Development Of Pulmonary Edema Research Articles

A combination of left ventricular outflow tract velocity time integral and lung ultrasound to predict mortality in ST elevation myocardial infarction.

Development of ventricular failure and pulmonary edema is associated with a worse prognosis in ST-elevation myocardial infarction (STEMI). We aimed to evaluate the prognostic ability of a novel classification combining lung ultrasound (LUS) and left ventricular outflow tract (LVOT) velocity time integral (VTI) in patients with STEMI. LUS and LVOT-VTI were performed within 24h of admission in STEMI patients. A LUS combined with LVOT-VTI (LUV) classification was developed based on LUS with < or ≥ 3 positive zone scans, combined with LVOT-VTI > or ≤ 14. Patients were classified as A (< 3zones/ > 14cm VTI), B (≥ 3zones/ > 14cm VTI), C (< 3zones/ ≤ 14cm VTI) and D (≥ 3zones/ ≤ 14cm VTI). Primary outcome was occurrence of in-hospital mortality. Development of cardiogenic shock (CS) within 24h was also assessed. A total of 308 patients were included. Overall in-hospital mortality was 8.8%, while mortality for LUV A, B, C, and D was 0%, 3%, 12%, and 45%, respectively. The area under the curve (AUC) for predicting in-hospital mortality was 0.915. Moreover, after exclusion of patients admitted in Killip IV, at each increasing degree of LUV, a higher proportion of patients developed CS within 24h: LUV A = 0.0%, LUV B 5%, LUV C = 12.5% and LUV D = 30.8% (p < 0.0001). The AUC for predicting CS was 0.908 (p < 0.001). In a cohort of STEMI patients, LUV provided to be an excellent method for prediction of in-hospital mortality and development of CS. LUV classification is a fast, non-invasive and very user-friendly ultrasonographic evaluation method to stratify the risk of mortality and CS.

Neurogenic Pulmonary Edema Associated with Hyponatremia, Primary Polydipsia, and Cannabis Use: A Case Report

Introduction: Neurogenic pulmonary edema is a rare and potentially life-threatening condition that can present as severe pulmonary edema after significant neurologic insults. This is the first documented instance that shows a plausible causal link between cannabis consumption, psychogenic polydipsia, and the subsequent development of neurogenic pulmonary edema associated with status epilepticus secondary to acute hyponatremia. Case Report: We report a case of a 34-year-old female who presented to the emergency department altered and postictal after a witnessed new-onset seizure. She developed significant respiratory distress that required intubation. Her sodium was 121 millimoles per liter (mmol/L), from 137 mmol/L 36 hours prior on routine outpatient labs. Further history revealed excessive water ingestion after eating a cannabis edible prior to the seizure. Conclusion: This case highlights the importance of recognizing neurogenic pulmonary edema in connection with psychogenic polydipsia, severe hyponatremia, and status epilepticus subsequent to cannabis consumption.

RETROSPECTIVE ANALYSIS OF CLINICAL, EPIDEMIOLOGY AND PATHOMORPHOLOGICAL FEATURES OF MYOCARDIAL INFARCTION

The aim of this study is to conduct a retrospective analysis of the clinical, epidemiological, and pathomorphological features of myocardial infarction. Materials and methods: A retrospective analysis was conducted using data from medical records and autopsy results from the pathology department for the year 2023. Results. In 2023, the pathology department performed 182 autopsies, with 123 patients diagnosed with acute, repeated, or recurrent myocardial infarction (MI), accounting for 67.6% of all autopsies. The average age of the deceased was 74.4±0.9 years, with 81.3% being persons of incapacitated age. Women comprised the majority at 55.3% (T=2784.5; p=0.001). The highest proportion of MI-related deaths occurred in September, accounting for 12.2%. In the pathological diagnosis, myocardial infarction (MI) was the primary disease, with varying localization of the pathological process in the left ventricle. Transmural MI was detected in 95.9% of the deceased, while subendocardial MI was found in 4.1%. Acute MI developed against the background of a previously experienced MI in 43.9% of cases, and in 5.5% of cases, it was a repeated acute recurrent MI. Changes in the aorta, coronary vessels, and basal vessels of the brain were observed in 100.0% of the cases, with hypertensive disease detected in 95.9% of cases. Acute cardiopulmonary failure with the development of pulmonary edema was the immediate cause of death in 95.9% of cases. Macroscopic examination revealed hypertrophy of the left ventricle. The myocardium appeared reddish-brown and elastic, with white layers. Brown-gray infarct areas of different sizes were present in the left ventricular wall, while in cases of repeated acute myocardial infarction, the affected area was gray-white and hard to the touch. Microscopically, hypertrophy of cardiomyocytes of the left ventricle with perinuclear lipofuscinosis was observed in all deceased individuals. Sections of the infarct zone contained homogenized, anucleated, fragmented cardiomyocytes, dilated full blood vessels with small perivascular hemorrhages, and neutrophilic-macrophage infiltrates of varying intensity. Large centers of cardiosclerosis were detected in cases of repeated MI, while signs of angiogenesis with the formation of granulation tissue were observed in cases of recurrent MI. Conclusion. In 2023, 123 autopsies revealed a diagnosis of acute, repeated, or recurrent myocardial infarction (MI) in 67.6% of all cases. The average age of the deceased was 74.4±0.9 years, with 81.3% being individuals of incapacitated age. There was a predominance of women, accounting for 55.3% of cases. Acute MI developed against the background of a previously experienced one in 43.9% of the deceased, while repeated acute recurrent MI was detected in 5.5% of cases. Pathomorphological changes corresponded to the typical features of MI depending on its age.

Acute kidney injury in patients with acute coronary syndrome - risk profile

Abstract Funding Acknowledgements None. Introduction Acute kidney injury (AKI) is a strong predictor of in-hospital adverse outcomes, which is a common complication of acute coronary syndrome (ACS). Aim To analyse the risk profile of patients treated for acute coronary syndrome who develop acute kidney injury. Material and methods This is a single-centre cross-sectional cohort study on 3507 patients with ACS. The main exclusion criteria was left ventricular dysfunction. Demographical and clinical characteristics, biochemical parameters, the anatomical distribution of coronary artery disease (CAD) and the final outcomes were analysed according to RF at the moment of the indexed event. The estimated glomerular filtration rate (eGFR) was calculated by the Modification of Diet in Renal Disease Study Group Equation (MDRD), where patients with eGFR&amp;lt;60ml/min 1.73 m2 had moderate to severe renal dysfunction. Results 74 (2.1%) out of 3507 patients developed acute kidney injury (AKI). Those were predominantly males [62.2% (46), OR 1.55 (95% CI 0.98-2.47), p=0.044], significantly older (68.95±9.9. vs 62.5±11.2; p &amp;lt;0.000001), more often with preexisting HBI (OR 4.72 (95% CI 2.20-10.30, p=0.000070), HTA(OR 1.89 95%CI 1.11-3.23, p=0.020), diabetes(OR 1.88 95%CI 1.18-3.00, p=0.008), cancer(OR 2.92 95%CI 1.15-7.44, p=0.024), anaemia (beta -.104, p=0.000032), while less often were smokers (OR 0.51, 95% CI 0.31-0.83, p=0.006). They had statistically significantly higher values of cardiac troponin (beta .075, p=0.000011), stress glycemia (beta .104, p=0. 0.000019), and WBC (beta .074, p=0.000013), higher BUN (beta .325, p=0.000011), creatinine (beta .268, p=0.000016), and lower eGFR at admission (beta -.211, p=0.000032), lower sodium (beta -.101, p=0.000012), and higher potassium levels (beta .087, p=0.0008). Vice versa, total cholesterol, LDL-C and non-HDL-C (beta -.051, p=0.002, -.049, p=0.003, and -.047, p=0.005 respectively), were lower, the same for Hgb (beta -.107, p=0.000021). It is worth mentioning that 18(11.5%), of AKI patients were not PCI treated. Independent variables associated with AKI were: preexisting renal failure, cancer, and WBC. Outcomes: AKI carried a significantly higher in-hospital mortality rate (4.2% in general population, and 21.1% of all deaths were AKI patients, OR 23.01 (95% CI 14.04-47.03, p=0.00002)]. It was significantly associated with the development of pulmonary oedema (OR 17.94, 95% CI 9.67-33.26, p=0.000012), cardiogenic shock (OR 21.59, 95% CI 12.79-36.47, p=0.00006), any type of dysrhythmia (OR 1.83, 95%CI 1.53-2.18, p=0.0001), and any type of bleeding complications (OR 1.61, 95%CI 1.14-2.27, p=0.007). Conclusion AKI is a relatively rare complication in ACS patients, however is associated with significant in-hospital morbidity and mortality. Patients with pre-existing renal failure, and cancer, as well as patients who developed more pronounced inflammatory reaction were more prone to AKI.

Dynamic trend of lung fluid movement during exercise in heart failure: From lung imaging to alveolar-capillary membrane function

BackgroundIn chronic heart failure (HF), exercise-induced increase in pulmonary capillary pressure may cause an increase of pulmonary congestion, or the development of pulmonary oedema. We sought to assess in HF patients the exercise-induced intra-thoracic fluid movements, by measuring plasma brain natriuretic peptide (BNP), lung comets and lung diffusion for carbon monoxide (DLCO) and nitric oxide (DLNO), as markers of hemodynamic load changes, interstitial space and alveolar-capillary membrane fluids, respectively. Methods and resultsTwenty-four reduced ejection fraction HF patients underwent BNP, lung comets and DLCO/DLNO measurements before, at peak and 1 h after the end of a maximal cardiopulmonary exercise test. BNP significantly increased at peak from 549 (328–841) to 691 (382–1207, p < 0.0001) pg/mL and almost completely returned to baseline value 1 h after exercise. Comets number increased at peak from 9.4 ± 8.2 to 24.3 ± 16.7, returning to baseline (9.7 ± 7.4) after 1 h (p < 0.0001). DLCO did not change significantly at peak (from 18.01 ± 4.72 to 18.22 ± 4.73 mL/min/mmHg), but was significantly reduced at 1 h (16.97 ± 4.26 mL/min/mmHg) compared to both baseline (p = 0.0211) and peak (p = 0.0174). DLNO showed a not significant trend toward lower values 1 h post-exercise. ConclusionsModerate/severe HF patients have a 2-step intra-thoracic fluid movement with exercise: the first during active exercise, from the vascular space toward the interstitial space, as confirmed by comets increase, without any effect on diffusion, and the second, during recovery, toward the alveolar-capillary membrane, clearing the interstitial space but worsening gas diffusion.

Substantiation of the possibility of using bronchoalveolar lavage with perfluorocarbon fluids for the treatment of the alveolar stage of toxic pulmonary edema

Introduction. Toxic pulmonary edema is an acute syndrome characterized by the accumulation of fluid in the extravascular spaces of the lungs, impaired gas exchange, the formation of tissue hypoxia and acidosis, which can occur in acute inhalation poisoning with pulmonary toxicants at work. Existing methods of drug and respiratory therapy are ineffective in the development of alveolar pulmonary edema (end-stage acute respiratory distress syndrome; ARDS). In this regard, the search for new approaches to the treatment of this condition, which is characterized by almost 100 % mortality, is of great practical importance. One of such approaches is the use of perfluorocarbon (PFC) fluids, which, due to their unique physical and chemical properties, are able not only to ensure the evacuation of edematous fluid from the alveoli and respiratory tract, but also to restore gas exchange in the parts of the lungs filled with them. This article will present an experimental evaluation of the use of PFC fluids in a model of the alveolar stage of toxic pulmonary edema.&#x0D; The goal of the study is to determine the effect of bronchoalveolar lavage (BAL) using perfluorocarbons on the indicators of acute respiratory failure and the outcome of the alveolar stage of toxic pulmonary edema.&#x0D; Materials and methods. The study was carried out on male Wistar rats aged 4 months, weighing 180–230 g. Toxic pulmonary edema was initiated by endotracheal injection of 0.1 M HCl solution. Anesthetized rats were intubated with a cannula, then intratracheally injected with 0.1 M HCl solution at a dose of 2 ml/kg and connected to a ventilator. After that, the animals were randomized by weight into groups of 6 individuals each. Animals of the experimental group with a decrease in saturation below 80%, 2–6 procedures of bronchoalveolar lavage (BAL) with PFC-oxygenated liquid in a single dose of 2.0 ml/kg were performed. Heart rate, oxygen saturation, duration of survival, and overall survival by group were recorded.&#x0D; The resalts. In all rats, there was a decrease in oxygen saturation (SpO2) and heart rate (HR) after HCl administration, which was restored to the lower limits of normal within 5 minutes. However, after 25 to 30 minutes, the animals experienced a rapid decrease in SpO2, an increase in heart rate, the appearance of wet wheezing in the lungs, and the discharge of foamy fluid from the catheter. Against this background, there was a rapid death of animals, At the same time, the average duration of survival was 30.6±3.3 min. In turn, in the animals of the experimental group, after each BAL procedure, an increase in saturation was noted, it was possible to evacuate a total of 9.1±0.8 ml/kg of edematous fluid from the lungs. It was also noted that the average duration of survival of rats in the experimental group was 1.69 times and amounted to 51.6±3.8 minutes.&#x0D; Conclusions. The use of BAL with PFC fluids in the alveolar stage of toxic pulmonary edema makes it possible to evacuate a significant amount of edematous fluid from the lower parts of the lungs due to its displacement by a perfluorocarbon with a higher density; to short-term reduce the severity of manifestations of acute respiratory failure after instillation of oxygenated PFC liquid; to increase the duration of survival of animals by ensuring gas exchange in previously uninvolved parts of the lungs.&#x0D; Ethics. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki. The Clinical Study Protocol was reviewed at a meeting of the local Ethics Committee FSBSI IRIOH. Protocol No. 4 of May 25, 2022.

Circulatory support with venovenous ECMO in a patient with reperfusion pulmonary edema after pulmonary artery thromboendarterectomy

Chronic thromboembolic pulmonary hypertension (CTEPH) is a subtype of pulmonary hypertension characterized by the obstruction of pulmonary arteries secondary to chronic thromboembolism. Pulmonary thromboendarterectomy surgery (PTE) is the main treatment for patients with CTEPH, as it removes the chronic thrombi from the pulmonary arteries. Pulmonary reperfusion syndrome is a common complication of the surgery, which involves the development of pulmonary edema in the area where blood perfusion improves after the surgery. The incidence of this syndrome varies from 8 to 91% depending on the criteria used for diagnosis, and it is one of the most serious complications of pulmonary thromboendarterectomy. In such cases, circulatory support with extracorporeal membrane oxygenation (ECMO) has become a valuable therapeutic modality. We present the case of a 60-year-old woman with a history of acute pulmonary embolism due to deep vein thrombosis of the right pelvic limb who was diagnosed later with CTEPH who was admitted for scheduled surgical treatment involving bilateral PTE. However, during the immediate postoperative period, she developed cardiogenic shock and refractory hypoxemia secondary to pulmonary reperfusion syndrome following the surgical procedure. As a result, she required veno-venous ECMO circulatory support for 6 days, leading to resolution of the pulmonary condition and clinical improvement.

Role of neutrophil myeloperoxidase in the development and progression of high-altitude pulmonary edema

BackgroundNeutrophil infiltration and hypoxic pulmonary vasoconstriction induced by hypobaric hypoxic stress are vital in high-altitude pulmonary edema (HAPE). Myeloperoxidase (MPO), an important enzyme in neutrophils, is associated with inflammation and oxidative stress and is also involved in the regulation of nitric oxide synthase (NOS), an enzyme that catalyzes the production of the vasodilatory factor nitric oxide (NO). However, the role of neutrophil MPO in HAPE's progression is still uncertain. Therefore, we hypothesize that MPO is involved in the development of HAPE via NOS. MethodsIn Xining, China (altitude: 2260 m), C57BL/6 N wild-type and mpo−/− mice served as normoxic controls, while a hypobaric chamber simulated 7000 m altitude for hypoxia. L-NAME, a nitric oxide synthase (NOS) inhibitor to inhibit NO production, was the experimental drug, and D-NAME, without NOS inhibitory effects, was the control. After measuring pulmonary artery pressure (PAP), samples were collected and analyzed for blood neutrophils, oxidative stress, inflammation, vasoactive substances, pulmonary alveolar-capillary barrier permeability, and lung tissue morphology. ResultsWild-type mice's lung injury scores, permeability, and neutrophil counts rose at 24 and 48 h of hypoxia exposure. Under hypoxia, PAP increased from 12.89 ± 1.51 mmHg under normoxia to 20.62 ± 3.33 mmHg significantly in wild-type mice and from 13.24 ± 0.79 mmHg to 16.50 ± 2.07 mmHg in mpo−/− mice. Consistent with PAP, inducible NOS activity, lung permeability, lung injury scores, oxidative stress response, and inflammation showed more significant increases in wild-type mice than in mpo−/− mice. Additionally, endothelial NOS activity and NO levels decreased more pronouncedly in wild-type mice than in mpo−/− mice. NOS inhibition during hypoxia led to more significant increases in PAP, permeability, and lung injury scores compared to the drug control group, especially in wild-type mice. ConclusionMPO knockout reduces oxidative stress and inflammation to preserve alveolar-capillary barrier permeability and limits the decline in endothelial NOS activity to reduce PAP elevation during hypoxia. MPO inhibition emerges as a prospective therapeutic strategy for HAPE, offering avenues for precise interventions.

Cardiogenic pulmonary edema - is it lone cardiogenic? "Missing link" between hemodynamic and other existing mechanisms.

The current traditional pathophysiologic concept of pulmonary edema of cardiogenic origin explains its development by a hydrostatic effect due to increased pulmonary capillary pressure resulting in fluid flux to alveolar and interstitial areas from capillaries. However, several experimental studies and clinical data of poor response to hemodynamic and diuretic treatment in many scenarios provide further evidence of the involvement of several other contributing factors to the development of cardiogenic pulmonary edema. Several experimental and clinical studies have found that sympathetic overactivity with elevated plasma catecholamine concentrations may play an important role in the development of cardiovascular-associated pulmonary edema. Catecholamine-induced pulmonary injury may be one of the key mechanisms in acute cardiogenic pulmonary edema triggering proinflammatory cytokine overactivation, oxidative stress and myocardial injury. In the everyday treatment of acute heart failure, physicians should consider the possibility of other noncardiogenic mechanisms involved in the progression of acute pulmonary edema, particularly catecholamine overactivity, lymphatic drainage, inflammatory and oxidative stress, high surfactant protein. The classic, hemodynamic treatment approach in pulmonary edema with the coexistence of other contributing factors may not provide adequate clinical benefit during treatment.

Computational modeling of heart failure in microgravity transitions.

The space tourism industry is growing due to advances in rocket technology. Privatised space travel exposes non-professional astronauts with health profiles comprising underlying conditions to microgravity. Prior research has typically focused on the effects of microgravity on human physiology in healthy astronauts, and little is known how the effects of microgravity may play out in the pathophysiology of underlying medical conditions, such as heart failure. This study used an established, controlled lumped mathematical model of the cardiopulmonary system to simulate the effects of entry into microgravity in the setting of heart failure with both, reduced and preserved ejection fraction. We find that exposure to microgravity eventuates an increased cardiac output, and in patients with heart failure there is an unwanted increase in left atrial pressure, indicating an elevated risk for development of pulmonary oedema. This model gives insight into the risks of space flight for people with heart failure, and the impact this may have on mission success in space tourism.

Нові підходи до лікування отруєнь синтетичними опіоїдами: застосування великих доз Налоксону та перспективи створення альтернативних антидотів

Introduction. In the conditions of the spread of powerful synthetic opioids, the traditionally recommended doses of Naloxone may be insufficient; instead, a significant increase in the dose of Naloxone leads to side effects, which in turn creates a threat to life. Aim. Analysis of the results of own research and scientific information regarding the use of Naloxone in the treatment of synthetic opioids poisoning and the development of alternative antidotes. Materials and Methods. The medical data of 174 patients treated with the diagnosis: "Acute narcotic poisoning" (ICD-10:Т40.0-Т40.3) were studied. Laboratory studies were carried out by the method of immunochromatographic analysis and chromatographymass spectrometry. Statistical data processing was performed using the IBM SPSS Statistics 29.0.0.0 program, using Spearman's rank correlation analysis (r), with p ≤ 0.05. Results. Among patients who received Naloxone, the best dynamics according to the Glasgow coma scale at the 4th and 6th hours of observation were those who received 2-6 mg of Naloxone. A significant part of patients (76 cases, 43.68 %) required repeated administration of Naloxone due to the renarcotization, in such cases a direct correlation was established with the occurrence of undesirable clinical effects (r = 0.864, p = 0.05). A direct relationship between an increase in the dose of Naloxone and the development of arterial hypertension (r = 0.945, p = 0.01), convulsions (r = 0.887, p = 0.01), withdrawal and pain syndrome (r = 0.881, p = 0.01). In general, the occurrence of clinical effects was correlated with an increase in the dose of Naloxone (R2 = 0.92), however, the rank correlation analysis did not confirm the relationship between the dose of Naloxone and the development of pulmonary edema (r = 0.938, p &gt; 0.05), cardiac arrhythmia (r= 0.598, p &gt; 0.05), cardiac arrest (r= -0.146, p &gt; 0.05). Conclusions. The use of high doses of Naloxone does not solve the problem of prevention of opioid overdoses and their effective treatment. The development of new models of antidotes to opioids using сovalent Naloxone nanoparticles, serotonin 5-HT1A agonists, Fentanyl-binding Cyclodextrin scaffolds, specific vaccines, etc. is considered promising. Keywords: opioids, antidotes, Naloxone, Fentanyl.

Sarcoidosis-Associated Pulmonary Hypertension

Sarcoidosis is characterized by non-necrotizing granulomatous aggregations affecting a range of organs, with thoracic structures involved in 90% to 95% of cases. This granulomatous disease can impact the pulmonary vasculature via different mechanisms resulting in sarcoidosis-associated pulmonary hypertension (SAPH). These include postcapillary disease (left heart disease), immune-mediated granulomatous vasculopathy, hypoxemia, thromboembolism, pulmonary vascular compression and/or stenosis by mediastinal lymph nodes/fibrosis, or sarcoidosis-related portal hypertension. SAPH is a serious complication, especially in those with end-stage lung disease. A thorough evaluation is crucial to delineate the predominant mechanism of PH in the affected individual. The management of SAPH is complex and necessitates a personalized, multifaceted approach, targeting the specific mechanisms and underlying pathologies. Such patients are best served at specialized Pulmonary Hypertension and Sarcoidosis Centers. A notable phenotype within SAPH is the “pulmonary arteriopathy” group, characterized by milder parenchymal disease and a favorable response to PAH-targeted therapy, whereas patients with active granulomatous inflammation are likely to respond to immunosuppression. Several PAH therapies have been used to treat SAPH, however, clear direction on the use of PAH therapies in SAPH is still lacking. Patients receiving pulmonary vasodilators should be carefully monitored for potential deterioration in gas exchange or development of pulmonary edema, which could suggest underlying left heart disease or pulmonary veno-occlusive disease. Timely referral for lung transplant evaluation is crucial for those with SAPH and severe parenchymal lung disease, ensuring a comprehensive and patient-centered care approach. Much work remains to be done to understand the exact pathogenesis of SAPH, as well as to develop therapies that clearly improve outcomes for these patients.

LUV Score - a combination of bedside lung ultrasound and velocity-time integral (VTI) to predict mortality risk in STEMI patients

Abstract Background Early risk stratification is essential for in-hospital management of ST-segment–elevation myocardial infarction (STEMI). Development of acute heart failure and pulmonary edema is associated with poorer prognosis in this setting. Velocity–time integral (VTI) estimates stroke volume and cardiac output and has never been tested in acute coronary syndromes. Purpose Our aim was to evaluate the prognostic ability of a novel cardiothoracic ultrasound protocol for hemodynamic assessment with lung ultrasound (LUS) and VTI in patients with STEMI. Methods LUS and VTI were performed within 24h of admission for STEMI. LUS consisted of 8 scanning zones. A LUS combined with VTI (LUV) classification was developed. Receiver operating characteristic (ROC) analyses were performed to assess LUV score with in-hospital mortality, and it was compared with traditional Killip classification. Results From September 2022 and January 2023, 104 consecutive patients were admitted with ST-segment–elevation myocardial infarction. Fifteen patients were excluded from the analysis because were not assessed within 24h of admission. Therefore, 89 patients were included in the final analysis. Mean age was 62 years, 59% were male, 55% had hypertension, 32% had diabetes, 43% was anterior wall myocardial infarction and 16% had Killip 3 or 4 at admission. Overall in-hospital mortality was 7.9% and mortality across LUV categories were 0%, 0%, 8% and 50% for LUV A-D, respectively. A VTI ≥ 14 implied a negative predictive value for in-hospital mortality of 100%. The area under the ROC curve of LUV classification for in-hospital mortality was 0.92 (P=0.001), and Killip classification (0.85, P&amp;lt;0.001; P=0.48 for the difference between curves – Figure 1). Incidences of culprit vessel according to LUV categories are illustrated at Figure 2. There were no left main culprit vessel in our sample. The distribution of Cardiac Output (CO) and Cardiac index (CI) and Cardiac Power Output (CPO) were the following: LUV A: CO = 4.5 (1.2), CI = 4.0 (1.1) CPO = 0.9 (0.3); LUV B CO = 3.8 (0.9) CI = 3.4 (0.8) CPO = 0.7 (0.2); LUV C CO = 3.3 (0.8) CI = 3.0 (0.8) CPO = 0.6 (0.1) ; LUV D CO = 2.9 (0.7) CI = 2.7(0.5) CPO = 0.5(0.1). Conclusions In a cohort of patients with ST-segment–elevation myocardial infarction undergoing primary percutaneous coronary intervention, LUV score provided an excellent AUC for prediction of in-hospital mortality. LUV score is an easy, noninvasive, rapidly acquired, and accurate method for risk stratification in STEMI patients.

Effect of CPAP therapy on the reperfusion lung injury after transluminal balloon angioplasty of the pulmonary arteries in patients with chronic thromboembolic pulmonary hypertension

Aim. To evaluate the effect of non-invasive ventilation (NIV) in CPAP (continuous positive airway pressure) mode on the development of reperfusion pulmonary edema after percutaneous balloon pulmonary angioplasty (BPA) in patients with chronic thromboembolic pulmonary hypertension (CTEPH).Materials and methods. The study included 70 patients with CTEPH who underwent the first stage of BPA. Prevention of reperfusion edema was carried out using NIV in the CPAP mode starting from the early postoperative period in combination with oxygen and diuretic therapy (as nedeed). The presence and severity of pulmonary edema was assessed based on clinical signs and data from computed tomography or chest radiography.Results. Patients after BPA were on CPAP therapy: average pressure: 10.0±0,7 hPa. During 1st day, the average time of use was: 990±417 minutes. Prolongation of CPAP therapy &gt;1 day occurred in 26 (37%) patients. Depending on the severity of reperfusion edema to the lungs, patients were divided into 2 groups: group 1 (grade 1, n=42) and group 2 (grade 3-4, n=12). During the observation period, there were no cases of severe reperfusion edema (grade 5), and no cases required the use of invasive ventilation or extracorporeal membrane oxygenation. No complications of CPAP therapy were recorded. The number of PA segments and ΔPFG did not differ, but the PEPSI index was higher in group 2: 41,9 [16,0; 57,9] vs 80.5 [52,5; 111,25], p=0,0146. The number of days before discharge after BPA in patients of group 2 was higher: 4.0 [3,9; 5,5] vs 7,0 [4,6; 10,0] days, p=0,013. Despite the development of reperfusion edema, before discharge the SpO2 values in group 2 were comparable to the baseline: 93,0 [89,9; 94,2] vs 93,0 [89,7; 94,4]Conclusion. Preventive use of NIV in the CPAP mode, starting from the early postoperative period, is safe and makes it possible to achieve optimal clinical results in patients even with moderate and severe lung reperfusion edema after large volumes of surgical intervention.

Diagnosis of pulmonary edema of small pets

The respiratory system provides the body with oxygen, which is necessary for the vital activity of organs, tissues and cells of the animal. Respiratory diseases are widespread and therefore improving the methods of diagnosis and prevention of lung pathologies is important for veterinary medicine. Pulmonary edema is a life-threatening condition of the animal and requires immediate assistance. There are various types and causes of edema, however, knowing the symptoms, it is possible to carry out the necessary diagnostics, therefore, the study of the mechanism of development and types of pulmonary edema using radiological diagnostic methods is relevant. The research work was carried out on the basis of the veterinary clinic of LLC "Ringa", the object of the study were dogs and cats with clinical manifestations of respiratory failure, the main diagnostic method was digital radiography. Based on the conducted studies, cardiogenic and non–cardiogenic pulmonary edema was identified, the mechanism of development of which has differences: cardiogenic pulmonary edema manifests itself against the background of heart defects, cardiosclerosis, arterial hypertension; non-cardiogenic – due to impaired capillary permeability and the release of the liquid part of the blood into the interstitial tissue, and then into the alveoli. X-ray diagnostics allows you to differentiate the pathology of the lungs at the initial stages of its development, since a long process of diagnostic measures can have negative consequences on the animal, and the finished radiograph has high-quality detail of the picture in high resolution with specific changes in the lungs with edema, which ensures the exclusion of other pathologies that can also lead to respiratory failure (neoplasms, pulmonary fibrosis , etc.), and that contributes to the provision of rapid appropriate actions in emergency situations to eliminate this condition and the appointment of specific therapeutic and preventive measures, allowing you to reduce the time in diagnosis, to help the patient, increasing the chances of a favorable outcome.

Periprocedural acute hemodynamic decompensation associated with substrate-based ablation of ventricular tachycardia in patients with structural heart disease - rare and nonpredictable event

Abstract Funding Acknowledgements Type of funding sources: None. Background Radiofrequency (RF) catheter ablation is an established treatment method in patients with structural heart disease (SHD) and recurrent ventricular tachycardia (VT). Due to underlying SHD, concomitant heart failure and a high burden of comorbidities, these patients are at considerable risk of periprocedural complications including acute hemodynamic decompensation (AHD) with a reported rate of up to 11%. The PAINESD score [sum of 5, 3, 6, 6, 3, 5, and 3 points for chronic obstructive pulmonary disease (COPD), age &amp;gt;60 years, ischemic cardiomyopathy (ICM), NYHA Class &amp;gt;2, LV ejection fraction (LVEF) &amp;lt;25%, electrical storm (ES), and diabetes mellitus (DM), respectively] was proposed to predict the risk of AHD, and identify the patients who may benefit from pre-emptive use of percutaneous left ventricular assist device (pVAD). Purpose The single-centre, retrospective study investigated the incidence of AHD in large-volume, tertiary referral EP centre and the predictive power of the PAINESD score. Methods We included patients who had their first ablation for SHD-related VT between August 2006 and December 2020. The procedure was performed under conscious sedation except for patients who were on mechanical ventilation because of hemodynamical or electrical instability before the ablation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right-ventricular pacing. Induced VTs were terminated by overdrive pacing or cardioverted. Activation and entrainment mapping were used rarely – only in well-tolerated VTs. The goal of ablation was to abolish all inducible VTs. A purposely established institutional registry for complications of invasive procedures was used to collect all periprocedural complications that were subsequently adjudicated using the source medical records. AHD triggered by ablation procedure was defined as intraprocedural or early post-procedural (&amp;lt;12 h) development of acute pulmonary oedema or refractory hypotension, requiring urgent intervention including (but not limited to) inotropic agents and/or artificial ventilation and/or pVAD implant. Results The study cohort consisted of 1143 patients (age: 63±13 years, males: 87%, ICM: 67%, ES: 25%, NYHA Class: 2.1±1.0, LVEF: 34±13%, DM: 32%, COPD: 12%). Their PAINESD score was 11.4±6.6 (median: 12, interquartile range: 6–17). The ablation procedure (total duration 187±78 min, RF time: 23±15 min) was complicated by AHD in 13/1143 = 1.1% patients and these adverse events were not predicted by PAINESD score (Figure). Conclusions We observed a substantially lower rate (1.1%) of AHD than previously reported (up to 11%). These events did not accumulate in patients with upper-tertile PAINESD score in whom the highest AHD risk was reported (up to 24%). This observation may be explained by careful substrate-based ablation under conscious sedation that prevents prolonged low-output state related to repeated VT induction and mapping in general anaesthesia.

Abstract 635: ESAM Deficiency-related Coronary Microvascular Dysfunction Contributes To Left Ventricle Diastolic Dysfunction In HFpEF

Coronary microvascular dysfunction and vascular inflammation have been linked to heart failure with preserved ejection fraction (HFpEF), but the underlying molecular mechanisms remain incompletely understood. Endothelial cell-selective adhesion molecule (ESAM) has been recently implicated as one of the biomarkers for heart failure. The biological function of ESAM is to regulate inflammatory cell adhesion, permeability and angiogenesis. Here, we examined the mechanistic role of ESAM in contributing left ventricle (LV) diastolic dysfunction in a mouse model of human HFpEF. We employed wild type (WT) mice and mice with homozygous genetic deficiency of ESAM (ESAM -/- ), with or without uninephrectomy and aldosterone infusion (UNX-Aldo, for 4-week). Using echocardiography, we found that WT mice with UNX-Aldo develop LV diastolic dysfunction, as indicated by a significantly reduced E/A ratio (E=early, A=late mitral inflow peak velocities), increased E/e’ ratio, isovolumic relaxation time (IVRT) and E wave deceleration time. UNX-Aldo significantly increased the serum soluble ESAM levels, along with elevated MMP2/9 levels, as potential mediators of ESAM ectodomain shedding. When compared to WT, ESAM -/- mice with UNX-Aldo displayed significant worsening of LV diastolic dysfunction, as indicated by increased IVRT, and the development of pulmonary edema and fibrosis. An unbiased automated tracing and 3D reconstruction of coronary microvasculature revealed that ESAM -/- mice had a significantly reduced coronary microvascular density. Arteries of ESAM -/- mice exhibited impaired endothelial sprouting and in cultured endothelial cells siRNA-mediated ESAM knockdown reduced tube formation. Thus, we propose that ESAM plays a role in the proper myocardial vascularization, hence the maintenance of myocardial perfusion. Deficiency, or augmented ectodomain shedding of ESAM impairs myocardial vascularization, whereby it contributes to the development of LV diastolic dysfunction, and could have mechanistic and diagnostic implications in human HFpEF.

PO-05-039 PERIPROCEDURAL ACUTE HEMODYNAMIC DECOMPENSATION ASSOCIATED WITH SUBSTRATE-BASED ABLATION OF VENTRICULAR TACHYCARDIA IN PATIENTS WITH STRUCTURAL HEART DISEASE – RARE AND NONPREDICTABLE EVENT

Patients with structural heart disease (SHD) and recurrent ventricular tachycardia (VT) are at considerable risk of periprocedural complications of radiofrequency (RF) catheter ablation including acute hemodynamic decompensation (AHD). The PAINESD score [sum of 5, 3, 6, 6, 3, 5, and 3 points for chronic obstructive pulmonary disease (COPD), age >60 years, ischemic cardiomyopathy (ICM), NYHA Class >2, LV ejection fraction (LVEF) <25%, electrical storm (ES), and diabetes mellitus (DM), respectively] was proposed to predict the risk of AHD, and identify the patients who may benefit from pre-emptive use of percutaneous left ventricular assist device (pVAD). The single-center, retrospective study investigated the incidence of AHD in large-volume, tertiary referral EP center and the predictive power of the PAINESD score. We included patients who had their first ablation for SHD-related VT between August 2006 and December 2020. The procedure was performed under conscious sedation except for patients who were on mechanical ventilation because of hemodynamical or electrical instability before the ablation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right-ventricular pacing. Activation and entrainment mapping were used rarely, only in well-tolerated VTs. The goal of ablation was to abolish all inducible VTs. AHD triggered by ablation procedure was defined as intra- or early post-procedural (<12 h) development of acute pulmonary oedema or refractory hypotension, requiring urgent intervention like inotropic agents and/or artificial ventilation and/or pVAD implant. The study cohort consisted of 1143 patients (age: 63±13 years, males: 87%, ICM: 67%, ES: 25%, NYHA Class: 2.1±1.0, LVEF: 34±13%, DM: 32%, COPD: 12%). Their PAINESD score was 11.4 ± 6.6 (median: 12, interquartile range: 6–17). The ablation procedure (total duration 187±78 min, RF time: 23±15 min) was complicated by AHD in 13/1143 = 1.1% patients and these adverse events were not predicted by PAINESD score (Figure). We observed a substantially lower rate (1.1%) of AHD than previously reported (up to 11%). These events did not accumulate in patients with upper-tercile PAINESD score in whom the highest AHD risk was reported (up to 24%). This observation may be explained by careful substrate-based ablation under conscious sedation that prevents prolonged low-output state related to repeated VT induction and mapping in general anesthesia.

Reexpansion Pulmonary Edema After Intrapleural Fibrinolytic Therapy

We report an empyema treated with antimicrobial therapy that developed reexpansion pulmonary edema after intrapleural fibrinolytic and enzyme therapy. Rapid evacuation of pleural fluid likely contributed to the development of reexpansion pulmonary edema.

Whole-exome sequencing in searching for novel variants associated with the development of high altitude pulmonary edema

BackgroundHigh altitude pulmonary edema (HAPE) is a high-altitude idiopathic disease with serious consequences due to hypoxia at high altitude, and there is individual genetic susceptibility. Whole-exome sequencing (WES) is an effective tool for studying the genetic etiology of HAPE and can identify potentially novel mutations that may cause protein instability and may contribute to the development of HAPE. Materials and methodsA total of 50 unrelated HAPE patients were examined using WES, and the available bioinformatics tools were used to perform an analysis of exonic regions. Using the Phenolyzer program, disease candidate gene analysis was carried out. SIFT, PolyPhen-2, Mutation Taster, CADD, DANN, and I-Mutant software were used to assess the effects of genetic variations on protein function. ResultsThe results showed that rs368502694 (p. R1022Q) located in NOS3, rs1595850639 (p. G61S) located in MYBPC3, and rs1367895529 (p. R333H) located in ITGAV were correlated with a high risk of HAPE, and thus could be regarded as potential genetic variations associated with HAPE. ConclusionWES was used in this study for the first time to directly screen genetic variations related to HAPE. Notably, our study offers fresh information for the subsequent investigation into the etiology of HAPE.