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Seminars in Respiratory and Critical... Oct 2023
Review
Topics: Humans; Hypertension, Pulmonary; Lung; Pulmonary Artery; Pulmonary Circulation
PubMed: 37816343
DOI: 10.1055/s-0043-1771162 -
Scientific Reports Nov 2023In patients with heart failure, guideline directed medical therapy improves outcomes and requires close patient monitoring. Pulmonary artery pressure monitors permit...
In patients with heart failure, guideline directed medical therapy improves outcomes and requires close patient monitoring. Pulmonary artery pressure monitors permit remote assessment of cardiopulmonary haemodynamics and facilitate early intervention that has been shown to decrease heart failure hospitalization. Pressure sensors implanted in the pulmonary vasculature are stabilized through passive or active interaction with the anatomy and communicate with an external reader to relay invasively measured pressure by radiofrequency. A body mass index > 35 kg/m and chest circumference > 165 cm prevent use due to poor communication. Pulmonary vasculature anatomy is variable between patients and the pulmonary artery size, angulation of vessels and depth of sensor location from the chest wall in heart failure patients who may be candidates for pressure sensors remains largely unexamined. The present study analyses the size, angulation, and depth of the pulmonary artery at the position of implantation of two pulmonary artery pressure sensors: the CardioMEMS sensor typically implanted in the left pulmonary artery and the Cordella sensor implanted in the right pulmonary artery. Thirty-four computed tomography pulmonary angiograms from patients with heart failure were analysed using the MIMICS software. Distance from the bifurcation of the pulmonary artery to the implant site was shorter for the right pulmonary artery (4.55 ± 0.64 cm vs. 7.4 ± 1.3 cm) and vessel diameter at the implant site was larger (17.15 ± 2.87 mm vs. 11.83 ± 2.30 mm). Link distance (length of the communication path between sensor and reader) was shorter for the left pulmonary artery (9.40 ± 1.43 mm vs. 12.54 ± 1.37 mm). Therefore, the detailed analysis of pulmonary arterial anatomy using computed tomography pulmonary angiograms may alter the choice of implant location to reduce the risk of sensor migration and improve readability by minimizing sensor-to-reader link distance.
Topics: Humans; Pulmonary Artery; Heart Failure; Prostheses and Implants; Hemodynamics; Monitoring, Physiologic
PubMed: 37993563
DOI: 10.1038/s41598-023-47612-9 -
Journal of Vascular Surgery. Venous and... Mar 2024
Topics: Humans; Arteriovenous Fistula; Pulmonary Veins; Pulmonary Artery
PubMed: 37972756
DOI: 10.1016/j.jvsv.2023.101717 -
Methodist DeBakey Cardiovascular Journal 2024The presentation of pulmonary embolism (PE) varies from asymptomatic to life-threatening, and management involves multiple specialists. Timely diagnosis of PE is based... (Review)
Review
The presentation of pulmonary embolism (PE) varies from asymptomatic to life-threatening, and management involves multiple specialists. Timely diagnosis of PE is based on clinical presentation, D-dimer testing, and computed tomography pulmonary angiogram (CTPA), and assessment by a Pulmonary Embolism Response Team (PERT) is critical to management. Artificial intelligence (AI) technology plays a key role in the PE workflow with automated detection and flagging of suspected PE in CTPA imaging. HIPAA-compliant communication features of mobile and web-based applications may facilitate PERT workflow with immediate access to imaging, team activation, and real-time information sharing and collaboration. In this review, we describe contemporary diagnostic tools, specifically AI, that are important in the triage and diagnosis of PE.
Topics: Humans; Pulmonary Embolism; Predictive Value of Tests; Computed Tomography Angiography; Fibrin Fibrinogen Degradation Products; Biomarkers; Artificial Intelligence; Workflow; Prognosis; Radiographic Image Interpretation, Computer-Assisted; Pulmonary Artery
PubMed: 38765212
DOI: 10.14797/mdcvj.1342 -
European Journal of Pharmacology Jun 2024Idiopathic pulmonary fibrosis (IPF) associated to pulmonary hypertension (PH) portends a poor prognosis, characterized by lung parenchyma fibrosis and pulmonary artery...
Idiopathic pulmonary fibrosis (IPF) associated to pulmonary hypertension (PH) portends a poor prognosis, characterized by lung parenchyma fibrosis and pulmonary artery remodeling. Serum and parenchyma levels of Interleukin 11 (IL-11) are elevated in IPF-PH patients and contributes to pulmonary artery remodeling and PH. However, the effect of current approved therapies against IPF in pulmonary artery remodeling induced by IL-11 is unknown. The aim of this study is to analyze the effects of nintedanib and pirfenidone on pulmonary artery endothelial and smooth muscle cell remodeling induced by IL-11 in vitro. Our results show that nintedanib (NTD) and pirfenidone (PFD) ameliorates endothelial to mesenchymal transition (EnMT), pulmonary artery smooth muscle cell to myofibroblast-like transformation and pulmonary remodeling in precision lung cut slices. This study provided also evidence of the inhibitory effect of PFD and NTD on IL-11-induced endothelial and muscle cells proliferation and senescence. The inhibitory effect of these drugs on monocyte arrest and angiogenesis was also studied. Finally, we observed that IL-11 induced canonical signal transducer and activator of transcription 3 (STAT3) and non-canonical mitogen-activated protein kinase 1/2 (ERK1/2) phosphorylation, but, PFD and NTD only inhibited ERK1/2 phosphorylation. Therefore, this study provided evidence of the inhibitory effect of NTD and PFD on markers of pulmonary artery remodeling induced by IL-11.
Topics: Pulmonary Artery; Interleukin-11; Indoles; Animals; Myocytes, Smooth Muscle; STAT3 Transcription Factor; Endothelial Cells; Pyridones; Cell Proliferation; Rats; Humans; Male; Cellular Senescence; MAP Kinase Signaling System; Idiopathic Pulmonary Fibrosis; Monocytes; Vascular Remodeling
PubMed: 38561103
DOI: 10.1016/j.ejphar.2024.176547 -
European Journal of Pharmacology May 2024Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by remodeling of the pulmonary vasculature and elevated pulmonary arterial... (Review)
Review
Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by remodeling of the pulmonary vasculature and elevated pulmonary arterial pressure, ultimately leading to right heart failure and death. Despite its clinical significance, the precise molecular mechanisms driving PAH pathogenesis warrant confirmation. Compelling evidence indicates that during the development of PAH, pulmonary vascular cells exhibit a preference for energy generation through aerobic glycolysis, known as the "Warburg effect", even in well-oxygenated conditions. This metabolic shift results in imbalanced metabolism, increased proliferation, and severe pulmonary vascular remodeling. Exploring the Warburg effect and its interplay with glycolytic enzymes in the context of PAH has yielded current insights into emerging drug candidates targeting enzymes and intermediates involved in glucose metabolism. This sheds light on both opportunities and challenges in the realm of antiglycolytic therapy for PAH.
Topics: Humans; Pulmonary Arterial Hypertension; Hypertension, Pulmonary; Familial Primary Pulmonary Hypertension; Glycolysis; Lung; Pulmonary Artery; Vascular Remodeling
PubMed: 38503401
DOI: 10.1016/j.ejphar.2024.176492 -
PloS One 2023The ductus arteriosus is a muscular artery connecting the pulmonary trunk directly to the aorta in fetal circulation in order to by-pass the fluid filled lungs....
The ductus arteriosus is a muscular artery connecting the pulmonary trunk directly to the aorta in fetal circulation in order to by-pass the fluid filled lungs. Post-natally, this vessel is speculated to undergo obliteration, fibrosis and ultimately metamorphosize into a band of ligament, thereby changing name from the ductus arteriosus to the ligamentum arteriosum (LA). Earlier studies into the innervation of the ductus arteriosus reported innervation from the left aortic and vagus nerves. However, information of what becomes of the innervation is scanty and contradictory. I hypothesized that; this fetal shunt still receives innervation even in post-uterine life. To test this, LA of human, pig, and wild-type mice were studied using double-immunofluorescence labeling using antibodies directed against structural and general neuronal marker proteins (Smooth muscle actin and Protein gene product 9.5 (PGP 9.5, respectively). Additionally, TEM studies were performed on mouse LA. Results from the present study demonstrates an extensive innervation of the LA in animals (mice and pigs) and in senescent humans validated by two independent methods, i.e., immunolabeling with antibody directed against PGP 9.5 and TEM. Intense immunoreactivity was clearly visible in samples subjected to PGP-immunolabeling. TEM revealed the presence of nerve terminals with about 30% of all nerve terminals observed less than 1 μm away from smooth muscle cells within the LA. This clearly differs from elastic arteries, where the distance between autonomic terminals and smooth muscle cells is rarely less than 1 μm. Conceivably, these results imply that the so- called LA receives innervation representative of that present within the ductus arteriosus during fetal life. This provides the first reliable study of innervation of the LA and makes room for further investigation into the neurochemistry of this innervation. This is crucial as the presence of nerve terminals may play a role in vessel compliance or impedance of the two great vessels related to this structure. The substances released by these fibers may also have an influence on cells and tissues in the immediate microenvironment of this structure.
Topics: Animals; Humans; Mice; Antibodies; Aorta; Ductus Arteriosus; Pulmonary Artery; Swine
PubMed: 37733721
DOI: 10.1371/journal.pone.0291879 -
American Journal of Respiratory and... Aug 2023
Topics: Humans; Hypertension, Pulmonary; Pulmonary Artery; Pulmonary Circulation
PubMed: 37348119
DOI: 10.1164/rccm.202306-0990ED -
European Journal of Cardio-thoracic... Jul 2023Disconnected pulmonary artery (PA) is a rare anomaly that can be isolated or associated with complex intracardiac malformations. Early reimplantation of the disconnected... (Observational Study)
Observational Study
OBJECTIVES
Disconnected pulmonary artery (PA) is a rare anomaly that can be isolated or associated with complex intracardiac malformations. Early reimplantation of the disconnected PA is recommended to allow growth and satisfactory pulmonary perfusion while preventing collateral artery development. The aim of this study was to describe the characteristics of patients with disconnected PA and, for those who had surgical reimplantation, to determine the incidence, delay and predictive factors of reintervention for reconnected PA stenosis.
METHODS
We include patients with the diagnosis of congenitally disconnected PA and surgical repair at our institution.
RESULTS
Retrospective observational study of 55 patients with a disconnected PA. Fifty-one underwent surgical correction and were followed up at our institution between 2000 and 2022. Disconnected PAs were observed in isolation in 31% of the cases. The most frequent form was left PA originating from the arterial duct (58%). The reimplantation was done at the median age of 12 days. Anastomotic stenosis was observed during follow-up in 71% of the patients with 75% of them requiring reintervention (55% of the population). The median delay to reintervention was 3.2 years after reimplantation, and >25% of reinterventions on the reimplanted PA occurred within the first postoperative year. We found more reintervention if associated cardiac defect, without significant statistic difference. Weight at re-confluence, presence of ductal tissue at the origin of the PA and prior shunt placement on the disconnected PA were not found to be risk factors for reintervention.
DISCUSSION
After surgical reimplantation of PA, >50% of patients required reintervention for PA stenosis. Technical improvements should be sought to reduce the incidence of this complication.
Topics: Humans; Infant; Infant, Newborn; Pulmonary Artery; Follow-Up Studies; Constriction, Pathologic; Retrospective Studies; Risk Factors; Treatment Outcome
PubMed: 37348856
DOI: 10.1093/ejcts/ezad245 -
Arteriosclerosis, Thrombosis, and... Jun 2024Pulmonary hypertension (PH) is a progressive and life-threatening disease characterized by pulmonary vascular remodeling, which involves aberrant proliferation and...
BACKGROUND
Pulmonary hypertension (PH) is a progressive and life-threatening disease characterized by pulmonary vascular remodeling, which involves aberrant proliferation and apoptosis resistance of the pulmonary arterial smooth muscle cells (PASMCs), resembling the hallmark characteristics of cancer. In cancer, the HMGB2 (high-mobility group box 2) protein promotes the pro-proliferative/antiapoptotic phenotype. However, the function of HMGB2 in PH remains uninvestigated.
METHODS
Smooth muscle cell (SMC)-specific HMGB2 knockout or HMGB2-OE (HMGB2 overexpression) mice and HMGB2 silenced rats were used to establish hypoxia+Su5416 (HySu)-induced PH mouse and monocrotaline-induced PH rat models, respectively. The effects of HMGB2 and its underlying mechanisms were subsequently elucidated using RNA-sequencing and cellular and molecular biology analyses. Serum HMGB2 levels were measured in the controls and patients with pulmonary arterial (PA) hypertension.
RESULTS
HMGB2 expression was markedly increased in the PAs of patients with PA hypertension and PH rodent models and was predominantly localized in PASMCs. SMC-specific HMGB2 deficiency or silencing attenuated PH development and pulmonary vascular remodeling in hypoxia+Su5416-induced mice and monocrotaline-treated rats. SMC-specific HMGB2 overexpression aggravated hypoxia+Su5416-induced PH. HMGB2 knockdown inhibited PASMC proliferation in vitro in response to PDGF-BB (platelet-derived growth factor-BB). In contrast, HMGB2 protein stimulation caused the hyperproliferation of PASMCs. In addition, HMGB2 promoted PASMC proliferation and the development of PH by RAGE (receptor for advanced glycation end products)/FAK (focal adhesion kinase)-mediated Hippo/YAP (yes-associated protein) signaling suppression. Serum HMGB2 levels were significantly increased in patients with PA hypertension, and they correlated with disease severity, predicting worse survival.
CONCLUSIONS
Our findings indicate that targeting HMGB2 might be a novel therapeutic strategy for treating PH. Serum HMGB2 levels could serve as a novel biomarker for diagnosing PA hypertension and determining its prognosis.
Topics: Animals; HMGB2 Protein; Humans; Vascular Remodeling; Male; Myocytes, Smooth Muscle; Disease Models, Animal; Pulmonary Artery; Mice, Knockout; Muscle, Smooth, Vascular; Rats; Mice, Inbred C57BL; Mice; Cell Proliferation; Severity of Illness Index; Signal Transduction; Pulmonary Arterial Hypertension; Rats, Sprague-Dawley; Female; Cells, Cultured; Middle Aged; Hypertension, Pulmonary
PubMed: 38572649
DOI: 10.1161/ATVBAHA.123.319916