Pulmonary Arterial Circulation Research Articles

Focal alveolar hemorrhage following guide-wire progression into the pulmonary arterial circulation during fibrin sheath angioplasty and catheter exchange: Case report.

Central venous catheters are a frequently used vascular access for hemodialysis. Fibrin sheath formation is a common complication and is associated with catheter malfunction. Although fibrin sheath angioplasty with catheter exchange is a frequently employed procedure, it can be associated with mechanical complications. An important technical step in this procedure is progression of the guide-wire into the inferior vena cava. Focal alveolar hemorrhage is a very rare complication of this procedure. We report a case of a 70-year old patient on dual antiplatelet therapy who underwent fibrin sheath angioplasty with guide-wire catheter exchange and experienced focal alveolar hemorrhage presenting as hemoptysis and acute type 1 respiratory failure. Progression of the guide-wire into the pulmonary circulation and antithrombotic therapy played a significant role in the development of this complication. This report aims to call attention to a poorly described and potentially serious yet avoidable complication of fibrin sheath angioplasty with guide-wire catheter exchange.

Microcomputed tomography visualization and quantitation of the pulmonary arterial microvascular tree in mouse models of chronic lung disease.

Pulmonary vascular dysfunctionis characterized by remodeling and loss of microvessels in the lung and is a major manifestation of chronic lung diseases (CLD). In murine models of CLD, the small arterioles and capillaries are the first and most prevalent vessels that are affected by pruning and remodeling. Thus, visualization of the pulmonary arterial vasculature in three dimensions is essential to define pruning and remodeling both temporally and spatially and its role in the pathogenesis of CLD, aging, and tissue repair. To this end, we have developed a novel method to visualize and quantitate the murine pulmonary arterial circulation using microcomputed tomography(µCT) imaging. Using this perfusion technique, we can quantitate microvessels to approximately 6 µM in diameter. We hypothesize that bleomycin-induced injury would have a significant impact on the arterial vascular structure. As proof of principle, we demonstrated that as a result of bleomycin-induced injury at peak fibrosis, significant alterations in arterial vessel structure were visible in the three-dimensional models as well as quantification. Thus, we have successfully developed a perfusion methodology and complementary analysis techniques, which allows for the reconstruction, visualization, and quantitation of the mouse pulmonary arterial microvasculature in three-dimensions. This tool will further support the examination and understanding of angiogenesis during the development of CLD as well as repair following injury.

Advanced imaging in an adult dog with anomalous origin of the left coronary artery from the pulmonary artery and extensive collateral coronary circulation

A three-year-old, spayed female, Bichon Frise was diagnosed with an anomalous origin of the left coronary artery from the pulmonary artery, a rare congenital coronary artery defect which has only been reported in two other dogs. Echocardiography was initially performed, though the final diagnosis was made with angiography and computed tomography angiography. An extensive network of collateral coronary circulation allowed for communication between the dilated, tortuous right coronary artery, and the anomalous left coronary artery. Though collateral circulation likely prolonged the patient's life, it is suspected that coronary steal phenomenon and chronic myocardial ischemia ultimately led to fatal ventricular arrhythmias. The dog died suddenly at the age of six, three years after initial diagnosis.

Novel concepts of treating vascular inflammation underlying neonatal lung diseases.

Bronchopulmonary dysplasia (BPD) is the most common sequela of prematurity. While multifactorial in aetiology, there is increasing evidence that fetal growth restriction (FGR) and antenatal exposure of the fetus to inflammation play important roles in the postnatal pathophysiology of BPD. Recent studies have focussed on disrupted angiogenesis and its influence on alveolarization. While there are multiple mechanistic links, inflammation is known to be a key driver of this disruption, affecting pulmonary arterial circulation. Although postnatal corticosteroids are commonly used in extremely premature infants to treat inflammation, aimed at obviating the need for intubation and mechanical ventilation or to facilitate extubation, the use of dexamethasone has not reduced the incidence of BPD. Here, we summarize current knowledge on alternative anti-inflammatory treatment options, which have shown promising outcomes either pre-clinically or clinically. These include supplementation with vitamin C and E (antioxidants), ω-3 poly-unsaturated fatty acids, pentoxifylline, anti-inflammatory cytokines of the IL (interleukin)-1 family, namely IL-1 receptor antagonist and IL-37, and the beneficial properties of breast milk. Evaluating these alternative treatments, either individually or as combination therapies in randomized controlled trials stands to immensely benefit the clinical outlook, particularly regarding BPD, for extremely premature infants.

Pulmonary artery pulsatility index in patients with tricuspid valve regurgitation: a simple non-invasive tool for risk stratification.

Tricuspid valve regurgitation (TR) is a common valvular disease associated with increased mortality. There is a need for tools to assess the interaction between the pulmonary artery (PA) circulation and the right ventricle in patients with TR and to investigate their association with outcomes. The pulmonary artery pulsatility index (PAPi) has emerged as a haemodynamic risk predictor in left heart disease and pulmonary hypertension (PH). Whether PAPi discriminates risk in unselected patients with greater than or equal to moderate TR is unknown. In 5079 patients with greater than or equal to moderate TR (regardless of aetiology) and PA systolic and diastolic pressures measured on their first echocardiogram, we compared all-cause mortality at 5 years based on the presence or absence of PH and PAPi levels. A total of 2741 (54%) patients had PH. The median PAPi was 3.0 (IQR 1.9, 4.4). Both the presence of PH and decreasing levels of PAPi were associated with larger right ventricles, worse right ventricular systolic function, higher NT-pro BNP levels, greater degrees of right heart failure, and worse survival. In a subset of patients who had an echo and right heart catheterization within 24 h, the correlation of non-invasive to invasive PA pressures and PAPi levels was very good (r = 0.76). In patients with greater than or equal to moderate TR with and without PH, lower PAPi is associated with right ventricular dysfunction, right heart failure, and worse survival. Incorporating PA pressure and PAPi may help stratify disease severity in patients with greater than or equal to moderate TR regardless of aetiology.

Safety of Transbronchial Biopsies in Patients with Pulmonary Hypertension: Systematic Review and Meta-Analysis.

Rationale: Transbronchial lung biopsies (TBLBs) are commonly performed by pulmonologists. Most providers consider pulmonary hypertension to be at least a relative contraindication to TBLB. This practice is based primarily on expert opinion, as there are very few patient outcomes data backing it. Objectives: We performed a systematic review and meta-analysis of previously published studies to determine the safety of TBLB in patients with pulmonary hypertension. Methods: The MEDLINE, Embase, Scopus, and Google Scholar databases were searched for pertinent studies. The quality of the included studies was assessed using the Newcastle-Ottawa Scale. Meta-analysis was performed using MedCalc version 20.118 to calculate the weighted pooled relative risk of complications in patients with pulmonary hypertension. Results: Nine studies with a total of 1,699 patients were included in the meta-analysis. On the basis of the Newcastle-Ottawa Scale, the risk of bias was low in the included studies. The overall weighted relative risk of bleeding with TBLB in patients with pulmonary hypertension was 1.01 (95% confidence interval, 0.71-1.45) compared with patients without pulmonary hypertension. Heterogeneity was low; therefore, the fixed-effects model was used. In a subgroup analysis of three studies, the overall weighted relative risk of significant hypoxia in patients with pulmonary hypertension was 2.06 (95% confidence interval, 1.12-3.76). Conclusions: Our results show that the patients with pulmonary hypertension do not have a significantly elevated risk of bleeding with TBLB compared with control subjects. We hypothesize that significant postbiopsy bleeding might be preferentially originating from bronchial artery circulation as opposed to pulmonary artery circulation, much like episodes of massive spontaneous hemoptysis. This hypothesis can explain our results, as in this scenario, elevated pulmonary arterial pressure would not be expected to have a bearing on the risk of post-TBLB bleeding. Most of the studies in our analysis included patients with mild to moderate pulmonary hypertension and it is not clear if our results can be extrapolated to patients with severe pulmonary hypertension. We noted that the patients with pulmonary hypertension were at a higher risk of developing hypoxia and needing a longer duration of mechanical ventilation with TBLB compared with control subjects. Further studies are needed to better understand the origin and pathophysiology of post-TBLB bleeding.

Ruptured pulmonary artery pseudoaneurysm treated with stent graft: case report and literature review

BackgroundHemoptysis is a severe condition, associated with a high mortality rate from asphyxiation. Less than 5% of cases come from the pulmonary arterial circulation and large pseudoaneurysm are rarely treatable by stent graft.Case presentationWe present the case of a 74-year-old man who suffered from a new onset of hemoptysis despite a prior bronchial artery embolization. He underwent a rescue endovascular stent graft placement for a massive hemoptysis caused by a ruptured proximal pulmonary artery pseudoaneurysm. A short review of similar situations is provided.ConclusionSalvage endovascular stent graft placement for a massive hemoptysis caused by a ruptured proximal pulmonary artery pseudoaneurysm is a viable salvage technique for life-threatening hemoptysis.

Abstract 9548: Dual Energy Computed Tomography Perfusion Mapping of Coronary to Pulmonary Collaterals in Chronic Thromboembolic Pulmonary Hypertension

Introduction: Chronic thromboembolic pulmonary hypertension (CTEPH) is classified as group 4 pulmonary hypertension where unresolved thromboembolic disease obstructs the pulmonary artery. The resultant lung ischemia commonly leads to bronchopulmonary collateralization thought to lower pulmonary vascular resistance and reduce mortality. Here, we present a rare presentation of coronary-pulmonary collaterals in a 65-year-old former 40-pack year smoker with CTEPH, COPD requiring oxygen, AF, and DHF. Results: Dual-energy computed tomography (DECT) showed complete occlusion of the proximal right pulmonary artery. However, perfused blood volume (PBV) mapping of the DECT study revealed areas of the right lung that were still minimally perfused (Figure 1A, B). Pulmonary angiography confirmed occlusion of the right pulmonary artery (1C) . Subsequent coronary angiography revealed the presence of coronary to pulmonary collaterals that were providing limited perfusion to the right pulmonary circulation from the left circumflex artery (1D) . The patient underwent pulmonary thromboendarterectomy with removal of the clot en bloc without complication (1E) . Post-surgery DECT confirmed restoration of pulmonary arterial circulation and catheterization revealed an excellent hemodynamic response to surgery (1F, G) . Conclusions: DECT-derived PBV revealed significant perfusion to a proximally obstructed lung, hastening the discovery of rarely documented coronary-pulmonary artery collaterals via coronary angiography. We uniquely visualize via perfusion mapping that the collaterals provide an alternate vascular supply distal to the chronic pulmonary arterial obstruction until thromboendarterectomy can conclusively treat the occlusion. The presence of coronary-pulmonary collaterals may share similar pathophysiology to bronchial-pulmonary collaterals and be a positive prognosticator for robust post-operative hemodynamic improvement in CTEPH.

Pharmacological counseling in hepatotoxicity induced by macitentan and selexipag: a case report

BackgroundPulmonary arterial hypertension is a progressive, debilitating condition characterized by increased resistance in the pulmonary arterial circulation. Current treatments for pulmonary arterial hypertension include endothelin receptor antagonists such as bosentan, sitaxentan, ambrisentan, macitentan, and oral prostacyclin receptor agonists such as selexipag. Endothelin receptor antagonists have been associated with liver injury, while hepatotoxicity was not reported for selexipag. Although genetic variability has been indisputably associated with variability in drug response, no study has been designed until now to assess its effects on the pharmacokinetics of endothelin receptor antagonists or selexipag.Case presentationWe report the case of a 58-year-old female Caucasian patient with a dramatic increase in plasma levels of transaminases after treatment with macitentan and selexipag, drugs whose risk of causing liver injury has so far been considered limited. After therapy discontinuation, plasma levels of transaminases returned to baseline, thus suggesting a role of these drugs in the observed hepatotoxicity. After pharmacological counseling, we decided to introduce ambrisentan for the patient’s treatment. After 7 months of treatment, no liver injury has been reported. To evaluate the role of genetic factors in the observed hepatotoxicity, we genotyped the patient for single-nucleotide polymorphisms previously associated with macitentan, ambrisentan, or selexipag metabolism. We found a genetic profile associated with a poor metabolizer (PM) phenotype for CYP2C8 and CYP2C9, key enzymes for elimination of both macitentan and selexipag. The reported results suggest that an allelic profile associated with low activity for CYP2C8 and CYP2C9 enzyme could be a potential risk factor for macitentan and selexipag-induced liver injury and could provide a possible marker for early identification of subjects at higher risk of developing hepatotoxicity.ConclusionsA multidisciplinary approach based on clinical evaluation, as well as pharmacological counseling and evaluation of the patient’s genetic profile, might be useful for identification of patients with a high chance of drug-induced liver injury, avoiding unnecessary risks in therapy selection and prescription.

Interventional treatment of pulmonary embolism - where do we currently stand?

Acute pulmonary embolism is the third most common cause of cardiovascular mortality in the world. The sudden pressure overload of the right ventricle, caused by the thrombotic masses in the pulmonary artery, may quickly progress to profound cardiogenic shock. That results in a mortality rate of more than 50% in patients with a massive form of pulmonary embolism. In such cases, systemic fibrinolysis is warranted, which leads to rapid improvement of the right ventricular function and hemodynamic stabilization. The thrombolytic effect of systemic fibrinolysis is, unfortunately, accompanied by an almost 5 times increased risk of bleeding, especially intracranial one. Therefore, in most cases, for patients with uncompromised hemodynamics, only anticoagulation treatment is offered. Interventional treatment of acute pulmonary embolism consists of the usage of very low-dose fibrinolytic devices or percutaneous thrombus aspiration devices. The goal is to provide rapid removal of the thrombotic masses from the pulmonary artery circulation while keeping the hemorrhagic risk at a minimum. This paper will try to provide a concise review of the most widely used and available devices, together with the latest clinical data, supporting their use. Also, the future perspectives in the field of endovascular treatment of acute pulmonary embolism will be presented.

P157 THE UNFORESEEABLE LINK: A CASE OF CORONARY–PULMONARY ARTERY FISTULA BRIDGING THE RIGHT CORONARY AND FIRST SEPTAL BRANCH OF THE LEFT ANTERIOR DESCENDING ARTERY

Abstract Coronary–pulmonary artery fistulas are a rare clinical entity with a variety of potential clinical manifestations. Albeit rare, such anomalies may in some instances involve multiple coronary arteries and go unnoticed until old age producing little to no clinical manifestations. We hereby present the case of an 83–year–old man, heavy smoker, with a history of cor pulmonale due to severe chronic obstructive pulmonary disease (COPD) who was recently diagnosed with metastatic lung adenocarcinoma. Incidentally, one of the ECGs performed revealed negative T waves in the precordial leads in the absence of symptoms and with a negative troponin curve. Echocardiography was thus performed and revealed severe left ventricular systolic dysfunction (EF 31%) with infero–postero–lateral akinesia. The patient underwent CT coronary angiogram, which ruled out any significant coronary stenosis but revealed a most surprising finding. An ectatic arterial branch running anteriorly and draining into the pulmonary artery connected the the proximal segment of the right coronary artery to the first septal branch of the left anterior descending (LAD) artery. Unfortunately, the severe left ventricular failure contraindicated any chemotherapy and the patient was discharged with a plan to start palliative radiotherapy. Three months later, the patient returned to our Hospital due to worsening weakness, cachexia and one episode of pre–sincope. During this hospital stay, he developed atypical chest pain with a significant troponin curve. A HRCT and pulmonary angiogram was performed, which revealed neoplastic progression with bilateral lung involvement and bone metastases, as well as bilateral segmental pulmonary emboli. Echocardiography demonstrated new segmental areas of akinesia (apical septum and mid–apical anteroseptal segment) suggestive of focal ischemic damage. Given the documented pulmonary embolism and the anomalous connection between pulmonary artery and coronary circulation, this event may have been caused by paradoxical embolism travelling from pulmonary to coronary circulation (most likely affecting the LAD artery territory). Due to the patient’s frailty however, this hypothesis could not be confirmed by coronary angiography. Despite their relative rarity, coronary–pulmonary artery fistulas involving multiple coronary arteries can occur in the elderly population with no previous clinical manifestations and may give rise to apparently unfathomable clinical constellations.

Cardiac Imaging in Patients After Fontan Palliation: Which Test and When?

The Fontan operation represents the final stage of a series of palliative surgical procedures for children born with complex congenital heart disease, where a “usual” biventricular physiology cannot be restored. The palliation results in the direct connection of the systemic venous returns to the pulmonary arterial circulation without an interposed ventricle. In this unique physiology, systemic venous hypertension and intrathoracic pressures changes due to respiratory mechanics play the main role for propelling blood through the pulmonary vasculature. Although the Fontan operation has dramatically improved survival in patients with a single ventricle congenital heart disease, significant morbidity is still a concern. Patients with Fontan physiology are in fact suffering from a multitude of complications mainly due to the increased systemic venous pressure. Consequently, these patients need close clinical and imaging monitoring, where cardiac exams play a key role. In this article, we review the main cardiac imaging modalities available, summarizing their main strengths and limitations in this peculiar setting. The main purpose is to provide a practical approach for all clinicians involved in the care of these patients, even for those less experienced in cardiac imaging.

Angiographic and histopathological study on bronchial-to-pulmonary vascular anastomoses on explants from patients with cystic fibrosis after bronchial artery embolisation

Labelled backgroundHaemoptysis is a life-threatening complication of cystic fibrosis (CF). One treatment is bronchial artery embolisation (BAE) using embolic-microspheres (EMs). During BAE, pulmonary arteries can be seen on digital subtracted angiography while iodine containing contrast material injection is performed in the bronchial artery. This suggests that EMs could go from bronchial to nontarget pulmonary arteries. The aim was to evaluate if EMs could be found inside pulmonary arteries on lung explants after BAE in transplanted CF patients. MethodsRetrospective observational study including patients with CF who underwent lung transplantation and had previously needed BAE. Clinical, chest CT angiography, and angiographic data were reviewed from medical records. Pathology examination of lung explants was performed to analyze the EMs anatomical localisation. ResultsEight patients were included between 2013 and 2015, four males with a mean age of 29 (19-45) years. All patients had bronchial artery hypertrophy on CT and bronchial-to-pulmonary artery shunting during BAE. On pathology examination, EM ≤800 µm were found in the pulmonary arteries in all patients and were responsible for distal branch occlusions. Two pulmonary infarcts were observed on CT angiography after BAE and confirmed histopathologically. ConclusionsEM migration from the bronchial to pulmonary arteries is a common occurrence after BAE in patients with advanced stage CF. Although BAE is a highly effective means of controlling haemoptysis in CF, studies on the optimal particle size are needed to preserve pulmonary artery circulation, because these results suggest that low size EMs could lead to nontarget embolisation.

Circadian Rhythm Of Pulmonary Artery Pressures In HFpEF Assessed With Cardiomem: Preliminary Results

<h3>Purpose</h3> : Systemic blood pressure is known to display a circadian rhythm in most healthy individuals, characterized by a nocturnal fall and a diurnal rise. Dysregulation of this pattern is associated with higher risk of cardiovascular disease. However, the circadian rhythm in the pulmonary arterial circulation and its impact on cardiovascular disease is less established. The aim of this study is to perform a preliminary investigation of any circadian variations of pulmonary artery (PA) pressures in patients with implanted cardiomem devices. <h3>Methods</h3> : Among 15 subjects with heart failure with preserved ejection fraction (HFpEF) and an implanted cardiomem device who were offered participation in this study, four subjects enrolled. Study participants recorded PA pressure signals three times a day: AM (7-9AM), mid-day (Noon-2PM), and PM (7-9PM). We excluded the readings that were preceded by changes in the diuretic regimen (change in dose and/or prn use of metolazone) within 3 days prior to the reading. <h3>Results</h3> : In the first two subjects (#1 and #2), we identified a "steady trend or slight rise" in PA pressures from morning-to-evening. These subjects had clinical stability (defined as no hospitalizations within the last year or medication changes within last 3-months), and relatively well controlled risk factors (diabetes, hypertension, sleep apnea). In the other two subjects (#3 and #4), we identified a "drop" in PA pressures from morning-to-evening. Subjects #3 and #4 have poorly controlled sleep-disordered breathing and DM, respectively. Both of these disease processes have been implicated in circadian misalignment of systemic BP. <h3>Conclusion</h3> : Based on these preliminary findings, a diurnal rise or steady PA pressures may reflect well-controlled risk factors in HFpEF. However, a nocturnal rise may indicate poorly controlled risk factors like sleep apnea or metabolic syndrome. Future studies are needed to confirm the circadian misalignment and its impact on cardiovascular outcomes.

Impedance of the Systemic and Pulmonary Arterial Circulations by Cardiac Magnetic Resonance

In normal conditions, impedance of the pulmonary circulation (PA-Zc) is one-third lower than the systemic circulation (Ao-Zc) with ventricular function coupled to the arterial circulation by relative matching between contractility and afterload. Simultaneous measurement of Ao-Zc and PA-Zc using a cardiac magnetic resonance (CMR) technique has not previously been performed.

Congenital isolated absence of a single cusp of pulmonary valve.

A 25-year-old, previously asymptomatic female, presented to the outpatient clinic with episodic palpitations for past 6 months. She was acyanotic and showed no peripheral stigmata of infective endocarditis. Transthoracic echocardiography revealed dilated right ventricle with severe low-pressure pulmonary regurgitation. A cardiac computed tomography angiography performed for evaluation of pulmonary arterial circulation and intracardiac anatomy revealed isolated absence of posterior pulmonary cusp. The two other (right anterior and left anterior) cusps were normal and covered only part of the valve orifice, resulting in pulmonary insufficiency. The main pulmonary artery showed asymmetric dilatation. No other structural heart defects were noted.

Systems analysis of the mechanisms governing the cardiovascular response to changes in posture and in peripheral demand during exercise

Blood flows and pressures throughout the human cardiovascular system are regulated in response to various dynamic perturbations, such as changes to peripheral demands in exercise, rapid changes in posture, or loss of blood from hemorrhage, via the coordinated action of the heart, the vasculature, and autonomic reflexes. To assess how the systemic and pulmonary arterial and venous circulation, the heart, and the baroreflex work together to effect the whole-body responses to these perturbations, we integrated an anatomically-based large-vessel arterial tree model with the TriSeg heart model, models capturing nonlinear characteristics of the large and small veins, and baroreflex-mediated regulation of vascular tone and cardiac chronotropy and inotropy. The model was identified by matching data from the Valsalva maneuver (VM), exercise, and head-up tilt (HUT). Thirty-one parameters were optimized using a custom parameter-fitting tool chain, resulting in an unique, high-fidelity whole-body human cardiovascular systems model. Because the model captures the effects of exercise and posture changes, it can be used to simulate numerous clinical assessments, such as HUT, the VM, and cardiopulmonary exercise stress testing. The model can also be applied as a framework for representing and simulating individual patients and pathologies. Moreover, it can serve as a framework for integrating multi-scale organ-level models, such as for the heart or the kidneys, into a whole-body model. Here, the model is used to analyze the relative importance of chronotropic, inotropic, and peripheral vascular contributions to the whole-body cardiovascular response to exercise. It is predicted that in normal physiological conditions chronotropy and inotropy make roughly equal contributions to increasing cardiac output and cardiac power output during exercise. Under upright exercise conditions, the nonlinear pressure-volume relationship of the large veins and sympathetic-mediated venous vasoconstriction are both required to maintain preload to achieve physiological exercise levels. The developed modeling framework is built using the open Modelica modeling language and is freely distributed.

Analysis of flow resistance in the pulmonary arterial circulation: implications for hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction (HPV) plays an essential role in distributing blood in the lung to enhance ventilation-perfusion matching and blood oxygenation. In this study, a theoretical model of the pulmonary vasculature is used to predict the effects of vasoconstriction over specified ranges of vessel diameters on pulmonary vascular resistance (PVR). The model is used to evaluate the ability of hypothesized mechanisms of HPV to account for observed levels of PVR elevation during hypoxia. The vascular structure from pulmonary arteries to capillaries is represented using scaling laws. Vessel segments are modeled as resistive elements and blood flow rates are computed from physical principles. Direct vascular responses to intravascular oxygen levels have been proposed as a mechanism of HPV. In the lung, significant changes in oxygen level occur only in vessels less than 60 μm in diameter. The model shows that observed levels of hypoxic vasoconstriction in these vessels alone cannot account for the elevation of PVR associated with HPV. However, the elevation in PVR associated with HPV can be accounted for if larger upstream vessels also constrict. These results imply that upstream signaling by conducted responses to engage constriction of arterioles plays an essential role in the elevation of PVR during HPV.NEW & NOTEWORTHY A theoretical model of the pulmonary vasculature is used to predict the effects of vasoconstriction over specified ranges of vessel diameters on pulmonary vascular resistance (PVR). The model shows that observed levels of hypoxic vasoconstriction in terminal vessels cannot account for the elevation of PVR associated with hypoxic pulmonary vasoconstriction (HPV). Upstream signaling by conducted responses to engage constriction of arterioles, therefore, plays an essential role in the elevation of PVR during HPV.

Large-bore Aspiration Thrombectomy for Acute Venous Thromboembolism

Pulmonary embolism can occur following dislodgement of deep venous thrombosis into the pulmonary artery circulation, which results in obstruction of the pulmonary artery system and can be fatal. The consequences of pulmonary embolism include hypotension, right heart strain, and hypoxia. In the long term, pulmonary embolism may lead to Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Patients who develop hypotensive massive and submassive pulmonary embolism can be treated with large-bore aspiration thrombectomy. In the acute setting, this improves short-term outcomes by decreasing the ICU stay. It can also reduce the risk of CTEPH. Options for large-bore aspiration thrombectomy include the FlowTriever™ system (Inari Medical, Irvine, CA) and the Lightning 12 vascular thrombectomy system (Penumbra Inc., Alameda, CA). This review discusses the pathophysiology of pulmonary embolism, management, and options for large-bore aspiration thrombectomy.

Assessment of pulmonary arterial circulation 3 months after hospitalization for SARS-CoV-2 pneumonia: Dual-energy CT (DECT) angiographic study in 55 patients.

BackgroundDuring COVID-19, the main manifestations of the disease are not only pneumonia but also coagulation disorders. The purpose of this study was to evaluate pulmonary vascular abnormalities 3 months after hospitalization for SARS-CoV-2 pneumonia in patients with persistent respiratory symptoms.MethodsAmong the 320 patients who participated in a systematic follow-up 3 months after hospitalization, 76 patients had residual symptoms justifying a specialized follow-up in the department of pulmonology. Among them, dual-energy CT angiography (DECTA) was obtained in 55 patients.FindingsThe 55 patients had partial (n = 40; 72.7%) or complete (n = 15; 27.3%) resolution of COVID-19 lung infiltration. DECTA was normal in 52 patients (52/55; 94.6%) and showed endoluminal filling defects in 3 patients (3/55; 5.4%) at the level of one (n = 1) and two (n = 1) segmental arteries of a single lobe and within central and peripheral arteries (n = 1). DECT lung perfusion was rated as non-interpretable (n = 2;3.6%), normal (n = 17; 30.9%) and abnormal (n = 36; 65.5%), the latter group comprising 32 patients with residual COVID-19 opacities (32/36; 89%) and 4 patients with normal lung parenchyma (4/36; 11%). Perfusion abnormalities consisted of (a) patchy defects (30/36; 83%), (b) PE-type defects (6/36; 16.6%) with (n = 1) or without proximal thrombosis (n = 5); and (c) focal areas of hypoperfusion (2/36; 5.5%). Increased perfusion was seen in 15 patients, always matching GGOs, bands and/or vascular tree-in- bud patterns.InterpretationDECT depicted proximal arterial thrombosis in 5.4% of patients and perfusion abnormalities suggestive of widespread microangiopathy in 65.5% of patients. Lung microcirculation was abnormal in 4 patients with normal lung parenchyma.