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PURPOSE: Right ventricular strain (RVS) is used to risk stratify patients with acute pulmonary embolism (PE) and influence treatment decisions. Guidelines suggest that either computed tomography pulmonary angiography (CTPA) or transthoracic echocardiography (TTE) can be used to assess RVS. We sought to determine how often CTPA and TTE yield discordant results and to assess the test characteristics of CTPA compared to TTE.METHODS: We analyzed data from a single-center registry of PE cases severe enough to warrant activation of the hospital's Pulmonary Embolism Response Team (PERT). We defined RVS as a right ventricular to left ventricular ratio (RV/LV) ≥ 1 or radiologist's interpretation of RVS on CTPA or as the presence of either RV dilation, hypokinesis, or septal bowing on TTE.RESULTS: We included 554 patients in our analysis, of whom 333 (60%) had concordant RVS findings on CTPA and TTE. Using TTE as the reference standard, CTPA had a sensitivity of 95% (95% CI 92-97%) and a specificity of 4% (95% CI 2-8%) for identifying RVS.CONCLUSIONS: In a selected population of patients with acute PE for which PERT was activated, CTPA is highly sensitive but not specific for the detection of RVS when compared to TTE.

New Findings: What is the central question of this study? Is it possible to combine the hyperpolarized magnetic resonance technique and the hyperinsulinaemic clamp method in order to evaluate skeletal muscle metabolism in a large animal model? What is the main finding and its importance? The logistical set-up is possible, and we found substantial increments in glucose infusion rates representing skeletal muscle glucose uptake but no differences in ratios of [1- 13C]lactate to [1- 13C]pyruvate, [1- 13C]alanine to [1- 13C]pyruvate, and 13C-bicarbonate to [1- 13C]pyruvate, implying that the hyperpolarization technique might not be optimal for detecting effects of insulin in skeletal muscle of anaesthetized animals, which is of significance for future studies. Abstract: In skeletal muscle, glucose metabolism is tightly regulated by the reciprocal relationship between insulin and adrenaline, with pyruvate being at the intersection of both pathways. Hyperpolarized magnetic resonance (hMR) is a new approach to gain insights into these pathways, and human trials involving hMR and skeletal muscle metabolism are imminent. We aimed to combine the hyperinsulinaemic clamp technique and hMR in a large animal model resembling human physiology. Fifteen anaesthetized pigs were randomized to saline (control group), hyperinsulinaemic euglycaemic clamp technique (HE group) or hyperinsulinaemic hypoglycaemic clamp technique (HH group). Skeletal muscle metabolism was evaluated by hyperpolarized [1- 13C]pyruvate injection and hMR at baseline and after intervention. The glucose infusion rate per kilogram increased by a statistically significant amount in the HE and HH groups (P 13C]lactate to [1- 13C]pyruvate in the HH group versus control group (P = 0.19); and 13C-bicarbonate to [1- 13C]pyruvate ratio in the HE group versus the control group (P = 0.12). We found evidence of profound increments in glucose infusion rates representing skeletal muscle glucose uptake, but interestingly, no signs of significant changes in aerobic and anaerobic metabolism using hMR. These results imply that hyperpolarized [1- 13C]pyruvate might not be optimally suited to detect effects of insulin in anaesthetized resting skeletal muscle, which is of significance for future studies.

INTRODUCTION: Pulmonary embolism is a common cause of cardiopulmonary mortality and morbidity worldwide. Survivors of acute pulmonary embolism may experience dyspnea, report reduced exercise capacity, or develop overt pulmonary hypertension. Clinicians must be alert for these phenomena and appreciate the modalities and investigations available for evaluation.AREAS COVERED: In this review, the current understanding of available contemporary imaging and physiologic modalities is discussed, based on available literature and professional society guidelines. The purpose of the review is to provide clinicians with an overview of these modalities, their strengths and disadvantages, and how and when these investigations can support the clinical work-up of patients post-pulmonary embolism.EXPERT OPINION: Echocardiography is a first test in symptomatic patients post-pulmonary embolism, with ventilation/perfusion scanning vital to determination of whether there is chronic residual emboli. The role of computed tomography and magnetic resonance in assessing the pulmonary arterial tree in post-pulmonary embolism patients is evolving. Functional testing, in particular cardiopulmonary exercise testing, is emerging as an important modality to quantify and determine cause of functional limitation. It is possible that future investigations of the post-pulmonary embolism recovery period will better inform treatment decisions for acute pulmonary embolism patients.

Aims Right ventricular (RV) failure causes death from acute pulmonary embolism (PE), due to a mismatch between RV systolic function and increased RV afterload. We hypothesized that an echocardiographic ratio of this mismatch [RV systolic function by tricuspid annular plane systolic excursion (TAPSE) divided by pulmonary arterial systolic pressure (PASP)] would predict adverse outcomes better than each measurement individually, and would be useful for risk stratification in intermediate-risk PE. Methods and results This was a retrospective analysis of a single academic centre Pulmonary Embolism Response Team registry from 2012 to 2019. All patients with confirmed PE and a formal transthoracic echocardiogram performed within 2 days were included. All echocardiograms were analysed by an observer blinded to the outcome. The primary endpoint was a 7-day composite outcome of death or haemodynamic deterioration. Secondary outcomes were 7- and 30-day all-cause mortality. A total of 627 patients were included; 135 met the primary composite outcome. In univariate analysis, the TAPSE/PASP was associated with our primary outcome [odds ratio = 0.028, 95% confidence interval (CI) 0.010–0.087; P Conclusion A combined echocardiographic ratio of RV function to afterload is superior in prediction of adverse outcome in acute intermediate-risk PE. This ratio may improve risk stratification and identification of the patients that will suffer short-term deterioration after intermediate-risk PE.

PURPOSE: Comparison of deep learning algorithm, radiomics and subjective assessment of chest CT for predicting outcome (death or recovery) and intensive care unit (ICU) admission in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.METHODS: The multicenter, ethical committee-approved, retrospective study included non-contrast-enhanced chest CT of 221 SARS-CoV-2 positive patients from Italy (n = 196 patients; mean age 64 ± 16 years) and Denmark (n = 25; mean age 69 ± 13 years). A thoracic radiologist graded presence, type and extent of pulmonary opacities and severity of motion artifacts in each lung lobe on all chest CTs. Thin-section CT images were processed with CT Pneumonia Analysis Prototype (Siemens Healthineers) which yielded segmentation masks from a deep learning (DL) algorithm to derive features of lung abnormalities such as opacity scores, mean HU, as well as volume and percentage of all-attenuation and high-attenuation (opacities >-200 HU) opacities. Separately, whole lung radiomics were obtained for all CT exams. Analysis of variance and multiple logistic regression were performed for data analysis.RESULTS: Moderate to severe respiratory motion artifacts affected nearly one-quarter of chest CTs in patients. Subjective severity assessment, DL-based features and radiomics predicted patient outcome (AUC 0.76 vs AUC 0.88 vs AUC 0.83) and need for ICU admission (AUC 0.77 vs AUC 0.0.80 vs 0.82). Excluding chest CT with motion artifacts, the performance of DL-based and radiomics features improve for predicting ICU admission.CONCLUSION: DL-based and radiomics features of pulmonary opacities from chest CT were superior to subjective assessment for differentiating patients with favorable and adverse outcomes.

Acute pulmonary embolism is a frequent condition in emergency medicine and potentially fatal. Cause of death is right ventricular failure due to increased right ventricular afterload from both pulmonary vascular obstruction and vasoconstriction. Inodilators are interesting drugs of choice as they may improve right ventricular function and lower its afterload. We aimed to investigate the cardiovascular effects of three clinically relevant inodilators: levosimendan, milrinone, and dobutamine in acute pulmonary embolism. We conducted a randomized, blinded, animal study using 18 female pigs. Animals received large autologous pulmonary embolism until doubling of baseline mean pulmonary arterial pressure and were randomized to increasing doses of each inodilator. Effects were evaluated with bi-ventricular pressure-volume loop recordings, right heart catheterization, and blood gas analyses. Induction of pulmonary embolism increased right ventricular afterload and pulmonary pressure (p

What is the central question of this study? Is it possible to combine the hyperpolarized magnetic resonance technique and the hyperinsulinaemic clamp method in order to evaluate skeletal muscle metabolism in a large animal model? What is the main finding and its importance? The logistical set-up is possible, and we found substantial increments in glucose infusion rates representing skeletal muscle glucose uptake but no differences in ratios of [1-In skeletal muscle, glucose metabolism is tightly regulated by the reciprocal relationship between insulin and adrenaline, with pyruvate being at the intersection of both pathways. Hyperpolarized magnetic resonance (hMR) is a new approach to gain insights into these pathways, and human trials involving hMR and skeletal muscle metabolism are imminent. We aimed to combine the hyperinsulinaemic clamp technique and hMR in a large animal model resembling human physiology. Fifteen anaesthetized pigs were randomized to saline (control group), hyperinsulinaemic euglycaemic clamp technique (HE group) or hyperinsulinaemic hypoglycaemic clamp technique (HH group). Skeletal muscle metabolism was evaluated by hyperpolarized [1

OBJECTIVES: To investigate if oxygen could unload the right ventricle and improve right ventricle function in a porcine model mimicking intermediate-high risk acute pulmonary embolism.DESIGN: Controlled, blinded, animal study.SETTING: Tertiary university hospital, animal research laboratory.SUBJECTS: Female, Danish pigs (n = 16, approximately 60 kg).INTERVENTIONS: Acute autologous pulmonary embolism was induced until doubling of baseline mean pulmonary arterial pressure. Group 1 animals (n = 8) received increasing FIO2 (40%, 60%, and 100%) for time intervals of 15 minutes returning to atmospheric air between each level of FIO2. In group 2 (n = 8), the effects of FIO2 40% maintained over 75 minutes were studied. In both groups, pulmonary vasodilatation from inhaled nitric oxide (40 parts per million) was used as a positive control.MEASUREMENTS AND MAIN RESULTS: Effects were evaluated by biventricular pressure-volume loop recordings, right heart catheterization, and arterial and mixed venous blood gasses. Pulmonary embolism increased mean pulmonary arterial pressure from 15 ± 4 to 33 ± 6 mm Hg (p = 0.0002) and caused right ventricle dysfunction (p < 0.05) with troponin release (p < 0.0001). In group 1, increasing FIO2 lowered mean pulmonary arterial pressure (p < 0.0001) and pulmonary vascular resistance (p = 0.0056) and decreased right ventricle volumes (p = 0.0018) and right ventricle mechanical work (p = 0.034). Oxygenation was improved and pulmonary shunt was lowered (p < 0.0001). Maximal hemodynamic effects were seen at FIO2 40% with no additional benefit from higher fractions of oxygen. In group 2, the effects of FIO2 40% were persistent over 75 minutes. Supplemental oxygen showed the same pulmonary vasodilator efficacy as inhaled nitric oxide (40 parts per million). No adverse effects were observed.CONCLUSIONS: In a porcine model mimicking intermediate-high risk pulmonary embolism, oxygen therapy reduced right ventricle afterload and lowered right ventricle mechanical work. The effects were immediately present and persistent and were similar to inhaled nitric oxide. The intervention is easy and safe. The study motivates extended clinical evaluation of supplemental oxygen in acute pulmonary embolism.

BackgroundInhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE.MethodsAnesthetized pigs (n = 18) were randomized into three subgroups. An acute PE iNO-group (n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals (n = 6) received PE, but no active treatment. A third group of sham animals (n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements.ResultsThe administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p ConclusionsiNO is a safe and effective pulmonary vasodilator both in the immediate and prolonged phase of acute PE in an in-vivo porcine model of intermediate-risk PE.

Aim To assess differences in qualitative and quantitative parameters of pulmonary perfusion from dual-energy computed tomography (CT) pulmonary angiography (DECT-PA) in patients with COVID-19 pneumonia with and without pulmonary embolism (PE). Materials and methods This retrospective institutional review board-approved study included 74 patients (mean age 61 ± 18 years, male:female 34:40) with COVID-19 pneumonia in two countries (one with 68 patients, and the other with six patients) who underwent DECT-PA on either dual-source (DS) or single-source (SS) multidetector CT machines. Images from DS-DECT-PA were processed to obtain virtual mono-energetic 40 keV (Mono40), material decomposition iodine (MDI) images and quantitative perfusion statistics (QPS). Two thoracic radiologists determined CT severity scores based on type and extent of pulmonary opacities, assessed presence of PE, and pulmonary parenchymal perfusion on MDI images. The QPS were calculated from the CT Lung Isolation prototype (Siemens). The correlated clinical outcomes included duration of hospital stay, intubation, SpO2 and death. The significance of association was determined by receiver operating characteristics and analysis of variance. Results One-fifth (20.2%, 15/74 patients) had pulmonary arterial filling defects; most filling defects were occlusive (28/44) located in the segmental and sub-segmental arteries. The parenchymal opacities were more extensive and denser (CT severity score 24 ± 4) in patients with arterial filling defects than without filling defects (20 ± 8; p=0.028). Ground-glass opacities demonstrated increased iodine distribution; mixed and consolidative opacities had reduced iodine on DS-DECT-PA but increased or heterogeneous iodine content on SS-DECT-PA. QPS were significantly lower in patients with low SpO2 (p=0.003), intubation (p=0.006), and pulmonary arterial filling defects (p=0.007). Conclusion DECT-PA QPS correlated with clinical outcomes in COVID-19 patients.

OBJECTIVES: To compare the hemodynamic effects of increased versus decreased preload in a porcine model of acute intermediate-risk pulmonary embolism.DESIGN: Randomized, controlled animal study.SETTING: Tertiary medical center, animal research laboratory.SUBJECTS: Female, Danish slaughter pigs (n = 22, ~ 60 kg).INTERVENTIONS: Acute pulmonary embolism was induced by large emboli made from clotting of autologous blood. Sixteen animals were randomized to either fluid loading (n = 8, isotonic saline, 1 L/hr for 2 hr) or diuretic treatment (n = 8, furosemide, 40 mg every 30 min, total 160 mg) and compared with a vehicle group (n = 6, no treatment).MEASUREMENTS AND MAIN RESULTS: Hemodynamics were evaluated at baseline, after pulmonary embolism and after each dose by biventricular pressure-volume loops, invasive pressures, diuretic output, respiratory variables, and blood analysis. Pulmonary embolism increased mean pulmonary arterial pressure (p < 0.0001), pulmonary vascular resistance (p = 0.008), right ventricular arterial elastance (p = 0.003), and right ventricular end-systolic volume (p = 0.020) while right ventricular stroke volume and right ventricular ejection fraction were decreased (p = 0.047 and p = 0.0003, respectively) compared with baseline. Fluid loading increased right ventricular end-diastolic volume (+31 ± 13 mL; p = 0.004), right ventricular stroke volume (+23 ± 10 mL; p = 0.009), cardiac output (+2,021 ± 956 mL; p = 0.002), and right ventricular ejection fraction (+7.6% ± 1.5%; p = 0.032), whereas pulmonary vascular resistance decreased (-202 ± 65 dynes; p = 0.020) compared with vehicle. Diuretic treatment decreased right ventricular end-diastolic volume (-84 ± 11 mL; p < 0.001), right ventricular stroke volume (-40 ± 6 mL; p = 0.001), cardiac output (-3,327 ± 451 mL; p = 0.005), and mean pulmonary arterial pressure (-7 ± 1 mm Hg; p < 0.001) and increased right ventricular end-systolic elastance (+0.72 ± 0.2 mm Hg/mL; p < 0.001) and systemic vascular resistance (+1,812 ± 767 dynes; p < 0.001) with no effects on mean arterial pressure.CONCLUSIONS: In a porcine model of acute intermediate-risk pulmonary embolism, fluid loading increased right ventricular preload and right ventricular stroke volume, whereas diuretics decreased right ventricular preload and right ventricular stroke volume without affecting mean arterial pressure.

PURPOSE: Normothermic perfusion is an emerging strategy for donor organ preservation and therapy, incited by the high worldwide demand for organs for transplantation. Hyperpolarized MRI and MRS using [1-13 C]pyruvate and other 13 C-labeled molecules pose a novel way to acquire highly detailed information about metabolism and function in a noninvasive manner. This study investigates the use of this methodology as a means to study and monitor the state of ex vivo perfused porcine kidneys, in the context of kidney graft preservation research.METHODS: Kidneys from four 40-kg Danish domestic pigs were perfused ex vivo with whole blood under normothermic conditions, using an MR-compatible perfusion system. Kidneys were investigated using 1 H MRI as well as hyperpolarized [1-13 C]pyruvate MRI and MRS. Using the acquired anatomical, functional and metabolic data, the state of the ex vivo perfused porcine kidney could be quantified.RESULTS: Four kidneys were successfully perfused for 120 minutes and verified using a DCE perfusion experiment. Renal metabolism was examined using hyperpolarized [1-13 C]pyruvate MRI and MRS, and displayed an apparent reduction in pyruvate turnover compared with the usual case in vivo. Perfusion and blood gas parameters were in the normal ex vivo range.CONCLUSION: This study demonstrates the ability to monitor ex vivo graft metabolism and function in a large animal model, resembling human renal physiology. The ability of hyperpolarized MRI and MRS to directly compare the metabolic state of an organ in vivo and ex vivo, in combination with the simple MR implementation of normothermic perfusion, renders this methodology a powerful future tool for graft preservation research.

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism (n = 6) or sham (n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased (P Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.

OBJECTIVES: We investigated whether the vasopressin-analog, terlipressin induces systemic vasoconstriction and pulmonary vasodilation in a porcine model of acute pulmonary embolism.DESIGN: Controlled, animal study.SETTING: Tertiary medical center research laboratory.SUBJECTS: Female pigs (n = 12, Cross of Land Race, Duroc, and Yorkshire ~ 60 kg).INTERVENTIONS: Acute pulmonary embolism was induced by administration of three large autologous emboli. Animals then received four increasing doses of either terlipressin (n = 6) or vehicle (n = 6).MEASUREMENTS AND MAIN RESULTS: Effects were evaluated in vivo at baseline, after pulmonary embolism and after each dose by invasive hemodynamic measures, transesophageal echocardiography, and blood analysis. Isolated pulmonary arteries were evaluated ex vivo in a myograph. Pulmonary embolism caused a four-fold increase in pulmonary vascular resistance (p < 0.0001) and a two-fold increase in mean pulmonary arterial pressure (p < 0.0001) compared with baseline. Terlipressin increased mean systemic blood pressure (28 ± 5 mm Hg; p < 0.0001) and systemic vascular resistance (1,320 ± 143 dynes; p < 0.0001) compared with vehicle. In the pulmonary circulation, terlipressin decreased mean pulmonary arterial pressure (-6.5 ± 1.8 mm Hg; p = 0.005) and tended to decrease pulmonary vascular resistance (-83 ± 33 dynes; p = 0.07). Terlipressin decreased cardiac output (-2.5 ± 0.5 L/min; p < 0.0001) and increased plasma lactate (2.7 ± 0.2 mmol/L; p < 0.0001), possibly indicating systemic hypoperfusion. A biomarker of cerebral ischemia, S100b, remained unchanged, suggesting preserved cerebral perfusion (0.17 ± 0.11 µg/L; p = 0.51). Ex vivo, terlipressin relaxed pulmonary and constricted mesenteric arteries.CONCLUSIONS: Terlipressin caused systemic vasoconstriction and pulmonary vasodilation in a porcine in vivo model of acute pulmonary embolism and vasorelaxation in isolated pulmonary arteries. Despite positive vascular effects, cardiac output declined and plasma lactate increased probably due to a predominantly systemic vasoconstrictor effect of terlipressin. These findings should warrant careful translation to the clinical setting and does not suggest routine use in acute pulmonary embolism.

Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricularafterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of themechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased rightventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonaryvasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexesand hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin,thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenousadministration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemicvasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulatorsof the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandinpathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim ofthis review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimentaland human investigations of pulmonary vasodilation in acute pulmonary embolism.

Normothermic perfusion is an emerging strategy for donor organ preservation and therapy, incited by the high worldwide demand for organs for transplantation. Hyperpolarized MRI and MRS using [1-Kidneys from four 40-kg Danish domestic pigs were perfused ex vivo with whole blood under normothermic conditions, using an MR-compatible perfusion system. Kidneys were investigated usingFour kidneys were successfully perfused for 120 minutes and verified using a DCE perfusion experiment. Renal metabolism was examined using hyperpolarized [1-This study demonstrates the ability to monitor ex vivo graft metabolism and function in a large animal model, resembling human renal physiology. The ability of hyperpolarized MRI and MRS to directly compare the metabolic state of an organ in vivo and ex vivo, in combination with the simple MR implementation of normothermic perfusion, renders this methodology a powerful future tool for graft preservation research.

Purpose: Patients with acute pulmonary embolism (PE) can quickly deteriorate and the condition has high mortality due to right ventricular (RV) failure. Immediately available predictors of adverse outcome are of major interest to the treating physician in the acute setting. The purpose of the present study was to evaluate if easily attainable measurements of RV function from the diagnostic computed tomography pulmonary angiography (CTPA) provide information for fast risk stratification in patients with acute PE. Methods: We retrospectively evaluated images from CTPA in 261 patients (age median 60 years, 50% females) enrolled in a prospective study. RV and left ventricular (LV) diameters and their ratio, the presence of septal bowing, contrast reflux in the inferior vena cava, and the diameter of the central pulmonary arteries (PA) were measured. The composite outcome was 5-day severe adverse events including death, acute decompensation, or need for emergent treatment. We used Wilcoxon rank sum test and Fischer’s exact test to test between groups and multivariate logistic regression for prediction. Results: In multivariate analysis, increased diameter of the main PA (OR = 1.08 per 1 mm increase, p = 0.047) and the presence of septal bowing (OR = 2.23, p = 0.055) were associated with severe adverse events. RV/LV > 1 did not predict severe outcomes (OR = 0.73, p = 0.541). Conclusions: Two easily attainable parameters of RV function on CTPA, septal bowing and main PA diameter, are associated with short-term adverse outcomes in patients with acute PE. Further study is required to determine whether these findings can be incorporated into clinical treatment algorithms. Purpose Patients with acute pulmonary embolism (PE) can quickly deteriorate and the condition has high mortality due to right ventricular (RV) failure. Immediately available predictors of adverse outcome are of major interest to the treating physician in the acute setting. The purpose of the present study was to evaluate if easily attainable measurements of RV function from the diagnostic computed tomography pulmonary angiography (CTPA) provide information for fast risk stratification in patients with acute PE. Methods We retrospectively evaluated images from CTPA in 261 patients (age median 60 years, 50% females) enrolled in a prospective study. RV and left ventricular (LV) diameters and their ratio, the presence of septal bowing, contrast reflux in the inferior vena cava, and the diameter of the central pulmonary arteries (PA) were measured. The composite outcome was 5-day severe adverse events including death, acute decompensation, or need for emergent treatment. We used Wilcoxon rank sum test and Fischer’s exact test to test between groups and multivariate logistic regression for prediction. Results In multivariate analysis, increased diameter of the main PA (OR = 1.08 per 1 mm increase, p = 0.047) and the presence of septal bowing (OR = 2.23, p = 0.055) were associated with severe adverse events. RV/LV > 1 did not predict severe outcomes (OR = 0.73, p = 0.541). Conclusions Two easily attainable parameters of RV function on CTPA, septal bowing and main PA diameter, are associated with short-term adverse outcomes in patients with acute PE. Further study is required to determine whether these findings can be incorporated into clinical treatment algorithms.

Right ventricular (RV) failure induced by sustained pressure overload is a major contributor to morbidity and mortality in several cardiopulmonary disorders. Reliable and reproducible animal models of RV failure are therefore warranted in order to investigate disease mechanisms and effects of potential therapeutic strategies. Banding of the pulmonary trunk is a common method to induce isolated RV hypertrophy but in general, previously described models have not succeeded in creating a stable model of RV hypertrophy and failure. We present a rat model of pressure overload induced RV hypertrophy caused by pulmonary trunk banding (PTB) that enables different phenotypes of RV hypertrophy with and without RV failure. We use a modified ligating clip applier to compress a titanium clip around the pulmonary trunk to a pre-set inner diameter. We use different clip diameters to induce different stages of disease progression from mild RV hypertrophy to decompensated RV failure. RV hypertrophy develops consistently in rats subjected to the PTB procedure and depending on the diameter of the applied banding clip, we can accurately reproduce different disease severities ranging from compensated hypertrophy to severe decompensated RV failure with extra-cardiac manifestations. The presented PTB model is a valid and robust model of pressure overload induced RV hypertrophy and failure that has several advantages to other banding models including high reproducibility and the possibility of inducing severe and decompensated RV failure.