production by twofold and 56%, respectively. Compared with controls, 5-HT2A R expression was increased in lung homogenates and pulmonary artery smooth muscle cell lysates by 35% and 32%, respectively. We concluded that increased 5-HT contributes to high PVR in experimental PPHN through activation of the 5-HT2A receptor and that SSRI infusion further increases PVR in this model.

scholarly journals Untargeted Metabolic Profiling Cell-Based Approach of Pulmonary Artery Smooth Muscle Cells in Response to High Glucose and the Effect of the Antioxidant Vitamins D and E

Metabolites ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 87 ◽  
Author(s):  
Abdulwahab Alamri ◽  
Abdulhadi Burzangi ◽  
Paul Coats ◽  
David Watson
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
High Glucose ◽  
Muscle Cells ◽  
Oxygen Species ◽  
Pulmonary Arterial ◽  
Pulmonary Artery Smooth Muscle

Pulmonary arterial hypertension (PAH) is a multi-factorial disease characterized by the hyperproliferation of pulmonary artery smooth muscle cells (PASMCs). Excessive reactive oxygen species (ROS) formation resulted in alterations of the structure and function of pulmonary arterial walls, leading to right ventricular failure and death. Diabetes mellitus has not yet been implicated in pulmonary hypertension. However, recently, variable studies have shown that diabetes is correlated with pulmonary hypertension pathobiology, which could participate in the modification of pulmonary artery muscles. The metabolomic changes in PASMCs were studied in response to 25 mM of D-glucose (high glucose, or HG) in order to establish a diabetic-like condition in an in vitro setting, and compared to five mM of D-glucose (normal glucose, or LG). The effect of co-culturing these cells with an ideal blood serum concentration of cholecalciferol-D3 and tocopherol was also examined. The current study aimed to examine the role of hyperglycemia in pulmonary arterial hypertension by the quantification and detection of the metabolomic alteration of smooth muscle cells in high-glucose conditions. Untargeted metabolomics was carried out using hydrophilic interaction liquid chromatography and high-resolution mass spectrometry. Cell proliferation was assessed by cell viability and the [3H] thymidine incorporation assay, and the redox state within the cells was examined by measuring reactive oxygen species (ROS) generation. The results demonstrated that PASMCs in high glucose (HG) grew, proliferated faster, and generated higher levels of superoxide anion (O2·−) and hydrogen peroxide (H2O2). The metabolomics of cells cultured in HG showed that the carbohydrate pathway, especially that of the upper glycolytic pathway metabolites, was influenced by the activation of the oxidation pathway: the pentose phosphate pathway (PPP). The amount of amino acids such as aspartate and glutathione reduced via HG, while glutathione disulfide, N6-Acetyl-L-lysine, glutamate, and 5-aminopentanoate increased. Lipids either as fatty acids or glycerophospholipids were downregulated in most of the metabolites, with the exception of docosatetraenoic acid and PG (16:0/16:1(9Z)). Purine and pyrimidine were influenced by hyperglycaemia following PPP oxidation. The results in addition showed that cells exposed to 25 mM of glucose were oxidatively stressed comparing to those cultured in five mM of glucose. Cholecalciferol (D3, or vitamin D) and tocopherol (vitamin E) were shown to restore the redox status of many metabolic pathways.

Norepinephrine and dobutamine improve cardiac index equally by supporting opposite sides of the heart in an experimental model of chronic pulmonary hypertension

2021 ◽  
Author(s):  
Janus Adler Hyldebrandt ◽  
Nikolaj Bøgh ◽  
Camilla Omann Christensen ◽  
Peter Agger
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Index ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
End Diastolic Volume ◽  
Chronic Pulmonary Hypertension ◽  
Blood Pressures ◽  
The Right

Abstract Background: Pulmonary hypertension is a significant risk factor in patients undergoing surgery. The combined effects of general anaesthesia and positive pressure ventilation can aggravate this condition and cause increased pulmonary blood pressures, reduced systemic blood pressures and ventricular contractility. Although perioperative use of inotropic support or vasopressors is almost mandatory for these patients, preference is disputed. In this study, we investigated the effects of norepinephrine and dobutamine and their ability to improve the arterio-ventricular relationship and haemodynamics in pigs suffering from chronic pulmonary hypertension.Method: Pulmonary hypertension was induced in five pigs by banding the pulmonary artery at 2–3 weeks of age. Six pigs served as controls. After 16 weeks of pulmonary artery banding, the animals were re-examined under general anaesthesia using biventricular conductance catheters and a pulmonary artery catheter. After baseline measurements, the animals were exposed to both norepinephrine and dobutamine infusions in incremental doses, with a stabilizing period in between the infusions. The hypothesis of differences between norepinephrine and dobutamine with incremental doses was tested using repeated two-way ANOVA and Bonferroni multiple comparisons post-test. Results: At baseline, pulmonary artery banded animals had increased right ventricular pressure (+39%, p=0.04), lower cardiac index (-23% p=0.04), lower systolic blood pressure (-13%, p=0.02) and reduced left ventricular end-diastolic volume (-33%, p=0.02). When incremental doses of norepinephrine and dobutamine were administered, the right ventricular arterio-ventricular coupling was improved only by dobutamine (p<0.05). Norepinephrine increased both left ventricular end-diastolic volume and left ventricular contractility to a greater extent (p<0.05) in pulmonary artery banded animals. While the cardiac index was improved equally by norepinephrine and dobutamine treatments in pulmonary artery banded animals, norepinephrine had a significantly greater effect on mean arterial pressure (p<0.05) and diastolic arterial pressure (p<0.05).Conclusion: While norepinephrine and dobutamine improved cardiac index equally, it was obtained in different manners. Dobutamine significantly improved the right ventricular function and the arterio-ventricular coupling. Norepinephrine increased systemic resistance, thereby improving arterial pressures and left ventricular systolic function by maintaining left ventricular end-diastolic volume.

P6478Resting and exercise pulmonary artery systolic pressure to rule out later development of pulmonary arterial hypertension in systemic sclerosis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Gargani ◽  
V Codullo ◽  
P Argiento ◽  
A Moreo ◽  
F Pieri ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Systemic Sclerosis ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Peak Exercise ◽  
Exercise Doppler Echocardiography ◽  
Pulmonary Arterial ◽  
Further Development ◽  
Rule Out

Abstract Background Patients with systemic sclerosis (SSc) are at risk of developing pulmonary arterial hypertension (PAH), which is often diagnosed late when the benefits of vasoactive therapies are limited. The concept of exercise pulmonary hypertension as a possible transitional phase anticipating resting PAH has been assessed in several pathologies, but has not been endorsed by the latest European Guidelines, because not supported by sufficient data. Purpose To evaluate whether PASP values at rest and at peak exercise, estimated at echocardiography, could be predictors of further development of PAH. Methods Four hundred and twenty-nine SSc patients without a previous diagnosis of PAH, enrolled at 4 referral Centres, underwent standard exercise Doppler echocardiography with PASP estimation at rest and at peak stress. Patients were then followed-up to assess the development of PAH, as diagnosed by a complete diagnostic work-up including right heart catheterization. PAH was defined by pre-capillary pulmonary hypertension (mean pulmonary artery pressure ≥25 mmHg with pulmonary arterial wedge pressure ≤15 mmHg), without significant interstitial lung disease and/or left heart disease. Results During the median follow-up of 75 months (IQR 29–114), 16 patients developed PAH. A combined cut-off of ≥24 mmHg as resting PASP and ≥40 as peak PASP was identified as the best predictor of further development of PAH (see Figure). Both resting PASP and peak PASP were predictors of PAH at univariate analysis (resting PASP OR 1.13, 95% C.I. 1.07–1.19, p<0.0001; peak PASP OR 1.13, 95% C.I. 1.07–1.18, p<0.0001). At multivariate analysis, only peak PASP was independently associated to PAH development (OR 1.13, 95% C.I. 1.04–1.18, p<0.001). Only one patient among those with resting PASP <24 mmHg and peak PASP <40 mmHg (34.7% of the total population) developed PAH during the follow-up (after 10 years from normal exercise Doppler echocardiography). Kaplan-Meier curves Conclusions Exercise increase in PASP is an independent predictor of later development of PAH in SSc. An increase in exercise PASP is frequent and is not necessarily associated with a later development of PAH, whereas the very high negative predictive value of a normal PASP both at rest and at peak exercise can be used in the clinical practice to confidently rule out about one third of patients. Acknowledgement/Funding Italian Ministry of Health (Ricerca Finalizzata 2011-2012)

Sex Differences in Right Ventricular-Vascular Coupling and Pulmonary Artery Impedance in Response to Chronic Hypoxia and Recovery

2012 ◽  
Author(s):  
Aiping Liu ◽  
Lian Tian ◽  
Diana M. Tabima ◽  
Naomi C. Chesler
Keyword(s):  
Pulmonary Artery ◽  
Chronic Hypoxia ◽  
Pulmonary Arteries ◽  
Pulmonary Artery Hypertension ◽  
Vascular Impedance ◽  
Female Predominance ◽  
Collagen Accumulation ◽  
Dominant Disease ◽  
Pulmonary Arterial

Pulmonary artery hypertension (PAH) is a female dominant disease (the female-to-male ratio is 4:1), characterized by small distal pulmonary arterial narrowing and large proximal arterial stiffening, which increase right ventricle (RV) afterload and ultimately lead to RV failure [1,2]. Our recent studies have shown that collagen accumulation induced by chronic hypoxia increases the stiffness of the large extralobar pulmonary arteries (PAs) [3], and affects pulmonary vascular impedance (PVZ) [4]. The role of collagen in the female predominance in developing PAH has not been explored to date.

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