Pulmonary Artery Occlusion Research Articles

Mechanical Circulatory Support in Patients with End-Stage Heart Failure

Objective. The aim of the study is to establish the effectiveness of mechanical support of blood circulation of patients with end-stage heart failure depending on the method of surgical correction.
 Materials and methods. The results of the study are based on the data of examination and dynamic observation of 73 patients (median age 44 (16-69) years, 68 men, 5 women) who were treated from 2008-2019 іn the following medical institutions: Republican Scientific and Practical Center «Cardiology» (Minsk, Republic of Belarus) and Center of cardiac surgery on the basis of Hospital «Feofania». Patients were examined during the initial examination, after 3 months and after 1 year.
 Results and discussion. As a result of the study found, indications for surgical treatment of patients with end-stage heart failure those are the following criteria: left ventricular ejection fraction (LV EF) <20%, (p < .0001). Pulmonary artery occlusion pressure (PAL) from 25 mm Hg up to 35 mm Hg (p < .0001). Peak myocardial oxygen consumption <14 ml/kg/min on the background of maximum drug therapy (p < .0001). Pulmonary vascular resistance (PVR) <5 units by Wood, (p < .0001). Transpulmonary gradient up to 15 mm Hg (p < .0001). Indications for LVAD therapy are the following criteria: left ventricular ejection fraction (LV EF) <20%, (p <0001). Pulmonary artery occlusion pressure > 35 mm Hg (p < .0001). Pulmonary vascular resistance (PVR) >5 units by Wood, (p < .0001). Transpulmonary gradient >15 mm Hg (p < .0001). Against the background of work LVAD after 3 months there was a decrease in the left ventricular cavity by 30%, (p < .0001), decrease in the pancreatic cavity by 25.5%, (p < .0001), increase in fraction LV emission by 21%, (p < .0001). According to direct pulmonary arterial tonometry with LVAD therapy, there was a decrease in pulmonary vascular resistance «Wood» by 34%, (p < .0001), reduction in pulmonary arterial pressure by 24%, (p < .0001), a decrease of transpulmonary gradient by 21%, (p < .0001). The results of the change in functional indicators in patients on LVAD therapy after 3 months: increase maximum myocardial oxygen consumption by 6% (p < .0001), increase exercise tolerance by 15% (p < .0001). Indications for BiVAD-therapy are the following criteria: biventricular insufficiency, (p < .0001). Pulmonary artery occlusion pressure >35 mm Hg, (p < .0001). Pulmonary vascular resistance >5 units by Wood, (p < .0001). Transpulmonary gradient >15 mm Hg, (p < .0001). Against the background of BiVAD work in 3 months was noted reduction of the right ventricular (RV) enddiastolic volume (EDV) by 6% (p <0001), reduction of the RV end-systolic volume (ESV) by 10%, (p < .0001), increase in LV EF by 33%, (p < .0001), decrease in left ventricular (LV) ESV (M-mode) by 36.3%, (p < .0001), a decrease in LV EDV (M-mode) by 30%, (p < .0001), a decrease in LV ESV (B-mode) by 22.5%, (p < .0001), increase in tricuspid systolic excursion (TAPSE) by 21.4%, (p < .0001). According to the direct pulmonary arterial tonometry during use BiVAD-therapy: reduction of pulmonary vascular resistance «Wood» by 22%, (p < .0001), reduction of pulmonary arterial pressure by 15%, (p <0001), reduction of transpulmonary gradient by 14%, (p <0001). The results of surgical treatment of patients with critical heart failure: after direct orthotopic heart transplantation (OHT): 24 patients were treated with positive result (92%), 2 patients died (8%). There were 18 patients performed secondary OHT, patients who were on LVAD therapy (46%). 18 patients (46%) continue LVAD-therapy. On LVAD-therapy 3 patients died (8%). The cause of death is purulent-septic lesions. Which patients were on BiVAD-therapy: secondary OHT performed 4 patients (50%). 4 patients (50%) died on BIVAD-therapy. The cause of death in 2 cases was purulent-septic lesions (50%), and in 2 other cases it was multisystem organ failure (50%)
 Conclusions. Analysis of the results of the differential approach to surgical treatment patients with heart failure NYHA functional class III-IV: patients with critical heart failure in the presence of contraindications to direct heart transplantation, it is advisable to consider the use of long-term mechanical circulatory support based on LVAD therapy (p < .0001) and BiVAD-therapy (p < .0001) as a mechanical bridge to heart transplantation. Applied long-term mechanical support of blood circulation in patients with high indicators of pulmonary hypertension (p < .0001), allows in a short time (4-6 weeks) to normalize pulmonary artery pressure and consider performing a secondary heart transplant.

Evaluation of intramuscular sodium nitroprusside injection to improve oxygenation in white-tailed deer (Odocoileus virginianus) anesthetized with medetomidine–alfaxalone–azaperone

ObjectiveIn ungulates, α2-adrenergic agonists can decrease oxygenation possibly through alteration of pulmonary perfusion. Sodium nitroprusside can decrease pulmonary vascular resistance (PVR) and increase cardiac output (Q˙t) through vasodilation. The objective was to determine if sodium nitroprusside would improve pulmonary perfusion and attenuate the increased alveolar–arterial (a–a) gradient resulting from medetomidine–azaperone–alfaxalone (MAA) administration. Study designProspective, randomized, crossover study with a 2 week rest period. AnimalsA group of eight adult female captive white-tailed deer (Odocoileus virginianus). MethodsDeer were administered MAA intramuscularly (IM), and auricular artery and pulmonary artery balloon catheters were placed. Deer spontaneously breathed air. Saline or sodium nitroprusside (0.07 mg kg–1) were administered IM 40 minutes after MAA injection. Heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary artery occlusion pressure (PAOP), right atrial pressure (RAP), Q˙t, arterial pH, PaCO2 and PaO2 were obtained immediately before nitroprusside injection (baseline) and 5, 10 and 15 minutes afterwards. Mixed venous blood samples were obtained at baseline and at 5 minutes. Systemic vascular resistance (SVR), PVR, intrapulmonary shunt fraction (Q˙s/Q˙t), a–a gradient, oxygen delivery (D˙O2) and oxygen extraction ratio (O2ER) were calculated. Statistical analysis was performed with repeated measures analysis of variance with correction factors. A p value < 0.05 was considered significant. ResultsWith nitroprusside, MAP, MPAP, PAOP, RAP, SVR and O2ER significantly decreased and HR, Q˙t and D˙O2 increased compared with baseline and between treatments. There was a significant decrease in PVR and a–a gradient and increase in PaO2 compared with baseline and saline treatment. Changes were not sustained. Conclusions and clinical relevanceNitroprusside temporarily changed hemodynamic variables, increased PaO2 and decreased a–a gradient. Nitroprusside possibly led to better pulmonary perfusion of ventilated alveoli. However, IM nitroprusside at this dose is not recommended because of severe systemic hypotension and short action.

High rates of pulmonary artery occlusions in COVID-19. A meta-analysis.

BackgroundCOVID‐19 patients are considered at high risk of venous thromboembolism (VTE). The real nature of pulmonary artery occlusions (PAO) in COVID‐19 has been questioned, suggesting that it is caused also by in situ thrombi, rather than only by emboli (PE) from peripheral thrombi.MethodsWe searched MEDLINE for studies published until 6 June 2020 that included COVID‐19 patients or non‐COVID‐19 medical patients at VTE risk, treated with heparins, in whom VTE (PE and deep vein thrombosis, DVT) had been reported. Systematic review and results reporting were conducted in accordance with PRISMA guidelines. Data were independently extracted by two observers, and estimates were pooled using random‐effects meta‐analysis.ResultsWe identified 17 studies including 3224 COVID‐19 patients and 7 including 11 985 non‐COVID‐19 patients. Two analyses were performed: in all COVID‐19 patients and only in those (n = 515) who, like non‐COVID‐19 patients, were screened systematically for DVT. The latter analysis revealed that the prevalence of DVT was 15.43% (95%CI, 4.08‐31.77) in COVID‐19 and 4.21% (2.27‐6.68) in non‐COVID‐19 patients (P = .0482). The prevalence of PE was 4.85% (40.33‐13.01) in COVID‐19 patients and 0.22% (0.03‐0.55) in non‐COVID‐19 patients (P = .0128). The percentage of PE among VTE events was 22.15% (5.31‐44.60) in COVID‐19 and 6.39% (3.17‐10.41) in non‐COVID‐19 patients (P = .0482). Differences were even more marked when all COVID‐19 patients were analysed.ConclusionsThe results of our meta‐analysis highlight a disproportion in the prevalence of PE among all VTE events in COVID 19 patients, likely reflecting PAO by pulmonary thrombi, rather than emboli from peripheral vein thrombi.

A CASE OF PULMONARY VEIN THROMBOSIS WITH EXTENSION INTO THE LEFT ATRIUM

SESSION TITLE: Medical Student/Resident Signs and Symptoms of Chest Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary vein thrombosis (PVT) is a rare and often misdiagnosed condition due to nonspecific symptoms at presentation. PVT is most commonly associated with lung malignancy, recent major pulmonary surgery, or atrial fibrillation. Symptoms generally include cough, dyspnea, nonspecific chest pain, and hemoptysis, similar to pulmonary embolism. Delay in diagnosis can be lethal. CASE PRESENTATION: A 76-year-old female with hyperthyroidism, history of DVT in 2018 previously on rivaroxaban, venous insufficiency and hypertension presented with cough, congestion, and progressive fatigue for 3 days. She was increasingly dyspneic at rest and with activity the day prior to admission. She required supplemental oxygenation with 2 L/minute via nasal cannula on evaluation at our emergency center. She additionally tested positive for influenza A and B. She denied chest pain, palpitations, or orthopnea, but did have associated worsening right lower extremity edema. Bilateral lower extremity venous duplex showed evidence of an acute thrombus in the right common femoral, superficial femoral, deep femoral, and popliteal veins; the left leg had no thromboses. Given evidence of acute DVT and acute hypoxemic respiratory failure on presentation, a CT PE protocol was done, noting a thrombus in the left lower pulmonary vein that extended into the left atrium (figures 1-3), with chronic occlusion of the left lower lobe pulmonary arteries as well as enlarged pulmonary arteries. She was initially treated with a heparin drip from 1/23/2020 to 1/27/2020, then she was transitioned to oral anticoagulation with rivaroxaban 20 mg PO daily. She maintained resting oxygen saturations on room air for three days prior to discharge on 1/28/2020 and her respiratory symptoms improved significantly. She had no evidence of underlying malignancy at the time. She has followed up twice with her primary care physician, remains on oral anticoagulation, and has had no respiratory complaints since discharge. Pending outpatient hypercoagulable workup and repeat chest imaging, which was recommended in 6 months. DISCUSSION: PVT is a rare yet life threatening condition if undiagnosed. It can lead to pulmonary hypertension, cor pulmonale, TIA or stroke, and even pulmonary infarction or gangrene. Though there is no present gold standard for diagnosis of PVT, CT pulmonary angiography led to the diagnosis in this case. CONCLUSIONS: Chronic anticoagulation is the mainstay of therapy for PVT. Though some cases may be idiopathic, it is prudent to investigate further for hypercoagulable states, including malignancy. Reference #1: Chaaya, G., & Vishnubhotla, P. (2017). Pulmonary Vein Thrombosis: A Recent Systematic Review. Cureus, 9(1), e993. https://doi.org/10.7759/cureus.993 Reference #2: Rana, M. A., Tilbury, N., & Kumar, Y. (2016). Idiopathic pulmonary vein thrombus extending into left atrium: a case report and review of the literature. Hindawi Publishing Corporation: Case Reports in Medicine, 2016, (article ID 3528393), 1-3. https://www.hindawi.com/journals/crim/2016/3528393/ Reference #3: Sahay, S., & Lodato, R. (2013). Pulmonary vein thrombosis: a rare entity. CHEST Journal, 144 (4_MeetingAbstracts). https://journal.chestnet.org/article/S0012-3692(16)42762-5/fulltext DISCLOSURES: No relevant relationships by Kendall Creed, source=Web Response No relevant relationships by Peter Khalil, source=Web Response No relevant relationships by Victor Test, source=Web Response No relevant relationships by Alexandra Wichmann, source=Web Response

TUMORAL PULMONARY HYPERTENSION: A RARE BUT DEADLY COMPLICATION OF METASTATIC CANCER

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary tumor microembolism (PTE) and pulmonary tumor thrombotic microangiopathy (PTTM) are rare complications of metastatic cancer that can mimic acute pulmonary embolism (PE). They can present as fulminant right heart failure and are invariably fatal. They are usually associated with gastric and bronchogenic carcinomas. We report a patient with metastatic breast cancer who rapidly developed severe right ventricular failure with no evidence of PE on imaging, thought to be due to tumoral pulmonary hypertension (PH). CASE PRESENTATION: A 33-year-old female with recently diagnosed invasive ductal breast cancer with liver metastases presented with dyspnea for a few days. She had tachycardia, tachypnea and tender hepatomegaly, along with elevated D-dimer and liver enzymes. CT angiogram (CTA) of the lung was negative for PE. Echocardiogram (ECHO) showed severe PH and mildly dilated right ventricle (RV). She received one dose of paclitaxel. On day 3, the patient was intubated for worsening respiratory distress. Repeat CTA of the lung was negative for PE. ECHO now showed a severely dilated RV with decreased systolic function highly suggestive of thromboembolism for which alteplase was administered empirically. Despite thrombolysis and vasopressor support, she continued to deteriorate and developed multiorgan failure leading to death within 24 hours of intubation. DISCUSSION: Tumoral PH includes microvascular conditions (PTE and PTTM), tumor macroembolism, and intravascular invasion of tumors. PTE is the occlusion of small pulmonary arteries by tumor cells. PTE along with activation of coagulation and growth factors causing intimal proliferation becomes PTTM. PTTM is commonly seen in adenocarcinoma with only 3% cases occurring with breast cancer. Patients present with dyspnea, hypoxemia, and PH of unknown origin invariably progressing to right heart failure and death. Routine imaging such as CTA of the lung is usually normal. Cytology of the aspirate from a wedged pulmonary artery catheter has a reported sensitivity of 80–88% and a specificity of 82– 94%. However, there is rapid clinical deterioration and associated high mortality. High index of suspicion is required for diagnosis which is rarely made antemortem. Decreasing tumor burden with chemotherapy in combination with dexamethasone, warfarin and aspirin, also immunotherapy with PDGF inhibitor (imatinib) and VEGF inhibitor (bevacizumab) can be beneficial. CONCLUSIONS: Unexplained acute PH in patients with metastatic cancer should prompt concern for tumoral PH. Some advances in antemortem diagnosis have given hope for the treatment of this once thought to be an exclusively postmortem diagnosis. Treatment targeting growth factors looks promising and needs further investigation. Reference #1: Price LC, Seckl MJ, Dorfmüller P, Wort SJ. Tumoral pulmonary hypertension. Eur Respir Rev. 2019;28(151):180065. Published 2019 Feb 6. doi:10.1183/16000617.0065-2018 Reference #2: Mury, C., Schneider, A. G., Nobile, A., Rotman, S., & Liaudet, L. (2015). Acute Pulmonary Hypertension Caused by Tumor Embolism: A Report of Two Cases. Pulmonary Circulation, 5(3), 577-579. doi:10.1086/682225 Reference #3: Mury, C., Schneider, A. G., Nobile, A., Rotman, S., & Liaudet, L. (2015). Acute Pulmonary Hypertension Caused by Tumor Embolism: A Report of Two Cases. Pulmonary Circulation, 5(3), 577-579. doi:10.1086/682225 Ho, A. L., Szulakowsi, P., & Mohamid, W. H. (2015). The diagnostic challenge of pulmonary tumour thrombotic microangiopathy as a presentation for metastatic gastric cancer: A case report and review of the literature. BMC Cancer, 15(1). doi:10.1186/s12885-015-1467-7 DISCLOSURES: No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Delyse Garg, source=Web Response No relevant relationships by Davita Mabourakh, source=Web Response No relevant relationships by Nirav Mistry, source=Web Response No relevant relationships by Aditi Saha, source=Web Response No relevant relationships by Sohaib Tariq, source=Web Response No relevant relationships by Lalithaa Thirunavukarasu Murugan, source=Web Response

Postpartum pulmonary circulation in pregnant rats with monocrotaline-induced pulmonary arterial hypertension.

BackgroundThis is the first study to evaluate changes in postpartum pulmonary circulation in a novel pregnant rat model of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH).MethodsFemale rats were randomly divided into two groups: the MCT-treated pregnant group, in which rats were injected with MCT (40 mg/kg) at the age of 7 weeks, and the pregnant group, in which rats were injected with the same volume of 0.9% saline at the same age. Rats from both groups were mated at the age of 9 weeks. General condition information, hemodynamic data and pulmonary tissues were collected from pregnant rats from the two groups on the 18th day after successful mating (T1) and the 1st (T2), 3rd (T3), and 7th days after delivery (T4).ResultsThe MCT-treated pregnant group exhibited a greater mean pulmonary artery pressure (mPAP) (P<0.01) and Fulton’s Index (P<0.01) than the pregnant group at each time point. Lung tissues from the MCT-treated pregnant group showed pulmonary vascular hyperplasia and occlusive changes. The mPAP and the occluded pulmonary artery density in the MCT-treated pregnant group increased after delivery (P<0.01) and significantly increased at T3 compared with T2 (P<0.05) but was not further increased at T4 (P>0.05).ConclusionsPregnant rats with PAH exhibited increased mPAP after delivery accompanied by a significant increase in the occluded pulmonary artery density, which may have contributed to the increased mortality rate of pregnant rats with PAH after delivery.

Prevalence and Clinical Correlates of Echo-Estimated Right and Left Heart Filling Pressures in Hospitalized Patients With Coronavirus Disease 2019.

Objectives:The prevalence of elevated right and left heart filling pressures in coronavirus disease 2019 is not well characterized. We aimed to characterize the prevalence of pulmonary hypertension and concurrent elevated left heart filling pressure in hospitalized patients with coronavirus disease 2019. We hypothesized that a significant proportion of coronavirus disease 2019 patients has evidence of pulmonary hypertension associated with elevated left heart filling pressure on transthoracic echocardiography.Design:Retrospective cohort study.Setting:Academic tertiary-care center.Patients:Hospitalized coronavirus disease 2019 patients who underwent clinical transthoracic echocardiography.Interventions:None.Measurements and Main Results:The exposure variable of interest was right ventricular systolic pressure, calculated using the American Society of Echocardiography guidelines. Pulmonary hypertension was defined as right ventricular systolic pressure greater than 40 mm Hg. Left heart filling pressure was estimated with Nagueh’s method for pulmonary artery occlusion pressure using E/e’ ratio, and normal was considered pulmonary artery occlusion pressure less than 16 mm Hg. Clinical characteristics and outcomes were compared between the patients with and without pulmonary hypertension. A total of 73 patients (median age 66 yr [57–75 yr]; 46% women) were included. Median right ventricular systolic pressure was 39 mm Hg (interquartile range, 32–50 mm Hg), and 36 patients (49.3%) had evidence of pulmonary hypertension. Patients with pulmonary hypertension were more likely to require ICU admission (86% vs 65%; p = 0.035) and have acute respiratory distress syndrome (72% vs 49%; p = 0.0053) than those without. In-hospital mortality was 26% for those with pulmonary hypertension compared with 14% for those without (p = 0.19). Patients with pulmonary hypertension had higher median-estimated pulmonary artery occlusion pressure (17.4 mm Hg [12.7–21.3 mm Hg] vs 12.1 mm Hg [10.0–14.1 mm Hg]; p = 0.0008), and elevated left heart filling pressure was present in 59% of those with pulmonary hypertension.Conclusions:Pulmonary hypertension is common in hospitalized patients with coronavirus disease 2019 and is associated with poor clinical outcomes. Left ventricular filling pressure is elevated in over half of those with pulmonary hypertension and may represent a target to reduce right ventricular afterload and potentially improve outcomes in coronavirus disease 2019.

Continuous Estimation of Acute Changes in Preload Using Epicardially Attached Accelerometers.

A miniaturized accelerometer can be incorporated in temporary pacemaker leads which are routinely attached to the epicardium during cardiac surgery and provide continuous monitoring of cardiac motion during and following surgery. We tested if such a sensor could be used to assess volume status, which is essential in hemodynamically unstable patients. An accelerometer was attached to the epicardium of 9 pigs and recordings performed during baseline, fluid loading, and phlebotomy in a closed chest condition. Alterations in left ventricular (LV) preload alter myocardial tension which affects the frequency of myocardial acceleration associated with the first heart sound ( fS1). The accuracy of fS1 as an estimate of preload was evaluated using sonomicrometry measured end-diastolic volume (EDV[Formula: see text]). Standard clinical estimates of global end-diastolic volume using pulse index continuous cardiac output (PiCCO) measurements (GEDV[Formula: see text]) and pulmonary artery occlusion pressure (PAOP) were obtained for comparison. The diagnostic accuracy of identifying fluid responsiveness was analyzed for fS1, stroke volume variation (SVV[Formula: see text]), pulse pressure variation (PPV[Formula: see text]), GEDV[Formula: see text], and PAOP. Changes in fS1 correlated well to changes in EDV[Formula: see text] ( r2=0.81, 95%CI: [0.68, 0.89]), as did GEDV[Formula: see text] ( r2=0.59, 95%CI: [0.36, 0.76]) and PAOP ( r2=0.36, 95%CI: [0.01, 0.73]). The diagnostic accuracy [95%CI] in identifying fluid responsiveness was 0.79 [0.66, 0.94] for fS1, 0.72 [0.57, 0.86] for SVV[Formula: see text], and 0.63 (0.44, 0.82) for PAOP. An epicardially placed accelerometer can assess changes in preload in real-time. This novel method can facilitate continuous monitoring of the volemic status in open-heart surgery patients and help guiding fluid resuscitation.

Pulmonary artery hemodynamics are associated with duration of nocturnal desaturation but not apnea-hypopnea index.

Sleep-disordered breathing and nocturnal hypoxia are prevalent among patients with precapillary pulmonary hypertension (PAH). The rationale for these associations remains unclear and these relationships have not been well studied in other forms of pulmonary hypertension (PH). We hypothesized that severity of sleep-disordered breathing and nocturnal hypoxia are associated with worsening pulmonary hemodynamics, regardless of hemodynamic profile. Four hundred ninety-three patients were divided into 4 groups: 1) no PH, 2) postcapillary pulmonary hypertension, 3) PAH, and 4) mixed PAH/postcapillary pulmonary hypertension. The relationship between right heart catheterization measurements and apnea-hypopnea index or the percentage of sleep time spent with oxygen saturation < 90% (T90) was calculated using multiple linear regression. Analysis of variance was used for between-group comparisons. Statistical models were adjusted for known confounders. Apnea-hypopnea index did not differ between hemodynamic subgroups (P = .27) and was not associated with right atrial pressure (.11 ± .19, P = .55), cardiac index (.25 ± 1.64, P = .88), mean pulmonary artery pressure (-.004 ± .09, P = .97), or pulmonary artery occlusion pressure (.16 ± .14, P = .26). While patients with PH had a higher T90 than those without (mean 24.2% vs 11.7%, P < .001), there was no difference in T90 between individual PH subgroups (P = .70). T90 was associated with mean pulmonary artery pressure (.55 ± .10, P < .0001), PVR (1.61 ± .49, P = .001), and right atrial pressure (.50 ± .20, P = .01), but not cardiac index (-.76 ± 1.73, P = .66), or pulmonary artery occlusion pressure (.23 ± .15, P = .13). Increased PH severity was associated with longer duration of nocturnal hypoxia regardless of hemodynamic subgroup.

The Evaluation of Factors Affecting Hemodynamic Variability in Mechanically-Ventilated Patients After Cardiac Surgery.

BackgroundOptimizing cardiac preload is usually the first step in patients with unstable hemodynamic. However, it should be remembered that an unnecessary volume expansion may exacerbate the hemodynamic. In mechanically ventilated patients, the ventilatory induced hemodynamic variations (VIHV) can be used to predict the fluid requirement. These variations (called dynamic indices of cardiac filling pressure), are superior to static indices (central venous and pulmonary artery occlusion pressure) in diagnosing any volume requirement. We theorized that some conditions other than hypovolemia might affect these hemodynamic variations.ObjectivesThe current study aimed to discover these conditions in adult patients admitted to post-cardiac surgery ICU.MethodsThis antegrade cross-sectional study was conducted on 304 adult patients who were admitted to ICU after elective cardiac surgery in a teaching hospital (Tabriz-Iran). During the first 3 hours of the admission, the systolic (ΔSBP), diastolic (ΔDBP), mean (ΔMAP), and arterial blood pulse pressures (ΔPP) were invasively monitored and calculated in percent value. Because of the return of spontaneous breathing in most of the patients, the calculations were done only during the first 3-hour. All patients with spontaneous breathing, irregular cardiac rhythm, or re-admission to OR in this period were excluded from the study. We recorded demographic and surgical characteristics, perioperative hemodynamic and echocardiographic, and complications data and surveyed the correlation between VIHV and perioperative data.ResultsTwo hundred and ninety two patients met the inclusion criteria. Coronary artery bypass grafting (CABG) was the most common surgery (64.4 %). Cardiopulmonary bypass (CPB) was used in 95.55% of the surgeries. In the first 24-hour, 51 patients required re-operation because of sternum closure, bleeding control, cardiac tamponade, and coronary artery revascularization. Mortality and morbidity occurred in 2 (0.68%) and 50 (17.12%) patients, respectively. Among VIHVs, the ΔPP had the most significant value. Thus, mean ΔPP was calculated and the correlation between its severity (≤ 20% vs. > 20%) and other values surveyed. It was high in patients with cardiac dysfunction and tamponade (P value < 0.001). No significant correlation was found between mean ΔPP severity and hemorrhage rate, fluid balance, need to vasoactive agents, blood products, or bleeding control, redo CABG or sternum closure surgery, time to tracheal extubation, ICU stay, and postoperative complications. Patients with closed sternum were the same as those with the unclosed sternum.ConclusionsThe ΔPP was the most sensitive VIHV parameter. Cardiac dysfunction and tamponade increased ΔPP. Unclosed sternum did not affect its value. ΔPP value did not affect postoperative complications rate, time to tracheal extubation, or ICU stay.

Variation in Fluid and Vasopressor Use in Shock With and Without Physiologic Assessment: A Multicenter Observational Study.

To characterize the association between the use of physiologic assessment (central venous pressure, pulmonary artery occlusion pressure, stroke volume variation, pulse pressure variation, passive leg raise test, and critical care ultrasound) with fluid and vasopressor administration 24 hours after shock onset and with in-hospital mortality. Multicenter prospective cohort study between September 2017 and February 2018. Thirty-four hospitals in the United States and Jordan. Consecutive adult patients requiring admission to the ICU with systolic blood pressure less than or equal to 90 mm Hg, mean arterial blood pressure less than or equal to 65 mm Hg, or need for vasopressor. None. Of 1,639 patients enrolled, 39% had physiologic assessments. Use of physiologic assessment was not associated with cumulative fluid administered within 24 hours of shock onset, after accounting for baseline characteristics, etiology and location of shock, ICU types, Acute Physiology and Chronic Health Evaluation III, and hospital (beta coefficient, 0.04; 95% CI, -0.07 to 0.15). In multivariate analysis, the use of physiologic assessment was associated with a higher likelihood of vasopressor use (adjusted odds ratio, 1.98; 95% CI, 1.45-2.71) and higher 24-hour cumulative vasopressor dosing as norepinephrine equivalent (beta coefficient, 0.37; 95% CI, 0.19-0.55). The use of vasopressor was associated with increased odds of in-hospital mortality (adjusted odds ratio, 1.88; 95% CI, 1.27-2.78). In-hospital mortality was not associated with the use of physiologic assessment (adjusted odds ratio, 0.86; 95% CI, 0.63-1.18). The use of physiologic assessment in the 24 hours after shock onset is associated with increased use of vasopressor but not with fluid administration.

Dynamic right and left ventricular interactions in the pig.

What is the central question of this study? Are the mechanisms that cause ventricular interdependence different when due to primary right to left ventricular pressure loading? What is the main finding and its importance? An instantaneous selective increase in aortic pressure causes an immediate increase in right ventricular end-systolic pressure independent of the pericardium, whereas a selective increase in pulmonary artery pressure decreases left ventricular diastolic compliance owing to a subsequent increasing right ventricular end-diastolic volume as a function of an intact pericardium limiting biventricular volume. Changes in contraction synchrony of either ventricle do not appear to be causing these effects. I characterized the dynamic factors determining ventricular interdependence with and without the pericardium. I measured right (RV) and left ventricular (LV) pressures and volumes simultaneously using conductance catheters in seven pentobarbitone-anaesthetized open-chested 5- to 7-week-old piglets. I studied these effects during apnoea, inferior vena caval occlusion and rapid partial aortic and pulmonary arterial occlusions. Conductance catheter-defined long-axis regional volumes were assessed to define regional contractile synchrony. Closed-pericardium measures were made from an initial (baseline) volume, then after two 20mlkg-1 fluid loads followed by an open-pericardium step. Baseline RV and LV volumes were similar. Aortic occlusion increased LV pressures and volumes and RV end-systolic pressure such that RV end-systolic elastance increased without changes in RV contraction synchrony, not affected by the pericardium. Pulmonary artery occlusion increased RV end-systolic pressure but not end-systolic volume. On the subsequent beat, RV end-diastolic pressure increased, whereas LV end-diastolic volume and diastolic compliance decreased. These effects were attenuated by opening the pericardium. Contraction synchrony across longitudinal segments was unaltered by either aortic or pulmonary artery occlusion. I conclude that the determinants of systolic and diastolic ventricular interdependence are different. Increasing RV pressures causes diastolic RV-to-LV interdependence, decreasing LV diastolic compliance and dependent on an intact pericardium. An increase in LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium and has a minimal effect on RV diastolic function or contraction synchrony.

Pulmonary vessel casting in a rat model of monocrotaline-mediated pulmonary hypertension.

Pulmonary hypertension is a chronic vascular disease characterized by pulmonary vasoconstriction and pulmonary arterial remodeling. Pulmonary arterial remodeling is mainly due to small pulmonary arterial wall thickening and lumen occlusion. Previous studies have described intravascular changes in lung sections using histopathology, but few were able to obtain a fine detailed image of the pulmonary vascular system. In this study, we used Microfil compounds to cast the pulmonary arteries in a rat model of monocrotaline-induced pulmonary hypertension. High-quality images that enabled quantification of distal pulmonary arterial branching based on the number of vessel bifurcations/junctions were demonstrated in this model. The branch and junction counts of distal pulmonary arteries significantly decreased in the monocrotaline group compared to the control group, and this effect was inversely proportional to the mean pulmonary artery pressure observed in each group. The patterns of pulmonary vasculature and the methods for pulmonary vessel casting are presented to provide a basis for future studies of pulmonary arterial remodeling due to pulmonary hypertension and other lung diseases that involve the remodeling of vasculature.

Recombinant Adenosine Deaminase Ameliorates Inflammation, Vascular Disease, and Fibrosis in Preclinical Models of Systemic Sclerosis.

Systemic sclerosis (SSc) is characterized by fibrosis, vascular disease, and inflammation. Adenosine signaling plays a central role in fibroblast activation. We undertook this study to evaluate the therapeutic effects of adenosine depletion with PEGylated adenosine deaminase (PEG-ADA) in preclinical models of SSc. The effects of PEG-ADA on inflammation, vascular remodeling, and tissue fibrosis were analyzed in Fra-2 mice and in a B10.D2→BALB/c (H-2d ) model of sclerodermatous chronic graft-versus-host disease (GVHD). The effects of PEG-ADA were confirmed in vitro in a human full-thickness skin model. PEG-ADA effectively inhibited myofibroblast differentiation and reduced pulmonary fibrosis by 34.3% (with decreased collagen expression) (P = 0.0079; n = 6), dermal fibrosis by 51.8% (P = 0.0006; n = 6), and intestinal fibrosis by 17.7% (P = 0.0228; n = 6) in Fra-2 mice. Antifibrotic effects of PEG-ADA were also demonstrated in sclerodermatous chronic GVHD (reduced by 38.4%) (P = 0.0063; n = 8), and in a human full-thickness skin model. PEG-ADA treatment decreased inflammation and corrected the M2/Th2/group 2 innate lymphoid cell 2 bias. Moreover, PEG-ADA inhibited proliferation of pulmonary vascular smooth muscle cells (reduced by 40.5%) (P < 0.0001; n = 6), and prevented thickening of the vessel walls (reduced by 39.6%) (P = 0.0028; n = 6) and occlusions of pulmonary arteries (reduced by 63.9%) (P = 0.0147; n = 6). Treatment with PEG-ADA inhibited apoptosis of microvascular endothelial cells (reduced by 65.4%) (P = 0.0001; n = 6) and blunted the capillary rarefication (reduced by 32.5%) (P = 0.0199; n = 6). RNA sequencing demonstrated that treatment with PEG-ADA normalized multiple pathways related to fibrosis, vasculopathy, and inflammation in Fra-2 mice. Treatment with PEG-ADA ameliorates the 3 cardinal features of SSc in pharmacologically relevant and well-tolerated doses. These findings may have direct translational implications, as PEG-ADA has already been approved by the Food and Drug Administration for the treatment of patients with ADA-deficient severe combined immunodeficiency disease.

Complete occlusion of right pulmonary artery in Behçet disease.

Key messageWhen a patient with Behçet disease presents with haemoptysis, pulmonary vascular involvement should be considered.

Estimation of Pulmonary Artery Occlusion Pressure Using Doppler Echocardiography in Mechanically Ventilated Patients.

Evaluation of left atrial pressure is frequently required for mechanically ventilated critically ill patients. The objective of the present study was to evaluate the 2016 American Society of Echocardiography and the European Association of Cardiovascular Imaging guidelines for assessment of the pulmonary artery occlusion pressure (a frequent surrogate of left atrial pressure) in this population. A pooled analysis of three prospective cohorts of patients simultaneously assessed with a pulmonary artery catheter and echocardiography. Medical-surgical intensive care department of two university hospitals in France. Mechanically ventilated critically ill patients. None. Of 98 included patients (males: 67%; mean ± SD age: 59 ± 16; and mean Simplified Acute Physiology Score 2: 54 ± 20), 53 (54%) experienced septic shock. Using the 2016 American Society of Echocardiography and the European Association of Cardiovascular Imaging guidelines, the predicted pulmonary artery occlusion pressure was indeterminate in 48 of the 98 patients (49%). Of the 24 patients with an elevated predicted left atrial pressure (grade II/III diastolic dysfunction), only 17 (71%) had a pulmonary artery occlusion pressure greater than or equal to 18 mm Hg. Similarly, 20 of the 26 patients (77%) with a normal predicted left atrial pressure (grade I diastolic dysfunction) had a measured pulmonary artery occlusion pressure less than 18 mm Hg. The sensitivity and specificity of American Society of Echocardiography and the European Association of Cardiovascular Imaging guidelines for predicting elevated pulmonary artery occlusion pressure were both 74%. The agreement between echocardiography and the pulmonary artery catheter was moderate (Cohen's Kappa, 0.48; 95% CI, 0.39-0.70). In a proposed alternative algorithm, the best echocardiographic predictors of a normal pulmonary artery occlusion pressure were a lateral e'-wave greater than 8 (for a left ventricular ejection fraction ≥ 45%) or an E/A ratio less than or equal to 1.5 (for a left ventricular ejection fraction < 45%). The American Society of Echocardiography and the European Association of Cardiovascular Imaging guidelines do not accurately assess pulmonary artery occlusion pressure in ventilated critically ill patients. Simple Doppler measurements gave a similar level of diagnostic performance with less uncertainly.

A Model of Pediatric End-Stage Lung Failure in Small Lambs

One in five children with end-stage lung failure (ESLF) die while awaiting lung transplant. No suitable animal model of ESLF exists for the development of artificial lung devices for bridging to transplant. Small lambs weighing 15.7 ± 3.1 kg (n = 5) underwent ligation of the left anterior pulmonary artery (PA) branch, and gradual occlusion of the right main PA over 48 hours. All animals remained hemodynamically stable. Over seven days of disease model conditions, they developed pulmonary hypertension (mean PA pressure 20 ± 5 vs. 33 ± 4 mm Hg), decreased perfusion (SvO2 66 ± 3 vs. 55 ± 8%) with supplemental oxygen requirement, and severe tachypneic response (45 ± 9 vs. 82 ± 23 breaths/min) (all p < 0.05). Severe right heart dysfunction developed (tricuspid annular plane systolic excursion 13 ± 3 vs. 7 ± 2 mm, fractional area change 36 ± 6 vs. 22 ± 10 mm, ejection fraction 51 ± 9 vs. 27 ± 17%, all p < 0.05) with severe tricuspid regurgitation and balloon-shaped dilation of the right ventricle. This model of pediatric ESLF reliably produces pulmonary hypertension, right heart strain, and impaired gas exchange, and will be used to develop a pediatric artificial lung.

Physiologic Effects of Pulmonary Artery Occlusion: Comment.

Physiologic Effects of Pulmonary Artery Occlusion: Comment.

Physiologic Effects of Pulmonary Artery Occlusion: Reply.

Physiologic Effects of Pulmonary Artery Occlusion: Reply.

Microvascular Disease in Chronic Thromboembolic Pulmonary Hypertension: Hemodynamic Phenotyping and Histomorphometric Assessment.

Pulmonary endarterectomy (PEA) is the gold standard treatment for patients with operable chronic thromboembolic pulmonary hypertension. However, persistent pulmonary hypertension (PH) after PEA remains a major determinant of poor prognosis. A concomitant small-vessel arteriopathy in addition to major pulmonary artery obstruction has been suggested to play an important role in the development of persistent PH and survival after PEA. One of the greatest unmet needs in the current preoperative evaluation is to assess the presence and severity of small-vessel arteriopathy. Using the pulmonary artery occlusion technique, we sought to assess the presence and degree of small-vessel disease in patients with chronic thromboembolic pulmonary hypertension undergoing PEA to predict postoperative outcome before surgery. Based on pulmonary artery occlusion waveforms yielding an estimate of the effective capillary pressure, we partitioned pulmonary vascular resistance in larger arterial (upstream resistance [Rup]) and small arterial plus venous components (downstream resistance) in 90 patients before PEA. For validation, lung wedge biopsies were taken from nonobstructed and obstructed lung territories during PEA in 49 cases. Biopsy sites were chosen according to the pulmonary angiogram still frames that were mounted in the operating room. All vessels per specimen were measured in each patient. Percent media (%MT; arteries) and intima thickness (%IT; arteries, veins, and indeterminate vessels) were calculated relative to external vessel diameter. Decreased Rup was an independent predictor of persistent PH (odds ratio per 10%, 0.40 [95% CI, 0.23-0.69]; P=0.001) and survival (hazard ratio per 10%, 0.03 [95% CI, 0.00-0.33]; p=0.004). Arterial %MT and %IT of nonobstructed lung territories and venous %IT of obstructed lung territories were significantly increased in patients with persistent PH and nonsurvivors. Rup correlated inversely with %MT (r=-0.72, P<0.001) and %IT (r=-0.62, P<0.001) of arteries from nonobstructed lung territories and with %IT (r=-0.44, P=0.024) of veins from obstructed lung territories. Receiver operating characteristic analysis disclosed that Rup <66% predicted persistent PH after PEA, whereas Rup <60% identified patients with poor prognosis after PEA. Pulmonary artery occlusion waveform analysis with estimation of Rup seems to be a valuable technique for assessing the degree of small-vessel disease and postoperative outcome after PEA in chronic thromboembolic pulmonary hypertension.