Pulmonary Circulation最新文献

Pulmonary Hypertension (PH) is a critical disease characterized by increased pulmonary arterial pressure and the development of vascular resistance, which can lead to fatal outcomes if left untreated. Cardiovascular and Respiratory Nurses (CRNs) play a significant role in the management of PH; however, there is a lack of sufficient studies examining their role competence. This study aimed to investigate the role competencies of CRNs regarding PH. This cross-sectional and descriptive study was conducted at Istanbul Yedikule Chest Diseases Hospital with the participation of 85 CRNs. Data were collected using a personal characteristics form and Pulmonary Hypertension Inventory of the Role Competence (PHIRC). Data analysis was performed using Mann-Whitney U, Kruskal-Wallis, Chi-Square, and post hoc Bonferroni tests. Among the nurses, 76.5% held a bachelor's degree, and 78.9% were working in clinical settings. The CRNs scored above mean level in all sub-dimensions of the PHIRC. The moderate scores for knowledge and symptom management, risk factors awareness of CRNs, and symptom identification, and the total score were 12.75 ± 1.92, 11.52 ± 1.91, 10.34 ± 2.48, and 34.67 ± 5, respectively. A significant increase in the role competence was observed as the frequency of encountering PH patients increased (p < 0.05). The findings of this study indicate that CRNs had above-moderate role competence regarding PH management. Additionally, nurses who frequently encountered PH patients demonstrated higher role competence, which may be related to maintaining active knowledge. Nurses in their first year of practice had higher knowledge levels, highlighting the necessity of periodic and high-quality training programs and courses on PH.

Using lung immunohistochemistry and stereology, platelets were found to accumulate and co-localize with leukocytes, particularly monocytes, within the mural and adventitial space of remodeled vessels of patients with pulmonary arterial hypertension. The presumed signaling between these cell types invites further studies into the role of platelet-monocyte aggregates in pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a form of pulmonary hypertension that is caused by persistent obstruction of the pulmonary arteries by organized thrombi and associated microvascular disease. Pulmonary endarterectomy (PEA) is the gold standard treatment, but the extent of small vessel remodeling, which strongly influences treatment outcomes, remains difficult to quantify pre-operatively. We developed a multiscale, structure-based model of the pulmonary circulation using patient-specific vascular geometries from CT pulmonary angiography (CTPA) and haemodynamic data from right heart catheterization (RHC). Eleven CTEPH patients were included. The model estimated individual remodeling burden by fitting simulated to measured preoperative mean pulmonary artery pressure (mPAP). PEA was simulated by removing flow obstructions to predict Postoperative mPAP and pulmonary vascular resistance (PVR), both under pre- and post-PEA boundary conditions. Model predictions of post-PEA mPAP and PVR were in reasonable agreement with measured outcomes, especially when Postoperative boundary conditions were applied. Predicted changes in mPAP (∆mPAP) strongly correlated with clinical values (R = 0.81, p = 0.002), improving further with post-PEA flow parameters (R = 0.84, p = 0.001). The model captured variable haemodynamic responses to PEA, even among patients with similar Postoperative mPAP. This preliminary investigation demonstrates the feasibility of personalized computational modeling to non-invasively estimate the extent of microvascular disease and simulate postsurgical haemodynamic outcomes in CTEPH. The findings support the potential for this approach to serve as a clinical decision-making tool, with future validation in larger cohorts and integration of spatial remodeling and longitudinal data.

The natural history of late-onset pulmonary arterial hypertension (PAH) with features of venous/capillary involvement and the associations with rare variants in PAH genes are not well known. We report a case of a female patient who developed severe PAH at the age of 70. Two years before, lung histology was obtained showing features of pulmonary veno-occlusive disease. Genetic testing revealed that the patient was harbouring two rare genetic variants in the KDR and EIF2AK4 genes. She received a triple combination therapy alongside diuretics and survived remarkable 8 years after the PAH diagnosis.

Treatment options for acute pulmonary embolism (PE) have evolved rapidly, with an increasing number of interventional options, necessitating interhospital transfer for consideration of advanced therapies and optimal care. Utilizing the National PERT Consortium database, this study analyzed 12,346 patients from 35 institutions between October 16, 2015 and June 1, 2024. Patients were categorized as directly presenting to a PERT hospital or transferred from a referring hospital. Demographics, clinical presentations, treatments, and outcomes were compared. Multivariable logistic regression was used to evaluate the association between transfer status and outcomes. Transferred patients (n = 3277) were younger, more frequently White, more often obese, and had lower malignancy rates. They were more likely to be classified as high-risk PE (16.7% vs. 13.8%, p < 0.01) and intermediate-high risk PE (55.9% vs. 54.3%, p < 0.01). Transferred patients more frequently received advanced therapies, including ECMO (2.8% vs. 1.1%, p < 0.01), surgical embolectomy (2.0% vs. 0.8%, p < 0.01), systemic thrombolysis (5.3% vs. 3.8%, p < 0.001), and catheter-based interventions (32.3% vs. 17.1%, p < 0.01). After adjustment, transfer was associated with lower odds of 30-day mortality (OR 0.82, 95% CI 0.69-0.98), 1-year mortality (OR 0.77, 95% CI 0.67-0.89), and in-hospital mortality (OR 0.78, 95% CI 0.65-0.97), with no significant difference in major bleeding risk. Subgroup analysis showed mortality benefits were most evident among intermediate-low and high-risk patients. In conclusion, acute PE patients transferred to PERT hospitals were more likely to receive advanced therapies and had improved short- and long-term survival, with no increase in bleeding risk, despite presenting with higher clinical severity.

Mechanical ventilation (MV), though life-saving in acute respiratory distress syndrome (ARDS), can cause ventilator-induced lung injury (VILI). MicroRNA-24 (miR-24) has been implicated in regulating inflammation and apoptosis, but its role in VILI remains unexplored. Therefore, our study aimed to explore the role of mechanism of miR-24 in VILI. MiR-24 expression was analyzed in MV-induced ARDS rat models (GSE57223), plasma from ARDS patients, and cyclic stretch (CS)-treated alveolar epithelial cells. Functional studies included intratracheal delivery of miR-24-agomir in rats with VILI and transfection of miR-24 mimic in CS-exposed cells. Inflammatory cytokines, oxidative stress markers, apoptosis, and mitochondrial dysfunction were assessed using ELISA, RT-qPCR, TUNEL, JC-1 staining, and ATP assays. BOK was identified as a target of miR-24 via bioinformatics, luciferase reporter, and RNA pull-down assays. Rescue experiments using BOK overexpression vectors (pcDNA3.1/BOK) were conducted in both models to confirm functional interaction. MiR-24 was significantly downregulated in ARDS patients and VILI models and positively correlated with oxygenation index. Overexpression of miR-24 attenuated MV- and CS-induced inflammation, oxidative damage, and mitochondrial apoptosis dysfunction. BOK was confirmed as a direct target of miR-24; its expression was upregulated in ARDS and VILI and inversely correlated with miR-24 levels. Silencing of BOK attenuated MV-induced inflammation, oxidative damage, and apoptosis in rats. Importantly, BOK overexpression reversed the protective effects of miR-24 both in vivo and in vitro, confirming its role as a key downstream effector. Receiver operating characteristic (ROC) analysis showed that miR-24 had good diagnostic potential (AUC = 0.834). Overall, MiR-24 protects against MV-induced lung injury by targeting BOK and modulating key injury pathways. The miR-24/BOK axis offers a promising therapeutic avenue for ARDS-associated VILI.

Pulmonary perfusion assessment is essential for the management of chronic thromboembolic pulmonary hypertension (CTEPH). Lung perfusion scintigraphy and contrast-enhanced CT are occasionally limited by the need for radionuclides or allergy to the contrast agents. Dynamic chest radiography (DCR) can evaluate the pulmonary perfusion non-invasively using conventional X-ray technology. We validated pulmonary perfusion measurements using DCR by comparing them with those obtained using perfusion scintigraphy in CTEPH. Thirty-three patients with CTEPH who underwent both DCR and lung perfusion scintigraphy within 1-month interval from December 2019 to December 2022 were included. DCR was performed with patients in both standing and supine positions. To assess lung perfusion, each lung was divided into six fields (right and left; upper, middle, and lower). The blood flow rates per field were quantified by using analysis software as 100% of the sum of the six sites. The correlation between blood flow rates of each area in DCR and perfusion scintigraphy was evaluated using intraclass correlation coefficients (ICC). DCR showed a strong correlation with pulmonary perfusion scintigraphy in both standing (ICC(2,1) = 0.86; confidence interval [CI], 0.81-0.89) and supine (ICC(2,1) = 0.82; CI, 0.77-0.86) positions. When analyzed by region, all regions except the left lower lung showed significant correlations with perfusion scintigraphy findings. Intra- and intra-inspector reliabilities at both positions were excellent. The quantitative assessment of lung perfusion using DCR is reliable in patients with CTEPH. However, perfusion in the left lower lung was underestimated using DCR.