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Surgical and Radiologic Anatomy : SRA Nov 2020Previous studies have shown a correlation between axial pulmonary trunk diameter (PTD) on chest computed tomography (CT) and pulmonary artery pressure. However, it is...
PURPOSE
Previous studies have shown a correlation between axial pulmonary trunk diameter (PTD) on chest computed tomography (CT) and pulmonary artery pressure. However, it is not known whether the PTD slices measured on chest CT have been recorded during the systolic or diastolic phase. The aim of this study was to demonstrate the variations in PTD during the cardiac cycle by measuring coronary CT angiography (CCTA) images.
METHODS
A retrospective analysis was made of 101 patients who underwent CCTA for coronary artery disease assessment. CCTA images were reconstructed during a full cardiac cycle and measurements were taken of the systolic and diastolic PTD and ascending aorta diameter (AAD) from the same slice by two independent observers.
RESULTS
Inter-observer agreement was excellent (intraclass correlation coefficient = 0.99) for all CT measurements. The mean systolic PTD of all patients was 26.3 ± 3.6 mm and the mean diastolic PTD was 22.8 ± 3.2 mm (p < 0.001). The mean difference between systole and diastole was found to be 3.5 ± 1.2 mm for PTD, 1.2 ± 0.7 mm for AAD, and 0.1 ± 0.04 for the PTD/AAD ratio (p values < 0.001). There was no statistical significance of PTD variations according to gender, age, height, weight, body mass index, and body surface area.
CONCLUSION
When an increased PTD is detected in a chest CT compared to normal limits or a previous CT scan, this may be the result of the variation in PTD due to the cardiac cycle.
Topics: Adult; Age Factors; Aged; Aorta; Biological Variation, Population; Computed Tomography Angiography; Coronary Angiography; Coronary Artery Disease; Diastole; Female; Humans; Hypertension, Pulmonary; Male; Middle Aged; Pulmonary Artery; Retrospective Studies; Sex Factors; Systole
PubMed: 32405785
DOI: 10.1007/s00276-020-02493-9 -
European Journal of Cardio-thoracic... May 2022
Topics: Constriction, Pathologic; Heart Defects, Congenital; Humans; Lung; Pulmonary Artery; Tomography, X-Ray Computed; Trachea; Tracheal Stenosis; Treatment Outcome; Vascular Malformations
PubMed: 35201297
DOI: 10.1093/ejcts/ezac127 -
International Journal of Legal Medicine Nov 2019Pulmonary fat embolism (PFE) is a relevant diagnosis playing a role as a sign of vitality or a cause of death. Its severity is assessed according to histological grading...
PURPOSE
Pulmonary fat embolism (PFE) is a relevant diagnosis playing a role as a sign of vitality or a cause of death. Its severity is assessed according to histological grading systems like that of Falzi. The aim of this study was to determine the utility of unenhanced postmortem computed tomography (PMCT) for PFE diagnosis based on the detection of fat layers.
METHODS
Consecutive cases with PMCT and autopsy were studied retrospectively. The case group consisted of cases with positive PFE, and the control group included cases with negative PFE. Three observers independently assessed PMCT data for fat layers in the pulmonary trunk and the right and left pulmonary artery. For cases with fat layers, autopsy protocols were assessed for the cause of death, relation to trauma, and undertaken resuscitation measures.
RESULTS
Eight hundred thirty cases were included: 366 PFE positive cases (144 of Falzi grade 1, 63 of 1.5, 99 of 2, 28 of 2.5, and 32 of 3) and 464 PFE negative cases. Interrater reliabilities varied between substantial and almost perfect, and discrepancies were solved according to majority. Eighteen cases showed fat layers on PMCT (2 controls-traumatic instantaneous deaths-, 16 PFE positive cases). PMCT showed low sensitivity but high specificity for PFE diagnosis. The layers were located at the same position in the pulmonary trunk directly adjacent to the pulmonary valve distal to the right ventricle.
CONCLUSION
Fat layer on PMCT is a rare finding but relates to PFE diagnosis, especially of severe histological grade. It is to be expected in a typical position within the pulmonary trunk.
Topics: Case-Control Studies; Embolism, Fat; Female; Forensic Pathology; Humans; Male; Middle Aged; Predictive Value of Tests; Pulmonary Artery; Pulmonary Embolism; Retrospective Studies; Sensitivity and Specificity; Tomography, X-Ray Computed
PubMed: 30972495
DOI: 10.1007/s00414-019-02055-8 -
Heart, Lung & Circulation Aug 2021Pulmonary artery stenosis is a frequent complication after arterial switch operation. This case study presented a complex pulmonary artery stenosis initially treated...
Pulmonary artery stenosis is a frequent complication after arterial switch operation. This case study presented a complex pulmonary artery stenosis initially treated with bilateral pulmonary artery stenting. The patient was found to have aortic valve endocarditis and recurrent pulmonary artery stenosis. The aortic valve was replaced and the pulmonary valve was repaired, followed by interposition of a Y-shaped graft from the sinotubular junction to both pulmonary arteries. The patient had an uneventful recovery and was discharged home asymptomatic after endocarditis antibacterial treatment.
Topics: Arterial Switch Operation; Follow-Up Studies; Humans; Postoperative Complications; Pulmonary Artery; Pulmonary Valve Stenosis; Reoperation; Transposition of Great Vessels
PubMed: 33745815
DOI: 10.1016/j.hlc.2021.01.011 -
Developmental Biology Jun 2023Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors...
Outflow tract (OFT) develops from cardiac progenitor cells in the second heart field (SHF) domain. APJ, a G-Protein Coupled Receptor, is expressed by cardiac progenitors in the SHF. By lineage tracing APJ+SHF cells, we show that these cardiac progenitors contribute to the cells of OFT, which eventually give rise to aorta and pulmonary trunk/artery upon its morphogenesis. Furthermore, we show that early APJ + cells give rise to both aorta and pulmonary cells but late APJ + cells predominantly give rise to pulmonary cells. APJ is expressed by the outflow tract progenitors in the SHF but its role is unclear. We performed knockout studies to determine the role of APJ in SHF cell proliferation and survival. Our data suggested that APJ knockout in the SHF reduced the proliferation of SHF progenitors, while there was no significant impact on survival. In addition, we show that ectopic overexpression of WNT in these cells disrupted aorta and pulmonary morphogenesis from OFT. Overall, our study has identified APJ + progenitor population within the SHF that give rise to aorta and pulmonary trunk/artery cells. Furthermore, we show that APJ signaling stimulates proliferation of these cells in the SHF.
Topics: Heart; Signal Transduction; Stem Cells; Pulmonary Artery; Aorta; Myocardium; Gene Expression Regulation, Developmental
PubMed: 37037405
DOI: 10.1016/j.ydbio.2023.04.003 -
The Journal of Thoracic and... Jun 2021
Topics: Humans; Hypertension, Pulmonary; Pulmonary Arterial Hypertension; Pulmonary Artery
PubMed: 32690412
DOI: 10.1016/j.jtcvs.2020.04.131 -
Interactive Cardiovascular and Thoracic... Nov 2020We aimed to describe the anatomic distribution of periarterial pulmonary sympathetic nerves and to observe the long-term morphometric and functional changes after...
OBJECTIVES
We aimed to describe the anatomic distribution of periarterial pulmonary sympathetic nerves and to observe the long-term morphometric and functional changes after pulmonary artery denervation (PADN), a novel therapy for pulmonary arterial hypertension (PAH).
METHODS
A total of 45 beagles were divided into a sympathetic innervation group (n = 3, 33.3% were females), a PAH group (n = 35, 34.3% were females) and a control group (n = 7, 28.5% were females). The PAH group was randomly divided into no-PADN (n = 7), instant-PADN (n = 7), 1M-PADN (n = 7), 2M-PADN (n = 7) and 3M-PADN (n = 7) subgroups. The sympathetic innervation group was sacrificed to reveal the sympathetic innervation of pulmonary arteries. PAH was induced by injecting dehydromonocrotaline (DHMCT) through the right atrium. The pulmonary capillary wedge pressure, right ventricular systolic pressure, right ventricular mean pressure, pulmonary artery systolic pressure and pulmonary artery mean pressure of each group were continuously measured. The cardiac output was detected to calculate the pulmonary vascular resistance. PAH and control groups were subjected to immunofluorescence assay, sympathetic nerve conduction velocity measurement and transmission electron microscopy.
RESULTS
The no-PADN group had significantly higher PVSP, PVMP, pulmonary artery systolic pressure, pulmonary artery mean pressure and pulmonary vascular resistance but lower cardiac output than those of the control group (P < 0.05). Instant-PADN, 1M-PADN, 2M-PADN and 3M-PADN groups had significantly lower PVSP, PVMP, pulmonary artery systolic pressure, pulmonary artery mean pressure and pulmonary vascular resistance but higher cardiac output than those of the no-PADN group (P < 0.05). Most sympathetic nerves were located within 2.5 mm of the intimae of the bifurcation and proximal trunk, mainly in the left trunk. The diameter and cross-sectional area of myelinated fibres in the PAH group were significantly larger than those of the control group. Sympathetic nerve conduction velocity of the PAH group gradually decreased, and nerve fibres were almost demyelinated 3 months after PADN.
CONCLUSIONS
PADN effectively relieved dehydromonocrotaline-induced canine PAH and decreased sympathetic nerve conduction velocity.
Topics: Animals; Disease Models, Animal; Dogs; Hypertension, Pulmonary; Lung; Monocrotaline; Pulmonary Artery; Sympathectomy; Sympathetic Nervous System; Vascular Resistance
PubMed: 33057705
DOI: 10.1093/icvts/ivaa166 -
The Journal of Thoracic and... Oct 2022Pulmonary artery (PA) reconstruction is performed to avoid pneumonectomy for non-small cell lung cancer (NSCLC). Our objective was to assess the safety and efficacy of...
OBJECTIVE
Pulmonary artery (PA) reconstruction is performed to avoid pneumonectomy for non-small cell lung cancer (NSCLC). Our objective was to assess the safety and efficacy of performing PA reconstruction without systemic heparinization during resections of NSCLC.
METHODS
Among 3537 patients with resected NSCLC between 2008 and 2019, 130 (3.7%) patients underwent PA reconstruction to avoid pneumonectomy without intraoperative systemic heparinization. We investigated surgical outcome. The median follow-up time was 37 months.
RESULTS
As to PA reconstruction, tangential suture, patch closure (autologous pericardium), end-to-end anastomosis, and conduit were performed in 56, 26, 32, and 16 patients (autologous pericardium, 13; resected pulmonary vein, 3), respectively. Combined bronchial sleeve resection was performed in 68 (52%) patients. The mean operative time was 261 minutes. The procedure-related complications were 2 PA thromboses with pericardial conduit requiring completion pneumonectomy and 2 massive hemoptysis of a bronchopulmonary fistula leading to death (operative mortality, 1.5%). PA bending and mechanical stenosis were due to the lengthening by the conduit. Seventy-five patients had other complications, the most frequent being arrhythmia. One patient was at stage 0 after induction chemoradiotherapy; 26, stage I (9 IA and 17 IB); 43, stage II (19 IA and 24 IB), 55 stage III (49 IIIA and 6 IIIB); and 5, stage IV. Five-year overall survival, cancer-specific survival, and recurrence-free survival rates were 49.2%, 61.8%, and 37.1%, respectively.
CONCLUSIONS
PA reconstruction without intraoperative systemic heparinization during resections of NSCLC was performed with a very low risk of thrombosis as well as perioperative bleeding.
Topics: Carcinoma, Non-Small-Cell Lung; Humans; Lung; Lung Neoplasms; Neoplasm Staging; Pneumonectomy; Pulmonary Artery
PubMed: 35219513
DOI: 10.1016/j.jtcvs.2022.01.017 -
Clinical Imaging Jul 2020Pulmonary hypertension (PH) is a progressive, potentially fatal disease, difficult to diagnose early due to non-specific nature of symptoms. PH is associated with...
OBJECTIVES
Pulmonary hypertension (PH) is a progressive, potentially fatal disease, difficult to diagnose early due to non-specific nature of symptoms. PH is associated with increased morbidity and death in many respiratory and cardiac disorders, and with all-cause mortality, independent of age and cardiopulmonary disease. The main pulmonary artery diameter (MPA), and ratio of MPA to adjacent ascending aorta (AA), MPA:AA, on Chest CT are strong indicators of suspected PH. Our goal was to determine the prevalence of abnormally high values of these indicators of PH in asymptomatic low-dose CT (LDCT) screening participants at risk of lung cancer, and determine the associated risk factors.
METHODS
We reviewed consecutive baseline LDCT scans of 1949 smokers in an IRB-approved study. We measured the MPA and AA diameter and calculated MPA:AA ratio. We defined abnormally high values as being more than two standard deviations above the average (MPA ≥ 34 mm and MPA:AA ≥ 1.0). Regression analyses were used to identify risk factors and CT findings of participants associated with high values.
RESULTS
The prevalence of MPA ≥ 34 mm and MPA:AA ≥ 1.0 was 4.2% and 6.9%, respectively. Multivariable regression demonstrated that BMI was a significant risk factor, both for MPA ≥ 34 mm (OR = 1.07, p < 0.0001) and MPA:AA ≥ 1.0 (OR = 1.04, p = 0.003). Emphysema was significant in the univariate but not in the multivariate analysis.
CONCLUSIONS
We determined that the possible prevalence of PH as defined by abnormally high values of MPA and of MPA:AA was greater than previously described in the general population and that pulmonary consultation be recommended for these participants, in view of the significance of PH.
Topics: Adult; Aorta; Early Detection of Cancer; Female; Humans; Hypertension, Pulmonary; Lung; Lung Neoplasms; Male; Middle Aged; Pulmonary Artery; Risk Factors; Smokers; Tomography, X-Ray Computed
PubMed: 32120308
DOI: 10.1016/j.clinimag.2019.11.011 -
Seminars in Thoracic and Cardiovascular... 2021
Topics: Carotid Stenosis; Humans; Pulmonary Artery
PubMed: 33171238
DOI: 10.1053/j.semtcvs.2020.10.010