Small Branches Of Pulmonary Artery Research Articles

Potential role of GcMAF in suppressing the severity of COVID-19-induced immune responses: Lesson learned from HIV

Over the last six months, there have been increasing numbers of reports that struggle to understand the pathogenesis of the coronavirus disease 2019 (COVID-19) pandemic. As of August 16, 2020, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been responsible for more than 21 294 000 infections and about 760 000 deaths worldwide [1], but the mechanisms of virus-induced host damage remain a mystery. Understanding the pathways behind viral pathogenicity just like cellular and tissue tropism, counteracting host defence processes and immunological responses are crucial to find new therapeutic strategies. Based on clinical reports, it is noteworthy that COVID-19 causes various degree of illness ranging from asymptomatic or milder symptomatic cases to severe lung injury or even multi-organ dysfunction with liver and kidney impairment [2], [3], [4]. Even in not severe patients, the heterogeneity of symptoms is consistent with the increasing evidence that SARS-CoV-2 shows a broad tissue tropism, being able to attack almost anything in the body [2], [3], [4], [5]. To date, the most commonly investigated hypothesis about the underlying mechanisms of multi-organ failure may be summarized into three main targets: microcirculation dysfunction, overwhelming inflammation and abnormal coagulation [7]. Radiologic and laboratory findings as well as preliminary autopsy studies seem to support this hypothesis. The most common patterns seen on chest CT were ground-glass opacity, interlobular septal thickening, air bronchogram, bilateral patchy shadowing, crazy-paving pattern, and thickening of the adjacent pleura, resembling an interstitial involvement in viral pneumonia [2], [3], [7], [8]. Under the light of microscope, the lungs revealed diffuse alveolar damage with formation of numerous hyaline membranes, very patchy and sparse interstitial chronic inflammation composed mainly of lymphocytes, thrombi within a few small pulmonary artery branches, congestion of alveolar septal capillaries, focal edema fluid, and macrophage infiltration within the airspaces [9], [10], [11], [12]. The more significant laboratory abnormalities were metabolic acidosis, lymphocytopenia, leukopenia, thrombocytopenia, elevated levels of C-reactive protein (CRP), interleukin-6 (IL-6), lactate dehydrogenase (LDH) and D-dimer [2], [3], [4], [5], [6], [7]. As firstly suggested by Huang C et al. [4], the systemic cytokine storm could play a key role in the virus-induced tissue damage. However, the question “what the link for the overproduction of pro-inflammatory mediators and the immune suppression, on the hand, and microvascular injury and thromboembolism, on the other, is”, remains unclear. Being the knowledge of this issue very scarce, lessons learned from other human pathogenic viruses, with specific reference to human immunodeficiency virus (HIV), could be diriment.

Features of local pulmonary hemostasis in patients who received surgical treatment for benign peripheral lung tumors

Objectives - to develop a method for prevention of thromboembolic events in small branches of pulmonary artery in post-operative period, based on features of local pulmonary hemostasis in patients who underwent lung surgery for benign tumors. Material and methods. 30 male patients aged 62 ± 2.4 years old were included in the study. All patients underwent lung surgery (mainly lobectomy). Blood was drawn intra-operationally from a. pulmonale (arriving venous blood), v. pulmonale (outflowing blood) and cubital vein. The following parameters of coagulative and thrombocytic-vascular hemostasis were examined: free endogenous heparin was evaluated by protamine titration, platelet count and platelet aggregative properties were registered, using hematology analyzer, activated partial thromboplastin time (aPTT), quantitative analysis of fibrinogen and protein C was performed using CoaLAB 1000 analyzer. Results. Study of hemostasis features in patients, who underwent lung surgery, has revealed an imbalance of coagulation and anticoagulation systems, which manifested itself as dysfunctions in thrombocytic-vascular hemostasis (increase in platelets aggregative properties, most notable in peripheral venous blood), plasma hemostasis (decrease in aPTT, most notable in arterial blood, and increased fibrinogen level) and anticoagulation (modestly decreased protein C and heparin levels in peripheral blood), which is characteristic of hypercoagulation, being the possible basis for development of thromboembolic complications in post-operative period. These changes are most typical for blood taken from cubital vein, which is indicative of increased possibility of clot formation specifically in systemic circulation, which is indicative of increased possibility of clot formation specifically in systemic circulation. The least risk of clot formation was established in pulmonary vein blood (outflowing blood). Moderate correlation between free heparin level in arterial blood and venous blood was established. Conclusion. The derived results have allowed us to develop an individual management plan for patients with increased risk of thromboembolic events, which includes early administration of anticoagulant agents in prophylactic doses.

Surgical Management of Tetralogy of Fallot with Inadequate Size Pulmonary Artery Branches

Background: Tetralogy of Fallot (TOF) with inadequate size pulmonary artery (PA) branches continues to be a problem in many developing countries due to late presentation. Surgical management is still debatable in clinical practice. Our aim is to review our experience with different surgical modalities for management of this subset of patients. Methods: Between 2012 and 2018, out of 314 operations for TOF at our unit, there were 26 cases judged either pre-operatively or intraoperatively to have PA branches inadequate for total correction (McGoon’s ratio ≤ 1.5 or pulmonary branch size <-2 Z-value of expected size). Modified Blalock-Taussig shunt (MBTS) was done in 11 cases (shunt strategy). Open-heart surgery, involving going on cardiopulmonary bypass and cardiac arrest, was done in 15 cases (right ventricular outflow tract, RVOT, reconstruction strategy). The main PA was opened and the PA branches were sized from inside using Hegar sizers and Z-scores obtained. In 6 cases, the measured PA branches were smaller than the -2 Z-value, so, RVOT reconstruction without ventricular septal defect (VSD) closure (antegrade palliation) was done. The PA patch was adjusted to get a main PA annular diameter of not more than Z-value of -4, and to get an oxygen saturation on 25% FiO2 not exceeding 90%. In the remaining 9 cases, the sizes of the PA branches were found to accommodate a Hegar sizer within -2 Z-values. So, in those 9 patients, we proceeded to total repair with VSD closure. Results: There were no statistically significant differences between the 2 strategies (shunt vs. RVOT reconstruction) as regarding the preoperative parameters (age, weight, preoperative oxygen saturation on room air and the preoperative McGoon’s ratio of branch pulmonary arteries size). As regarding the postoperative data, there was statistically significant difference in the total mortality being less in RVOT reconstruction (1/15, 6.6%) compared to MBTS (4/11, 36.4%). The ratio between the diameters of branch pulmonary arteries was significantly lower in antegrade palliation than with MBTS, denoting more equal and even growth of pulmonary artery branches after antegrade palliation. Conclusion: In TOF patients judged preoperatively to have small PA branches not suitable for total correction, intra-operative direct assessment of the sizes of pulmonary artery branches by Hegar sizers is more accurate and reliable than preoperative imaging studies, and offered to save many patients from a two-stage repair allowing them a primary total repair with perfect results. In cases that needed a two-stage repair because of small PA branches, antegrade palliation yielded better early outcome than MBTS and furthermore provides uniform branch pulmonary arteries growth, which facilitates the 2nd stage total correction.

Pulmonary Artery Sealing With an Ultrasonic Energy Device in Video-Assisted Thoracoscopic Surgery Lobectomy: An Animal Survival Study

Pulmonary artery (PA) sealing in video-assisted thoracoscopic surgery (VATS) lobectomy is typically accomplished using vascular endostaplers. Endostaplers may be associated with iatrogenic PA branch injury, especially in short, small PA branches. We evaluated PA branch sealing with the HARMONIC ACE+7 (ACE) shears (Ethicon, Cincinnati, OH) in VATS lobectomy in a canine survival model. Ten adult dogs underwent VATS lobectomy. Standard VATS lobectomy operative technique was used for the entire operation, except for PA branch sealing. The ACE was used for all PA branch sealing. Dogs were kept alive for 30 days. The 10 dogs underwent VATS right upper (n= 5) and right lower (n= 5) lobectomy. The ACE was used to seal 21 PA branches. No PA branch was divided with an endostapler. There were no intraoperative complications or conversions to thoracotomy. Mean invivo PA diameter was 5.6 mm (range, 2 to 12 mm). One 10-mm PA branch had a partial seal failure immediately at the time of sealing. The device was reapplied on the stump, and the PA branch was successfully sealed. All dogs survived 30 days without hemothorax. Necropsy at 30 days did not reveal any signs of postoperative bleeding. Pathology of the sealed PA branches at 30 days revealed fibrosis, giant cell reaction, neovascularization, and thermal changes of the vessel wall. The use of the ACE for PA branch sealing in VATS lobectomy is safe and effective in an animal survival model. Human studies are needed to determine the clinical safety of ultrasonic PA branch sealing before widespread clinical use.

Right ventricular failure and pulmonary hypertension at recurrent thromboembolism of small branches of the pulmonary artery in cancer patients

Aim. Develop new approaches to the diagnosis of right heart failure and pulmonary hypertension in recurrent thromboembolism of small branches of the pulmonary artery in patients with malignant tumors. &#x0D; Methods. 83 patients with malignant tumors of various localizations were examined and followed-up. The main group included 49 patients with malignant tumors of various localizations and related venous thrombosis. The control group included 34 patients who did not have venous thrombosis. Patients in both groups underwent ultrasonography of inferior vena cava system veins and echocardiography at intervals of 3-4 days during the diagnosis and treatment of malignant tumors. Right ventricle ejection fraction and systolic pressure in the pulmonary artery were calculated at echocardiography. &#x0D; Results. No signs of inferior vena cava system veins thromboses, right heart failure, pulmonary hypertension were identified in patients of the control group while setting up the diagnosis and treatment of malignancies. In 38 out of 49 patients of the main group, right ventricular failure and pulmonary hypertension of varying severity were detected. The condition of 46 patients of the main group gradually improved after treating with anticoagulants. &#x0D; Conclusion. Recanalization of venous thrombosis is accompanied by frequent rejection of micro thrombi and embolization of small branches of pulmonary artery, causing right heart failure and pulmonary hypertension, which can be promptly detected by repeated echocardiography.

Surgical Correction of Tetralogy of Fallot in Adulthood

Background: The aim of this study is to evaluate the short-term results of surgical correction of Tetralogy of Fallot in adult patients. Methods: Between 1999 and 2007, surgical correction was performed in 16 adult patients (mean age: 34.6 years; range: 18 to 62). Five previous procedures had been performed in 4 patients. Thirteen patients were in NYHA functional classification III or IV (81%), and 12 were cyanotic. Echocardiography was performed in all patients and 14 of them were catheterized. The mean gradient in the right ventricular outflow tract was 82 mmHg. Four patients had bad anatomy, consisting in coronary fistulas (2) and small pulmonary artery branches (2). Results: Infundibular resection was performed in all patients, ventricular septal defect closure in 15, pulmonary valve commissurotomy in 8, right ventricular outflow tract patch enlargement in 9 and transannular patch placement in 4. Three patients died during the postoperative hospital stay, 2 of them with sepsis. All of them had bad anatomy and severe preoperative condition. No residual defects were found. The other 13 patients had a good recovery. Eleven had less than 24 hours of mechanical ventilation. Early hospital discharge was possible in all survivors. Conclusion: Surgical correction of Tetralogy of Fallot in adulthood is an infrequent procedure. The short-term results depend mostly on the anatomic substrate and the preoperative clinical condition of the patient.

Embryonic and early fetal development of human lung vasculature and its functional implications.

Recently, we have identified in the mouse three processes involved in the early development of pulmonary vasculature: angiogenesis for branching of central vessels, vasculogenesis (lakes in the mesenchyme) for peripheral vessels, and a lytic process to establish luminal connection between the two. We have established that these three processes also operate in the human by studying serial sections of human embryos and early fetuses. Vascular lakes of hematopoietic cells appear at stage 13, i.e., 4+ weeks gestational age (GA), the first intrapulmonary vascular structure to appear. At stage 20 (50.5 days GA), a venous network with luminal connections to central pulmonary veins (PV) is present. Airways have not yet reached these regions of lung. At its first intrapulmonary appearance, the pulmonary artery (PA) is small and thick walled: it runs with the airway but its branching is slower, so many peripheral airways are not accompanied by a PA branch. By contrast, the PV has a peripheral patent network well before the PA. In the pseudoglandular phase, airway branching continues, and the PA catches up so that small PA branches are found with all airways. Later in this phase small nonmuscular vessels lie in the mesenchyme close to airway epithelium. By the early canalicular phase and the age of viability, continuity between pulmonary artery and the peripheral capillary network must be established. In a 10-week fetus several structures suggesting a breakthrough site were seen. Air-blood barrier structure is first seen at 19 weeks. Thus in the lung, the PA and PV are dissociated in their timing and pattern of branching. Early veins are present diffusely through the mesenchyme and establish central luminal connection to the main pulmonary vein before airway or artery are present at this level.

Fatal intraoperative pulmonary thrombosis after graft replacement of an aneurysm of the arch and descending aorta in association with deep hypothermic circulatory arrest and aprotinin therapy

J Thorac Cardiovasc Surg 1998;115:723-4

Morphologic particulars in the peripheral pulmonary artery of the lungs in neonates (author's transl)

Morphological particulars in small branches of the pulmonary artery in newborn children are described: small diameter; hypercellular intima; thick media; wide adventitia, consisting of connective tissue only; epitheloid cells between intima and media as well as media and adventitia. "Sperrarterien" are also seen. These structural changes in the small branches of pulmonary artery, the reduction of the hypertrophic wall of the right ventricle, and the increase of the magnitude of respiration--processes during the first 4 months of life--are considered important factors in explaining the frequency of sudden infant death during the first 4 months of life.

Potential artifact in measurement of left ventricular filling pressure with flow-directed catheters.

Artifactual pulmonary wedge pressure measurements were encountered during bedside use of Swan-Ganz catheters. These values were higher than pulmonary artery end diastolic pressure and devoid of typical phasic contours. Utilizing fluoroscopy these artifacts were reproduced by advancing the catheter tip 2-4 cm beyond the site of initial wedging and reinflating the balloon. Spurious increases of pulmonary wedge pressure of up to 15 mm Hg were thus obtained. In vitro catheter testing demonstrated overlapping of the catheter tip by the deformed balloon when it was fully inflated in a channel too small to accomodate it. These measurement artifacts are thus attributed to distal migration of the catheter tip into relatively small pulmonary artery branches and to subsequent occlusion of the catheter lumen by the balloon when it is reinflated. This can readily be avoided by routinely inflating the balloon with the minimum volume of air sufficient to yield a pulmonary wedge pressure tracing.