Pulmonary Artery Occlusion Research Articles

Assessment of fluid responsiveness as a component of hemodynamic monitoring in the operating room and intensive care unit

Fluid therapy is a critical, and often primary treatment modality in the management of various critical conditions. Like any therapeutic intervention, intravenous fluids require precise indications, contraindications, and dosing, all determined through the assessment of a patient’s volume status. Hemodynamic assessment plays a pivotal role in the treatment of critically ill patients, enabling clinicians to administer appropriate fluid therapy and cardiovascular support to optimize tissue perfusion and oxygenation. Traditional methods of assessing fluid responsiveness, which are predominantly static such as central venous pressure and pulmonary artery occlusion pressure, often fall short in their predictive accuracy under dynamic clinical conditions. Consequently, there is a growing interest in dynamic methods of fluid responsiveness assessment, which analyze cardiovascular response to specific preload changes. This literature review aims to explore various dynamic methods of hemodynamic assessment, discussing their advantages and limitations based on sources from databases like PubMed and MEDLINE.

Pulmonary hypertension induced by right pulmonary artery occlusion: Hemodynamic consequences of BMPR2 mutation

Pulmonary hypertension induced by right pulmonary artery occlusion: Hemodynamic consequences of BMPR2 mutation

Mechanical power ratio threshold for ventilator-induced lung injury

RationaleMechanical power (MP) is a summary variable incorporating all causes of ventilator-induced-lung-injury (VILI). We expressed MP as the ratio between observed and normal expected values (MPratio).ObjectiveTo define a threshold value of MPratio leading to the development of VILI.MethodsIn a population of 82 healthy pigs, a threshold of MPratio for VILI, as assessed by histological variables and confirmed by using unsupervised cluster analysis was 4.5. The population was divided into two groups with MPratio above or below the threshold.Measurements and main resultsWe measured physiological variables every six hours. At the end of the experiment, we measured lung weight and wet-to-dry ratio to quantify edema. Histological samples were analyzed for alveolar ruptures, inflammation, alveolar edema, atelectasis. An MPratio threshold of 4.5 was associated with worse injury, lung weight, wet-to-dry ratio and fluid balance (all p < 0.001). After 48 h, in the two MPratio clusters (above or below 4.5), respiratory system elastance, mean pulmonary artery pressure and physiological dead space differed by 32%, 36% and 22%, respectively (all p < 0.001), being worse in the high MPratio group. Also, the changes in driving pressure, lung elastance, pulmonary artery occlusion pressure, central venous pressure differed by 17%, 64%, 8%, 25%, respectively (all p < 0.001).LimitationsThe main limitation of this study is its retrospective design. In addition, the computation for the expected MP in pigs is based on arbitrary criteria. Different values of expected MP may change the absolute value of MP ratio but will not change the concept of the existence of an injury threshold.ConclusionsThe concept of MPratio is a physiological and intuitive way to quantify the risk of ventilator-induced lung injury. Our results suggest that a mechanical power ratio > 4.5 MPratio in healthy lungs subjected to 48 h of mechanical ventilation appears to be a threshold for the development of ventilator-induced lung injury, as indicated by the convergence of histological, physiological, and anatomical alterations. In humans and in lungs that are already injured, this threshold is likely to be different.

Pulmonary Hypertension Induced by Right Pulmonary Artery Occlusion: Hemodynamic Consequences of Bmpr2 Mutation.

The primary genetic risk factor for heritable pulmonary arterial hypertension is the presence of monoallelic mutations in the BMPR2 gene. The incomplete penetrance of BMPR2 mutations implies that additional triggers are necessary for pulmonary arterial hypertension occurrence. Pulmonary artery stenosis directly raises pulmonary artery pressure, and the redirection of blood flow to unobstructed arteries leads to endothelial dysfunction and vascular remodeling. We hypothesized that right pulmonary artery occlusion (RPAO) triggers pulmonary hypertension (PH) in rats with Bmpr2 mutations. Male and female rats with a 71 bp monoallelic deletion in exon 1 of Bmpr2 and their wild-type siblings underwent acute and chronic RPAO. They were subjected to full high-fidelity hemodynamic characterization. We also examined how chronic RPAO can mimic the pulmonary gene expression pattern associated with installed PH in unobstructed territories. RPAO induced precapillary PH in male and female rats, both acutely and chronically. Bmpr2 mutant and male rats manifested more severe PH compared with their counterparts. Although wild-type rats adapted to RPAO, Bmpr2 mutant rats experienced heightened mortality. RPAO induced a decline in cardiac contractility index, particularly pronounced in male Bmpr2 rats. Chronic RPAO resulted in elevated pulmonary IL-6 (interleukin-6) expression and decreased Gdf2 expression (corrected P value<0.05 and log2 fold change>1). In this context, male rats expressed higher pulmonary levels of endothelin-1 and IL-6 than females. Our novel 2-hit rat model presents a promising avenue to explore the adaptation of the right ventricle and pulmonary vasculature to PH, shedding light on pertinent sex- and gene-related effects.

Guidelines for the diagnosis and treatment of chronic thromboembolic pulmonary hypertension (2024 edition)

Chronic thromboembolic pulmonary hypertension (CTEPH) is classified as group 4 pulmonary hypertension, characterized by pulmonary arterial thrombotic occlusion leading to vascular stenosis or obstruction, progressive elevation of pulmonary vascular resistance and pulmonary arterial pressure, ultimately leading to right heart failure and even death. Recent years have seen rapid progress in the diagnostic and therapeutic in CTEPH field. More and more patients with CTEPH have been accurately diagnosed and assessed in time. Nevertheless, there is still a lot of work to do in the popularization of CTEPH diagnostic and therapeutic technique and the building of CTEPH expert center. To better guide clinical practice in our country, Pulmonary Embolism & Pulmonary Vascular Diseases Group of the Chinese Thoracic Society, Pulmonary Embolism & Pulmonary Vascular Disease Working Group of Chinese Association of Chest Physicians, National Cooperation Group on Prevention & Treatment of Pulmonary Embolism & Pulmonary Vascular Disease, National Expert Panel on the Development of a Standardized Framework for Pulmonary Arterial Hypertension, convened multidisciplinary experts for deliberation and Delphi expert consensus to develop the "Guidelines for the Diagnosis and Treatment of Chronic Thromboembolic Pulmonary Hypertension (2024 edition) ". These guidelines systematically evaluate domestic and international evidence-based medical research on CTEPH and propose recommendations tailored to clinical practice in our country. The key areas covered include definitions, epidemiology, pathogenesis, diagnosis and assessment, treatment, and management, with the aim of further standardizing the clinical diagnosis and treatment of CTEPH in our country.

Mycoplasma pneumoniae pneumonia-associated thromboembolism with plastic bronchitis: a series of five case reports and literature review

BackgroundMycoplasma pneumoniae pneumonia is a common respiratory infection among children. However, the occurrence of thromboembolism with plastic bronchitis in association with Mycoplasma pneumoniae pneumonia is extremely rare. This case series presents five cases of children with Mycoplasma pneumoniae pneumonia who developed thromboembolism and plastic bronchitis. The clinical presentation, diagnostic approach, and management strategies are discussed.MethodsA retrospective analysis was conducted on medical records from a pediatric hospital. Patient demographics, clinical features, laboratory findings, imaging results, treatment modalities, and outcomes were collected.ResultsThe patients in our case series presented with varying degrees of respiratory distress, cough, and fever. Imaging studies revealed evidence of thromboembolism based on pulmonary artery occlusion. Bronchial casts were observed by bronchoscopy. Laboratory tests demonstrated elevated D-dimer levels and fibrinogen degradation products. All patients received a combination of low molecular weight heparin anticoagulation and supportive care.ConclusionThromboembolism with plastic bronchitis associated with Mycoplasma pneumoniae pneumonia is a rare but potentially serious complication in children. Prompt recognition and management are crucial for improving patient outcomes. This case series highlights the diverse clinical presentations, diagnostic challenges, and treatment strategies for this unique clinical entity. Further research is needed to better understand the pathogenesis and optimal management of this condition.

An Enhanced Mask R-CNN Approach for Pulmonary Embolism Detection and Segmentation.

Pulmonary embolism (PE) refers to the occlusion of pulmonary arteries by blood clots, posing a mortality risk of approximately 30%. The detection of pulmonary embolism within segmental arteries presents greater challenges compared with larger arteries and is frequently overlooked. In this study, we developed a computational method to automatically identify pulmonary embolism within segmental arteries using computed tomography (CT) images. The system architecture incorporates an enhanced Mask R-CNN deep neural network trained on PE-containing images. This network accurately localizes pulmonary embolisms in CT images and effectively delineates their boundaries. This study involved creating a local data set and evaluating the model predictions against pulmonary embolisms manually identified by expert radiologists. The sensitivity, specificity, accuracy, Dice coefficient, and Jaccard index values were obtained as 96.2%, 93.4%, 96.%, 0.95, and 0.89, respectively. The enhanced Mask R-CNN model outperformed the traditional Mask R-CNN and U-Net models. This study underscores the influence of Mask R-CNN's loss function on model performance, providing a basis for the potential improvement of Mask R-CNN models for object detection and segmentation tasks in CT images.

Cardiopulmonary effects of apneustic anesthesia ventilation in anesthetized pigs: a new mode of ventilation for anesthetized veterinary species

ObjectiveTo compare the cardiopulmonary effects of apneustic anesthesia ventilation (AAV) and conventional mechanical ventilation (CMV) in anesthetized pigs and to describe a new mode of ventilation for anesthetized veterinary species.Study designRandomized, crossover design without washout.AnimalsTwelve healthy, female white Landrace pigs.MethodsFollowing ketamine-midazolam premedication and anesthetic induction with propofol, the trachea was intubated, and each pig was positioned in dorsal recumbency. Anesthesia was maintained with propofol and sufentanil infusions. Pigs were instrumented and their lungs were sequentially ventilated with each mode, in random order, for 1 h according to predefined criteria [fraction of inspired oxygen (FiO2) = 0.21, 10 mL kg−1 tidal volume (VT), and arterial carbon dioxide tension (PaCO2) within 40–45 mmHg]. Cardiopulmonary data were collected at baseline, 30 and 60 min. In 8 pigs, thoracic computed tomography (CT) was performed following the 60 min time point for each mode of ventilation and images were analyzed to quantify lung aeration. The effects of ventilation mode, time, and order were analyzed using repeated measures ANOVA. Paired t-tests were used to compare lung aeration between modes. Significance was defined as p &amp;lt; 0.05.ResultsData from 12 pigs were analyzed. A significant effect of mode was found for heart rate, mean arterial pressure (MAP), pulmonary artery occlusion pressure, cardiac index (CI), stroke volume index, systemic vascular resistance, pulmonary vascular resistance, oxygen delivery index (DO2I), oxygen extraction ratio (O2ER), VT, arterial oxygen tension, arterial hemoglobin saturation, PaCO2, end-tidal carbon dioxide tension, alveolar dead space (VDalv/VTalv), venous admixture (Q.s/Q.t), mean airway pressure, and dynamic compliance index (CRSI). Order effects were also observed for some cardiovascular and respiratory variables. For the eight pigs that underwent thoracic CT, AAV resulted in significantly larger proportions of normally and hyperaerated lung while CMV resulted in larger proportions of hypoaerated and atelectatic lung.ConclusionsIn dorsally recumbent anesthetized pigs, ventilated with FiO2 = 0.21, both modes of ventilation supported adequate oxygenation while AAV resulted in higher CRSI, and lower VDalv/VTalv and Q.s/Q.t, compared with CMV. AAV was also associated with lower MAP, CI, and DO2I and higher O2ER compared with CMV. Further investigation of AAV in anesthetized animals is warranted.

Clinical Characteristics and Prognoses of Mucormycosis in Four Children.

Mucormycosis is a fatal invasive fungal infection that commonly affects immunocompromised children. The aim of our study was to investigate the clinical manifestations, treatments, and prognosis of pediatric patients with mucormycosis. We conducted a retrospective search in Shenzhen Children's Hospital from July 2013 to July 2023 for all patients with mucormycosis. The clinical manifestation, pathogen detection, radiology, treatments, and prognosis were analyzed. Four cases were identified. Underlying conditions included acute myeloid leukemia with myeloid sarcoma (n = 1), thalassemia (post-allogeneic hematopoietic stem cell transplantation; n = 1), systemic lupus erythematosus (n = 1), and bilateral nephroblastoma (post-bilateral nephrectomy; n = 1). Two patients were disseminated mucormycosis, one case was pulmonary mucormycosis, and one case was cerebral mucormycosis. Fever, cough, and dyspnea were the main clinical symptoms of pulmonary mucormycosis, headache was the main clinical symptom of cerebral mucormycosis. Lung CT findings included consolidation, multiple nodules, halo sign, air crescent sign, and pleural effusion. The contrast-enhanced CT showed pulmonary artery and pulmonary vein occlusions in two patients and pseudoaneurysm in two patients. Amphotericin B formulations were administered as first-line therapy in all cases; in three cases, Triazole was administered in combination with amphotericin B. Mucormycosis is a life-threatening disease involving multiple systems. Aorta pseudoaneurysm is a rare and fatal complication, enhanced CT can assist in diagnosis. Early diagnosis and appropriate therapeutic strategies are needed.

Intrinsic mechanisms of right ventricular autoregulation

To elucidate the adaptation of the right ventricle to acute and intermittently sustained afterload elevation, targeted preload reductions and afterload increases were implemented in a porcine model involving 12 pigs. Preload reduction was achieved via balloon occlusion of the inferior vena cava before, immediately and 5 min after acute afterload elevation induced by pulmonary artery occlusion or thromboxane A2 analog (U46619) infusion. Ventricular response was monitored by registration of pressure–volume (PV) loops using a conductance catheter. The end-systolic pressure–volume relationship (ESPVR) during pure preload reduction was adequately described by linear regression (mean and SEM slope of ESPVR (Ees) 0.414 ± 0.064 mmHg/ml), reflecting the classical Frank-Starling mechanism (FSM). The ESPVR during acute afterload elevation exhibited a biphasic trajectory with significantly distinct slopes (mean and SEM Ees bilin1: 1.256 ± 0.066 mmHg ml; Ees bilin2: 0.733 ± 0.063 mmHg ml, p < 0.001). The higher slope during the first phase in the absence of ventricular dilation could be explained by a reduced amount of shortening deactivation (SDA). The changes in PV-loops during the second phase were similar to those observed with a preload intervention. The persistent increase in afterload resulted in an increase in the slopes of ESPVR and preload recruitable stroke work (PRSW) with a slight decrease in filling state, indicating a relevant Anrep effect. This effect became more pronounced after 5 min or TXA infusion. This study demonstrates, for the first time, the relevance of intrinsic mechanisms of cardiac autoregulation in the right ventricle during the adaptation to load. The SDA, FSM, and Anrep effect could be differentiated and occurred successively, potentially with some overlap. Notably, the Anrep effect serves to prevent ventricular dilation.

Epidemiology, Etiology, and Pathophysiology of Pulmonary Embolism

AbstractOver the last 20 years, there has been a progressive increase in the incidence of pulmonary embolism (PE) diagnosis in the United States, Europe, and Australia. Increased use of computed tomography pulmonary angiography has likely contributed in part to this rising incidence. However, it is pertinent to note that the burden of comorbidities associated with PE, such as malignancy, obesity, and advanced age, has also increased over the past 20 years. Time-trend analysis in North American, European, and Asian populations suggests that mortality rates associated with PE have been declining. The reported improved survival rates in PE over the past 20 years are likely, at least in part, to be the result of better adherence to guidelines, improved risk stratification, and enhanced treatment. Factors contributing to the development of venous thromboembolism (VTE) include stasis of blood, hypercoagulability, endothelial injury, and inflammation. In 70 to 80% of cases of PE, the thrombi embolizes from the proximal deep veins of the lower extremities and pelvis. Strong risk factors for VTE include lower extremity fractures and surgeries, major trauma, and hospitalization within the previous 3 months for acute myocardial infarction or heart failure with atrial fibrillation. Acute PE causes several pathophysiological responses including hypoxemia and right ventricle (RV) failure. The latter is a result of pulmonary artery occlusion and associated vasoconstriction. Hemodynamic compromise from RV failure is the principal cause of poor outcome in patients with acute PE.

IL-6/gp130 signaling in CD4+ T cells drives the pathogenesis of pulmonary hypertension

Pulmonary arterial hypertension (PAH) is characterized by stenosis and occlusions of small pulmonary arteries, leading to elevated pulmonary arterial pressure and right heart failure. Although accumulating evidence shows the importance of interleukin (IL)-6 in the pathogenesis of PAH, the target cells of IL-6 are poorly understood. Using mice harboring the floxed allele of gp130, a subunit of the IL-6 receptor, we found substantial Cre recombination in all hematopoietic cell lineages from the primitive hematopoietic stem cell level in SM22α-Cre mice. We also revealed that a CD4+ cell-specific gp130 deletion ameliorated the phenotype of hypoxia-induced pulmonary hypertension in mice. Disruption of IL-6 signaling via deletion of gp130 in CD4+ T cells inhibited phosphorylation of signal transducer and activator of transcription 3 (STAT3) and suppressed the hypoxia-induced increase in T helper 17 cells. To further examine the role of IL-6/gp130 signaling in more severe PH models, we developed Il6 knockout (KO) rats using the CRISPR/Cas9 system and showed that IL-6 deficiency could improve the pathophysiology in hypoxia-, monocrotaline-, and Sugen5416/hypoxia (SuHx)-induced rat PH models. Phosphorylation of STAT3 in CD4+ cells was also observed around the vascular lesions in the lungs of the SuHx rat model, but not in Il6 KO rats. Blockade of IL-6 signaling had an additive effect on conventional PAH therapeutics, such as endothelin receptor antagonist (macitentan) and soluble guanylyl cyclase stimulator (BAY41-2272). These findings suggest that IL-6/gp130 signaling in CD4+ cells plays a critical role in the pathogenesis of PAH.

The biased apelin receptor agonist, MM07, reverses Sugen/hypoxia-induced pulmonary arterial hypertension as effectively as the endothelin antagonist macitentan.

Introduction: Pulmonary arterial hypertension (PAH) is characterised by endothelial dysfunction and pathological vascular remodelling, resulting in the occlusion of pulmonary arteries and arterioles, right ventricular hypertrophy, and eventually fatal heart failure. Targeting the apelin receptor with the novel, G protein-biased peptide agonist, MM07, is hypothesised to reverse the developed symptoms of elevated right ventricular systolic pressure and right ventricular hypertrophy. Here, the effects of MM07 were compared with the clinical standard-of-care endothelin receptor antagonist macitentan. Methods: Male Sprague-Dawley rats were randomised and treated with either normoxia/saline, or Sugen/hypoxia (SuHx) to induce an established model of PAH, before subsequent treatment with either saline, macitentan (30mg/kg), or MM07 (10mg/kg). Rats were then anaesthetised and catheterised for haemodynamic measurements, and tissues collected for histopathological assessment. Results: The SuHx/saline group presented with significant increases in right ventricular hypertrophy, right ventricular systolic pressure, and muscularization of pulmonary arteries compared to normoxic/saline controls. Critically, MM07 was as at least as effective as macitentan in significantly reversing detrimental structural and haemodynamic changes after 4weeks of treatment. Discussion: These results support the development of G protein-biased apelin receptor agonists with improved pharmacokinetic profiles for use in human disease.

Predominance of M2 macrophages in organized thrombi in chronic thromboembolic pulmonary hypertension patients.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a debilitating disease characterized by thrombotic occlusion of pulmonary arteries and vasculopathy, leading to increased pulmonary vascular resistance and progressive right-sided heart failure. Thrombotic lesions in CTEPH contain CD68+ macrophages, and increasing evidence supports their role in disease pathogenesis. Macrophages are classically divided into pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages, which are involved in wound healing and tissue repair. Currently, the phenotype of macrophages and their localization within thrombotic lesions of CTEPH are largely unknown. In our study, we subclassified thrombotic lesions of CTEPH patients into developing fresh thrombi (FT) and organized thrombi (OT), based on the degree of fibrosis and remodeling. We used multiplex immunofluorescence histology to identify immune cell infiltrates in thrombotic lesions of CPTEH patients. Utilizing software-assisted cell detection and quantification, increased proportions of macrophages were observed in immune cell infiltrates of OT lesions, compared with FT. Strikingly, the proportions with a CD206+INOS- M2 phenotype were significantly higher in OT than in FT, which mainly contained unpolarized macrophages. Taken together, we observed a shift from unpolarized macrophages in FT toward an expanded population of M2 macrophages in OT, indicating a dynamic role of macrophages during CTEPH pathogenesis.

Carlino-Like Technique for Retrograde Recanalization of Chronic Thromboembolic Pulmonary Artery Occlusion

Carlino-Like Technique for Retrograde Recanalization of Chronic Thromboembolic Pulmonary Artery Occlusion

Chronic left pulmonary artery occlusion caused by a distal aortic arch aneurysm: Simultaneous Frozen Elephant Trunk and left sided pulmonary endarterectomy after livesaving TEVAR for aortic rupture

We present a case of a 62-year-old male patient with chronic distal aortic arch aneurysm causing recurrent nerve palsy and prolonged total occlusion of the left main pulmonary artery (PA). During diagnostic work up, the aneurysm ruptured requiring cardio-pulmonary resuscitation (CPR) and emergency retrograde stenting. After circulatory stabilization the patient was treated with controlled hypothermia for 24 h, and successive extubation without neurological deficit.Postinterventional imaging revealed a reversed perfusion of the aneurysmal sac through the PA, prompting open surgical treatment. Surgery consisted of reconstruction of the left PA by pulmonary endarterectomy (PEA), xenopericardial patchplasty of the left PA and frozen elephant trunk (FET) repair after removal of the bare springs of the previously inserted Gore Tag stent graft. Pre-discharge computed tomography angiography (CTA) demonstrated a fully recanalized left PA system and a completely excluded aneurysm. At ten-year follow-up the patient presented physically unimpaired (NYHA I). CTA confirmed a fully intact thoracic aorta and improved pulmonary function despite persisting left recurrent nerve palsy.

Cardiac Magnetic Resonance Studies in a Large Animal Model that Simulates the Cardiac Abnormalities of Human Septic Shock.

Septic shock, in humans and in our well-established animal model, is associated with increases in biventricular end diastolic volume (EDV) and decreases in ejection fraction (EF). These abnormalities occur over 2 days and reverse within 10 days. Septic non-survivors do not develop an increase in EDV. The mechanism for this cardiac dysfunction and EDV differences is unknown. Purpose-bred beagles randomized to receive intrabronchial Staphylococcus aureus (n=27) or saline (n=6) were provided standard ICU care including sedation, mechanical ventilation, and fluid resuscitation to a pulmonary arterial occlusion pressure of over 10mmHg. No catecholamines were administered. Over 96h, cardiac magnetic resonance imaging, echocardiograms, and invasive hemodynamics were serially performed, and laboratory data was collected. Tissue was obtained at 66h from six septic animals. From 0-96h after bacterial challenge, septic animals vs. controls had significantly increased left ventricular wall edema (6%) and wall thinning with loss of mass (15%) which was more pronounced at 48h in non-survivors than survivors. On histology, edema was located predominantly in myocytes, the interstitium, and endothelial cells. Edema was associated with significantly worse biventricular function (lower EFs), ventricular-arterial coupling, and circumferential strain. In septic animals, from 0-24h, the EDV decreased from baseline and, despite cardiac filling pressures being similar, decreased significantly more in non-survivors. From 24-48h, all septic animals had increases in biventricular chamber sizes. Survivors biventricular EDVs were significantly greater than baseline and in non-survivors, where biventricular EDVs were not different from baseline. Preload, afterload, or HR differences did not explain these differential serial changes in chamber size. Systolic and diastolic cardiac dysfunction during sepsis is associated with ventricular wall edema. Rather than differences in preload, afterload, or heart rate, structural alterations to the ventricular wall best account for the volume changes associated with outcome during sepsis. In non-survivors, from 0-24h, sepsis induces a more severe diastolic dysfunction, further decreasing chamber size. The loss of left ventricular mass with wall thinning in septic survivors may, in part explain, the EDV increases from 24-48h. However, these changes continued and even accelerated into the recovery phase consistent with a reparative process rather than ongoing injury.

Modified Starnes Procedure With Patch Occlusion of the Main Pulmonary Artery and Other Technical Modifications to Facilitate Subsequent Biventricular Repair of Ebstein Anomaly

The Starnes procedure, introduced in 1991, has been a valuable advancement in the surgical treatment of critically ill neonates with Ebstein's anomaly (EA). However, it used to be followed by the single ventricle pathway, which presents long-term outcome limitations. In 2019, this management concept was modified by taking down the Starnes procedure and performing the Cone repair of the tricuspid valve, which resulted in a biventricular reconstruction. This approach rehabilitates the right ventricle, likely improving the patients' long-term outcomes. However, it requires modifications in the classical Starnes operation and observing certain surgical details. In cases of circular shunting, we use a patch to occlude the pulmonary artery instead of dividing and oversewing it, simplifying the succeeding pulmonary artery reconstruction. We use a PTFE fenestrated patch placed in a supra-valvar position, preserving the underneath tricuspid valve integrity, facilitating the tricuspid valve repair, and decreasing the possibility of heart block.Central message: In the current era of biventricular repair after the Starnes procedure, using a non-stick supravalvar patch to exclude the tricuspid valve and preserving the pulmonary valve structure by patch occlusion of the main pulmonary artery instead of division and oversewing it are valuable modifications of the classic Starnes operation to optimize a future biventricular repair.

Unilateral Lung Removal in Combination with Monocrotaline or SU5416 in Rodents: A Reliable Model to Mimic the Pathology of the Human Pulmonary Hypertension.

Pulmonary hypertension (PH) is a chronic and progressive disorder characterized by elevated mean pulmonary arterial pressure, pulmonary vascular remodeling, and the development of concentric laminar intimal fibrosis with plexiform lesions. While rodent models have been developed to study PH, they have certain deficiencies and do not entirely replicate the human disease due to the heterogeneity of PH pathology. Therefore, combined models are necessary to study PH. Recent studies have shown that altered pulmonary blood flow is a significant trigger in the development of vascular remodeling and neointimal lesions. One of the most promising rodent models for increased pulmonary flow is the combination of unilateral left pneumonectomy with a "second hit" of monocrotaline (MCT) or SU5416. The removal of one lung in this model forces blood to circulate only in the other lung and induces increased and turbulent pulmonary blood flow. This increased vascular flow leads to progressive remodeling and occlusion of small pulmonary arteries. The second hit by MCT or SU5416 leads to endothelial cell dysfunction, resulting in severe PH and the development of plexiform arteriopathy.

Embolic Occlusion of Pulmonary Artery by Extended Floating Clots as the most Severe Variant of Venous Thromboembolism

Embolic Occlusion of Pulmonary Artery by Extended Floating Clots as the most Severe Variant of Venous Thromboembolism