Search

Background Pulmonary embolism (PE) is a common cause of death with an incidence of approximately 1–2 cases per 1000 inhabitants in Europe and the United States. Treatment for PE is the administration of anticoagulants for at least three months. Purpose To assess the feasibility of following the resolution rate of PE over time using repeated imaging with a non-contrast-enhanced magnetic resonance imaging (MRI) protocol. Material and Methods Patients (n = 18) diagnosed with acute PE via computed tomography pulmonary angiography (CTPA) underwent non-contrast-enhanced MRI at two tertiary hospitals. The first MRI was performed within 36 h of CTPA, with follow-up at one week, one, three, and six months. The MRI sequence used was a non-contrast-enhanced standard two-dimensional steady-state free precession under free-breathing and without respiratory or cardiac gating. All MRI scans were then compared to the initial CTPA. The emboli were assessed visually for location and size, and clot burden was calculated using the Qanadli score. Results MRI revealed complete resolution in seven cases at one week, in five cases at one month, and in three cases at three months. The most significant resolution of emboli occurred within the first few weeks, with only 10% of the diagnosed emboli persisting at the one-month examination. Conclusion The use of MRI imparts the ability to visualize PE without radiation and thus allows multiple examinations to be made, for example in studies investigating the resolution of PE or the evaluation of drug effect in clinical trials.

SARS-CoV-2 uses ACE2, an inhibitor of the Renin-Angiotensin-Aldosterone System (RAAS), for cellular entry. Studies indicate that RAAS imbalance worsens the prognosis in COVID-19. We present a consecutive retrospective COVID-19 cohort with findings of frequent pulmonary thromboembolism (17%), high pulmonary artery pressure (60%) and lung MRI perfusion disturbances. We demonstrate, in swine, that infusing angiotensin II or blocking ACE2 induces increased pulmonary artery pressure, reduces blood oxygenation, increases coagulation, disturbs lung perfusion, induces diffuse alveolar damage, and acute tubular necrosis compared to control animals. We further demonstrate that this imbalanced state can be ameliorated by infusion of an angiotensin receptor blocker and low-molecular-weight heparin. In this work, we show that a pathophysiological state in swine induced by RAAS imbalance shares several features with the clinical COVID-19 presentation. Therefore, we propose that severe COVID-19 could partially be driven by a RAAS imbalance., The SARS-CoV-2 receptor ACE2 is involved in the Renin-Angiotensin-Aldosterone System (RAAS). Over-activation of RAAS in swine results in a disease state similar to that of COVID-19 in human patients, suggesting that COVID-19 pathophysiology may be driven, at least in part, by an imbalance of this hormonal system.

Purpose: To follow up the clinical outcome of patients with suspected pulmonary embolism (PE), in those only imaged using unenhanced, free-breathing magnetic resonance imaging (MRI). Methods and materials: Fifty-seven patients aged 29–99 years (mean 70, SD 18) that could not undergo Computed Tomography Pulmonary Angiography (CTPA) were offered alternative imaging diagnostics in parallel with ongoing methodological studies validating MRI vs CTPA. Contraindications included renal failure (n = 44), severe iodine contrast allergy (n = 10), pregnancy (n = 2) and radioactive iodine therapy (n = 1). The unenhanced MRI protocol was based on free-breathing, steady-state free precession with no cardiac or respiratory gating. Retrospective review of the electronic medical record (EMR) was made of 0–12 months post-imaging and was collected during 2012–2018. Results: All 57 MRIs were of diagnostic quality and 12 pulmonary embolisms were diagnosed. Of the 57 patients, 44 were already on, or had started anticoagulation therapy due to clinical suspicion of PE. Four of the patients were put on anticoagulation after the positive MRI and 13 were taken off anticoagulation after a negative MRI report. Other diagnoses reported (considering dyspnea) were pleural effusion (n = 24), consolidation (n = 12) and pericardial effusion (n = 2). One patient had a deep vein thrombosis (DVT) within three months of our negative MRI result and then had a stroke within one year. Another patient suffered a stroke within three months of being diagnosed (by MRI) with PE and given anticoagulation as treatment. Conclusions: Our method supported or altered clinical decision-making and treatment in this cohort. A diagnostic tool for PE without intravenous contrast agent or radiation is of great benefit for certain patients. Keywords: Pulmonary embolism, MRI, Thoracic imaging

SARS-CoV-2 enters the cell through the ACE2 receptor, which is considered one of the main inhibitors in the Renin-Angiotensin-Aldosterone System (RAAS).1​ ,2 The virus has been shown to downregulate the ACE2 receptor, leading to a subsequent increase in the vasopressoragentangiotensinII.3​ Evidently,criticalcoronavirusdisease2019(COVID-19)is thought to be due to a dysregulated immune response, causing a cytokine-release syndrome eventually leading to acute respiratory distress syndrome (ARDS).4​ ,5 ​However, several reports on clinical laboratory features and case-descriptions of critically ill patients with COVID-19 show discrepancies compared to typical ARDS. Here, we show that infusing swines with angiotensin II induces a pathophysiological syndrome closely resembling that of patients with RT-PCR-positive COVID-19. By using multimodal clinical imaging of patients, comparing laboratory data and translational histological features, we show that it is highly likely that an increase in RAAS is one, if not the main, pathogenic feature in critical COVID-19. Furthermore, it is plausible that this large animal model can be used to screen for potential new treatments for patients with severe COVID-19 and that MRI lung perfusion can be used to evaluate the outcome of potential treatments targeting the pathophysiological syndrome.

SARS-CoV-2 enters the cell through the ACE2 receptor, which is considered one of the main inhibitors in the Renin-Angiotensin-Aldosterone System (RAAS).1​ ,2 The virus has been shown to downregulate the ACE2 receptor, leading to a subsequent increase in the vasopressoragentangiotensinII.3​ Evidently,criticalcoronavirusdisease2019(COVID-19)is thought to be due to a dysregulated immune response, causing a cytokine-release syndrome eventually leading to acute respiratory distress syndrome (ARDS).4​ ,5 ​However, several reports on clinical laboratory features and case-descriptions of critically ill patients with COVID-19 show discrepancies compared to typical ARDS. Here, we show that infusing swines with angiotensin II induces a pathophysiological syndrome closely resembling that of patients with RT-PCR-positive COVID-19. By using multimodal clinical imaging of patients, comparing laboratory data and translational histological features, we show that it is highly likely that an increase in RAAS is one, if not the main, pathogenic feature in critical COVID-19. Furthermore, it is plausible that this large animal model can be used to screen for potential new treatments for patients with severe COVID-19 and that MRI lung perfusion can be used to evaluate the outcome of potential treatments targeting the pathophysiological syndrome.

PURPOSE To evaluate the feasibility of an improved motion and flow robust methodology for imaging the pulmonary vasculature using non-contrast-enhanced, free-breathing, golden-angle radial MRI. METHODS Healthy volunteers (n = 10, age 46 ± 11 years, 50% female) and patients (n = 2, ages 27 and 84, both female) were imaged at 1.5 T using a Cartesian and golden-angle radial 2D balanced SSFP pulse sequence. The acquisitions were made under free breathing without contrast agent enhancement. The radial acquisitions were reconstructed at 3 temporal footprints. All series were scored from 1 to 5 for perceived diagnostic quality, artifact level, and vessel sharpness in multiple anatomical locations. In addition, vessel sharpness and blood-to-blood clot contrast were measured. RESULTS Quantitative measurements showed higher vessel sharpness for golden-angle radial (n = 76, 0.79 ± 0.11 versus 0.71 ± 0.16, p

Background Pulmonary embolism (PE) is a severe medical condition with non-specific clinical findings. Computed tomography angiography (CTA) using iodinated contrast agents is the golden standard for diagnosis, but many patients have contraindications for CTA. Purpose To investigate the diagnostic accuracy of repeated acquisitions of magnetic resonance imaging (MRI), without respiratory gating or breath holding, in diagnosing PE using CTA as the reference standard. Material and Methods Thirty-three patients with clinically suspected PE underwent MRI within 48 h after diagnostic CTA. A control group of 37 healthy participants underwent MRI and was matched with an equal number of negative CTA exams. The MRI protocol was based on free-breathing steady-state free precession producing 4.5 mm slices in axial, sagittal, and coronal planes. Instead of respiratory or cardiac gating five repetitive slices were obtained in each anatomical position to compensate for movement and artifacts. Clinical assessment including d-dimer and Well’s score was performed prior to imaging. One radiologist reviewed the CTA exams and two radiologists reviewed the MRI scans. Results All 70 MRI exams were of diagnostic quality and the total acquisition time for each MRI scan was 9 min 34 s. On CTA, 29 patients were diagnosed with PE and the MRI readers detected 26 and 27 of those, respectively. Specificity was 100% for both readers. Sensitivity was 90% and 93%, respectively. Inter-reader agreement using Cohen’s kappa was 0.97. Conclusion Our unenhanced MRI protocol shows a high sensitivity and specificity for PE, but further studies are required before considering it as a safe diagnostic test.

Background Magnetic resonance imaging (MRI) can be an alternative method to computed tomography angiography (CTA) for pulmonary embolism. Purpose To evaluate the feasibility of diffusion-weighted imaging (DWI) detecting acute pulmonary embolism (PE) in free-breathing humans. Material and Methods Twenty patients with PE verified by CTA and 20 controls were investigated with MRI (1.5 Aera, Siemens Healthcare). All sequences were performed in the transversal plane using free-breathing without gating. The protocol consisted of a two-dimensional steady-state free precession (SSFP) and a single-shot DWI echo-planar imaging sequence with a voxel resolution of 2 × 2 × 5 mm. Three b values were used: 50, 400, and 800 s/mm2. Images were analyzed in two orders: an open source analysis (OSA); and a blinded only DWI analysis (BDA) simulating clinical work. Results OSA of corresponding images showed 370 findings on CTA (i.e. one elongated emboli could be represented in multiple images). SSFP identified 237 of those (64%). DWI with b values of 50, 400, and 800 identified 327 (88%), 245 (66%), and 138 (37%), respectively. In BDA we found 160 true emboli (according to CTA) on b50, 78 on b400, and 54 on b800. Fifty-two of these findings at the subsegmental level could be correlated to PE on CTA but were not visible on SSFP. Conclusions DWI has a high sensitivity for detecting PE but suffers from poor specificity. It could potentially be used as an eye catcher, i.e. where to look for PE in other MRI sequences.