A 48-year-old patient was referred for anemia, jaundice, and right upper-quadrant pain, 5 months after a thorough evaluation for anemia resulting from obscure gastrointestinal bleeding. Abdominal imaging at admission showed a mass in the gallbladder, and endoscopic ultrasound confirmed the presence of a polyp-like lesion with a vascular stalk and clots within the gallbladder. During endoscopic ultrasound, hemobilia was visible (Figures A, B, and C, and Video 1). Laparoscopic cholecystectomy was performed with resolution of symptoms and the final diagnosis was gallbladder melanoma (Figure D). The patient had no history of melanoma and a search for an alternative primary site was unrevealing. Adjuvant treatment with nivolumab was initiated. Primary gallbladder and biliary tract melanoma is extremely rare, with only 37 and 14 cases reported in the literature, respectively. Most cases are caused by metastatic disease. No record of melanoma, the presence of a solitary lesion with a polypoid shape, and histologic examination showing junctional activity all indicate a primary tumor. Gallbladder melanoma most commonly is asymptomatic, but symptoms may occur including abdominal pain, nausea and vomiting, anemia, hemobilia, obstructive jaundice, and acute cholecystitis. Hemobilia associated with jaundice and right upper-quadrant pain, known as Quincke's triad, is an uncommon clinical manifestation, with only a handful of reported cases. eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiJmMTA0YmQ4ZDFmZTA1MjcyZDMwYmU2MDliZmEyMTg1NyIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNzAzMjY4NDA1fQ.bbrGxCioHz6UNzPkj229dcAXqLsQIkFRxyvqdVFR2jJDTI6QL0WHBuvlzkfM_WRaOcSUk9poyg7uT-Z91i9uFnCAxl5jqW13-1_5YWJhRcixAW3kiGVtsAf4DMZi-DHBqD1NH6dP6f1GP6CT7FV2hPGLkyDDsn5Js8GoZSQ_7ddjyBcLmSShcC2xIeFdn1wwPdL7SRGIDNObG6gosCWm2o12Dbos0eMJYjZtXL9voAQGrDytya-D4EwD4UsyP4h3QNUc6U7uP4rGR_k0Vdc9QlRVxgrTk0r8tQYuirs4o8lDNkUB0DNbJEAtdfU7TbZ1651TzDoes72uI6GZMV-H1A Download .mp4 (19.58 MB) Help with .mp4 files Video

Background and aims: The potential impact of coronary atherosclerosis, as detected by coronary artery calcium, on clinical outcomes in COVID-19 patients remains unsettled. We aimed to evaluate the prognostic impact of clinical and subclinical coronary artery disease (CAD), as assessed by coronary artery calcium score (CAC), in a large, unselected population of hospitalized COVID-19 patients undergoing non-gated chest computed tomography (CT) for clinical practice. Methods: SARS-CoV 2 positive patients from the multicenter (16 Italian hospitals), retrospective observational SCORE COVID-19 (calcium score for COVID-19 Risk Evaluation) registry were stratified in three groups: (a) "clinical CAD" (prior revascularization history), (b) "subclinical CAD" (CAC >0), (c) "No CAD" (CAC = 0). Primary endpoint was in-hospital mortality and the secondary endpoint was a composite of myocardial infarction and cerebrovascular accident (MI/CVA). Results: Amongst 1625 patients (male 67.2%, median age 69 [interquartile range 58-77] years), 31%, 57.8% and 11.1% had no, subclinical and clinical CAD, respectively. Increasing rates of in-hospital mortality (11.3% vs.27.3% vs. 39.8%, p < 0.001) and MI/CVA events (2.3% vs. 3.8% vs. 11.9%, p < 0.001) were observed for patients with no CAD vs. subclinical CAD vs clinical CAD, respectively. The association with in-hospital mortality was independent of in-study outcome predictors (age, peripheral artery disease, active cancer, hemoglobin, C-reactive protein, LDH, aerated lung volume): subclinical CAD vs. No CAD: adjusted hazard ratio (adj-HR) 2.86 (95% confidence interval [CI] 1.14-7.17, p=0.025); clinical CAD vs. No CAD: adj-HR 3.74 (95% CI 1.21-11.60, p=0.022). Among patients with subclinical CAD, increasing CAC burden was associated with higher rates of in-hospital mortality (20.5% vs. 27.9% vs. 38.7% for patients with CAC score thresholds<100, 101-400 and > 400, respectively, p < 0.001). The adj-HR per 50 points increase in CAC score 1.007 (95%CI 1.001-1.013, p=0.016). Cardiovascular risk factors were not independent predictors of in-hospital mortality when CAD presence and extent were taken into account. Conclusions: The presence and extent of CAD are associated with in-hospital mortality and MI/CVA among hospitalized patients with COVID-19 disease and they appear to be a better prognostic gauge as compared to a clinical cardiovascular risk assessment.

Recent clinical and demographical studies on COVID-19 patients have demonstrated that men experience worse outcomes than women. However, in most cases, the data were not stratified according to gender, limiting the understanding of the real impact of gender on outcomes. This study aimed to evaluate the disaggregated in-hospital outcomes and explore the possible interactions between gender and cardiovascular calcifications. Data was derived from the sCORE-COVID-19 registry, an Italian multicentre registry that enrolled COVID-19 patients who had undergone a chest computer tomography scan on admission. A total of 1683 hospitalized patients (mean age 67±14 years) were included. Men had a higher prevalence of cardiovascular comorbidities, a higher pneumonia extension, more coronary calcifications (63% vs.50.9%, p<0.001), and a higher coronary calcium score (391±847 vs. 171±479 mm3, p<0.001). Men experienced a significantly higher mortality rate (24.4% vs. 17%, p=0.001), but the death event tended to occur earlier in women (15±7 vs. 8±7 days, p= 0.07). Non-survivors had a higher coronary, thoracic aorta, and aortic valve calcium score. Female sex, a known independent predictor of a favorable outcome in SARS-CoV2 infection, was not protective in women with a coronary calcification volume greater than 100 mm3. There were significant differences in cardiovascular comorbidities and vascular calcifications between men and women with SARS-CoV2 pneumonia. The differences in outcomes can be at least partially explained by the different cardiovascular profiles. However, women with poor outcomes had the same coronary calcific burden as men. The presumed favorable female sex bias in COVID-19 must therefore be reviewed in the context of comorbidities, especially cardiovascular ones.

Background: Coronavirus disease 2019 (COVID-19) has spread worldwide determining dramatic impacts on healthcare systems. Early identification of high-risk parameters is required in order to provide the best therapeutic approach. Coronary, thoracic aorta and aortic valve calcium can be measured from a non-gated chest computer tomography (CT) and are validated predictors of cardiovascular events and all-cause mortality. However, their prognostic role in acute systemic inflammatory diseases, such as COVID-19, has not been investigated. Objectives: The aim was to evaluate the association of coronary artery calcium and total thoracic calcium on in-hospital mortality in COVID-19 patients. Methods: 1093 consecutive patients from 16 Italian hospitals with a positive swab for COVID-19 and an admission chest CT for pneumonia severity assessment were included. At CT, coronary, aortic valve and thoracic aorta calcium were qualitatively and quantitatively evaluated separately and combined together (total thoracic calcium) by a central Core-lab blinded to patients' outcomes. Results: Non-survivors compared to survivors had higher coronary artery [Agatston (467.76 +/- 570.92 vs 206.80 +/- 424.13 mm(2), p < 0.001); Volume (487.79 +/- 565.34 vs 207.77 +/- 406.81, p < 0.001)], aortic valve [Volume (322.45 +/- 390.90 vs 98.27 +/- 250.74 mm(2), p < 0.001; Agatston 337.38 +/- 414.97 vs 111.70 +/- 282.15, p < 0.001)] and thoracic aorta [Volume (3786.71 +/- 4225.57 vs 1487.63 +/- 2973.19 mm(2), p < 0.001); Agatston (4688.82 +/- 5363.72 vs 1834.90 +/- 3761.25, p < 0.001)] calcium values. Coronary artery calcium (HR 1.308; 95% CI, 1.046-1.637, p = 0.019) and total thoracic calcium (HR 1.975; 95% CI, 1.200-3.251, p = 0.007) resulted to be independent predictors of in-hospital mortality. Conclusion Coronary, aortic valve and thoracic aortic calcium assessment on admission non-gated CT permits to stratify the COVID-19 patients in-hospital mortality risk.

BACKGROUND AND AIMS:Extent of subclinical atherosclerosis has been associated with brain parenchymal loss in community-dwelling aged subjects. Identification of patient-related and plaque-related markers could identify subjects at higher risk of brain atrophy, independent of cerebrovascular accidents. Aim of the study was to investigate the relation between extent and characteristics of carotid plaques and brain atrophy in asymptomatic patients with no indication for revascularization. METHODS AND RESULTS:Sixty-four patients (aged 69 ± 8 years, 45% females) with carotid stenosis <70% based on Doppler flow velocity were enrolled in the study. Potential causes of cerebral damage other than atherosclerosis, including history of atrial fibrillation, heart failure, previous cardiac or neurosurgery and neurological disorders were excluded. All subjects underwent carotid computed tomography angiography, contrast enhanced ultrasound for assessment of plaque neovascularization and brain magnetic resonance imaging for measuring brain volumes. On multivariate regression analysis, age and fibrocalcific plaques were independently associated with lower total brain volumes (β = -3.13 and β = -30.7, both p < 0.05). Fibrocalcific plaques were also independently associated with lower gray matter (GM) volumes (β = -28.6, p = 0.003). On the other hand, age and extent of carotid atherosclerosis were independent predictors of lower white matter (WM) volumes. CONCLUSIONS:WM and GM have different susceptibility to processes involved in parenchymal loss. Contrary to common belief, our results show that presence of fibrocalcific plaques is associated with brain atrophy.

Purpose. A large number of patients affected by the SARS-Cov-2 virus worldwide undergo recovery of symptoms in about one month. Among these patients, the healing process is still under observation, with some patients in need of careful clinical monitoring. While the radiological findings have been shown to regress almost completely, little knowledge is available at the moment about other complications in the lung and in other organs. We then investigated the lung perfusion conditions in patients affected by COVID- 19 during recovery. Method. We retrospectively studied 20 patients, from 14 to 60 days after resolution of the COVID-19 symptoms, using chest CT. In a subgroup of 5 patients contrasted CT was used. Beside normal radiological evaluation of lung tissue, perfusion conditions were evaluated by digital image processing in the lung volume automatically segmented. Results. Pulmonary lung evaluation showed that COVID-19 pneumonia almost completely regressed, with mild focal areas affected by fibrous stripes. In patients that reported dyspnea, lung CT showed complete resolution of interstitial changes. Quantification of lung perfusion condition by contrasted CT, showed that dyspnea in 3 patients was associated with areas of hypoperfusion, while in 2 patients not reporting dyspnea perfusion conditions were comparable to normal controls. Conclusions. Although we obtained preliminary data, this is the first report on quantitative evaluation of hypoperfused lung tissue detected in recovering COVID-19 patients. These results suggest the need to further investigate these patients and to redefine the role of CT evaluation for diagnostic purposes as well as for evaluation of potential treatments.

The pathophysiology of SARS-CoV2 is becoming clearer with a number of recent reports in the literature after the fast viral outbreak in China and recently in other countries worldwide [[1]WHO Coronavirus Disease (COVID-2019) Situation Reports. Situation Report—114. May 13, 2020.2020https://www.who.int/docs/default-source/coronaviruse/situation-reportsGoogle Scholar]. The major symptoms is severe acute respiratory syndrome due to virus interaction with cells expressing angiotensin-converting enzyme 2 (ACE2) and TMPRSS2, triggering important immune response with the generation of cytokines and chemokines, which attract monocytes, macrophages and T cells promoting further inflammation [[2]Tay M.Z. Poh C.M. Rénia L. MacAry P.A. Ng L.F.P. The trinity of COVID-19: immunity, inflammation and intervention.Nat. Rev. Immunol. 2020; 20 (published online April 28): 363-374https://doi.org/10.1038/s41577-020-0311-8Crossref PubMed Scopus (2862) Google Scholar]. This may lead to further accumulation of immune cells in the lungs, with overproduction of pro-inflammatory cytokines and activation of complement and coagulation systems in lung microcirculation [[3]Klok F.A. Kruip M.J.H.A. van der Meer N.J.M. et al.Incidence of thrombotic complications in critically ill ICU patients with COVID-19.Thromb. Res. 2020; 191: 145-147Abstract Full Text Full Text PDF PubMed Scopus (3253) Google Scholar,[4]Li H. Liu L. Zhang D. et al.SARS-CoV-2 and viral sepsis: observations and hypotheses.Lancet. 2020; 395: 1517-1520Abstract Full Text Full Text PDF PubMed Scopus (828) Google Scholar]. This important immune response attracts virus-specific T cells to the site of infection, where they can eliminate the infected cells. Alveolar macrophages can then recognize neutralized viruses and apoptotic cells and clear them by phagocytosis, resulting in recovery [[5]Dou P. Zhang S. Wang C. et al.Serial CT features in discharged COVID-19 patients with positive RT-PCR re-test.Eur. J. Radiol. 2020; 127109010Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar]. Despite these pathophysiological mechanisms are under continuous investigation, there are only a few reports on the clinical course during the recovery phase of the disease. Recent investigations [[6]Belfiore M.P. Urraro F. Grassi R. et al.Artificial intelligence to codify lung CT in Covid-19 patients.Radiol. Med. 2020; 125: 500-504Crossref PubMed Scopus (86) Google Scholar,[7]Wang Y. Dong C. Hu Y. et al.Temporal changes of CT findings in 90 patients with COVID-19 pneumonia: a longitudinal study.Radiology. 2020; (Online ahead of print:)Crossref Scopus (639) Google Scholar] show that lung abnormalities on chest computerized tomography (CT) show the greatest severity approximately 6–11 days after the initial onset of symptoms, while in the following weeks recovery occurs consistently and in about 30 days lung tissue lesions are almost absorbed [[8]Pan F. Ye T. Sun P. et al.Time course of lung changes on chest CT during recovery from 2019 novel coronavirus (COVID-19) pneumonia.Radiology. 2020; 295: 715-721Crossref PubMed Scopus (1844) Google Scholar]. However, extended observation on COVID-19 patient during recovery are still object of investigation. More than 2,000 patients were admitted in our hospital (Bolognini Hospital, ASST Bergamo Est) during the COVID-19 outbreak, and we recently started to follow them during recovery. We reviewed CT findings in some of these patients in which CT scans were used to investigate potential thrombotic events with and without contrast media. We report here the preliminar results of these investigations in relation to lung perfusion conditions. We did identify perfusion defects in lungs of these patients, more than one month after remission of the symptoms, that deserve attention. During the period from April 15 to 30, twenty patients (12 male and 8 female; age range 35–86, mean age 58±10) previously treated for pneumonia SARS-CoV-2, with negative swab, have been admitted to our department to assess the outcome of SARS-CoV-2 pneumonia. Chest CT was performed at an interval between 14 and 60 days after remission of the fever (average 40±13 days). Twelve patients reported an almost complete resolution of the symptoms, while 8 patients reported residual dyspnea. Of these 8 patients, 3 reported dyspnea with minimal motor activity, while in the others after prolonged effort. Control CT was performed in 5 patients with contrast media for suspected thromboembolism (including those with dyspnea with minimal motor activity, or patients with D-Dimer value over normal range). Four patients not affected by COVID-19, studied by angioCT scan for other clinical indications and with normal lung tissue, were used as a control group. Ethical approval of this retrospective evaluation was obtained by the Bergamo province Ethics Committee (Reg. Sperim. N. 80/20 on 22/04/2020). Conventional chest CT was performed with the patient in the supine position during end-inspiration (CT 128 slice Ingenuity, Philips, Amsterdam, The Netherlands). The chest CT protocol used is as follows: from apices to mid-renal; slice thickness 1 mm; slice increment 1 mm; pitch 0.94; Rotation time 0.5 s; Field of view 411 mm; Voltage 120 kV; mAs modulation 100−200 mA. The contrasted acquisition consisted in arterial (80 mL/Iomeron 400, injection 4 mL/s in the antecubital vein; threshold 90 HU) and venous phase acquisition (60 s from the threshold). Images were viewed using IMPAX version 6.6.1 (Agfa-Gevaert NV Septestraat 27B-2640 Mortsel - Belgium). Every chest CT examination was evaluated by two double-blind experienced radiologists. The lung perfusion evaluation was performed by using PAA (Pulmonary Artery Analysis) Software [[9]Lahiji K. Kligerman S. Jeudy J. White C. Improved accuracy of pulmonary embolism computer-aided detection using iterative reconstruction compared with filtered back projection.Am. J. Roentgenol. 2014; 203: 763-771Crossref PubMed Scopus (21) Google Scholar] using Hounsfield Units (HU)-based colormap visualization tool (color palette ranging from −749 to −983 HU). The threshold level identified for normal lung tissue perfusion in control subjects was equal to −890 HU, with lower attenuation values considered as hypoperfusion. We quantified the volume of low perfusion lung tissue, independently by the amount of contrast media, using the following method. The previously mentioned range of HU for hypoperfused threshold (HU < −890) in the control group was on average 13.3 % of the total HU range air to contrast media in pulmonary artery. We then assumed this percentage, and calculated patient-specific threshold for hypoperfused tissue, on the basis of HU range from air to pulmonary artery. To estimate the percentage of lung volume characterized by hypoperfusion, we segmented the lung volume of the CT scans by automatic lung segmentation using the u-net (R231) convolutional network [[10]Hofmanninger J. Prayer F. Pan J. Rohrich S. Prosch H. Langs G. Automatic lung segmentation in routine imaging is a data diversity problem, not a methodology problem.arXiv. 2020; ([physics, stat]; published online January 31. http://arxiv.org/abs/2001.11767 (Accessed 15 May 2020))200111767Google Scholar], a model trained on a large dataset including COVID-19 CT slices. Segmentation on individual slices allowed to extract the right and left lung mask separately, with the trachea not included in the lung segmentation. We labeled each pixel inside the lung mask as low perfusion or normal perfusion based on the patient-specific thresholds using Python implementation of SimpleITK library (https://simpleitk.org/about.html). Out of the 20 patients who underwent follow-up, 12 patients had complete resolution of symptoms, with complete regression of the thickening areas detected with chest CT scan in 4 patients, and persistence of fibrous stripes areas in the other 8 patients. In the remaining patients, 5 reported dyspnea after prolonged effort, with 3 of them with complete remission of interstitial pneumonia and 2 with only partial remission. The 3 other patients reported dyspnea with minimal effort but showed a completely normal CT scan and remission of parenchymal opacity. These results indicate that persistent dyspnea is not associated with signs of interstitial pneumonia. In the 5 patients studied with contrast media, 3 were those that reported dyspnea with minimal effort, while the other 2 had no such symptom. At CT evaluation, no signs of thromboembolism were present in all these patients. Of interest, in the 3 patients affected by dyspnea color map representation (see Fig. 1) showed diffuse hypoperfused areas (dark red/violet) not uniform between the left and right lung. Quantification of hypoperfused lung volume showed that, while in normal controls this volume was in average 8.5 %, in these patients, that reported dyspnea, the volume ranged from 21.0 % to 48.4 % (Table 1). Of interest, tissue lung perfusion was normal in the two patients without dyspnea (see Table 1 and Fig. 1), with hypoperfused lung volume of 7.4 % and 8.5 %, respectively. Thus, the presence of dyspnea was associated with hypoperfused lung volume rather than with abnormal lung ventilation at CT.Table 1Percentage of lung volume occupied by hypoperfused tissue in COVID-19 patients and in controls.SubjectLeft LungRight LungTotalTime after symptoms remission (days)Patient symptomsPt 119.0 %29.3 %48.4 %54Dyspnea ++Pt 215.4 %11.0 %26.4 %30Dyspnea ++Pt 313.5 %7.5 %21.0 %30Dyspnea ++Pt 44.9 %2.4 %7.4 %25–Pt 53.7 %4.7 %8.5 %36–ControlsaMean + SD of 4 normal controls.4.3 ± 3.2 %4.0 + 2.7 %8.5 + 5.8 %–a Mean + SD of 4 normal controls. Open table in a new tab The lung tissue inflammation induced in COVID-19 patients by accumulation of immune cells, overproduction of pro-inflammatory cytokines and activation of complement and coagulation system in the microcirculation correlate with the initial appearance of areas of increased lung density with the "ground glass" appearance, which gradually tends to consolidate in areas preferentially located in the peripheral subpleural regions. Four stages of infection were recently proposed: early, progression, peak, and resolution [[11]Zu Z.Y. Jiang M.D. Xu P.P. et al.Coronavirus disease 2019 (COVID-19): a perspective from China.Radiology. 2020; (Online ahead of print)Crossref PubMed Scopus (1239) Google Scholar], and in the later stage of the infection, the pattern referred to as "crazy paving" and "reversed halo sign" have been found more frequently [[11]Zu Z.Y. Jiang M.D. Xu P.P. et al.Coronavirus disease 2019 (COVID-19): a perspective from China.Radiology. 2020; (Online ahead of print)Crossref PubMed Scopus (1239) Google Scholar]. Little is known, however, on the recovery phase of the disease. Our preliminar retrospective analysis, based on volumetric image processing, show that in symptomatic patients (dyspnea) one moths after remission from fever, despite the absence of pulmonary fibrous stripes residues, extended hypoperfused areas of lung parenchyma are still present. These findings suggest that during the recovery of COVID-19 important defects in lung blood perfusion of the microcirculation may persist even with normal lung CT. To our knowledge, this is the first report on quantitative estimation of lung microvasculature defect, without thromboembolism, in COVID-19 patients due incomplete healing of alveolar parenchyma microcirculation that persist during recovery. Thus, while the lung tissue damage related to interstitial fluid accumulation and impairment of ventilation is almost completely recovered within one month, a persistent defect of the microcirculation may remain, likely due to residual of viral-induced inflammation, with immune cell accumulation, platelet adhesion and micro-disseminated thrombi. Whether also fibrosis may be responsible for these microcirculation perfusion defects is worth to investigate. While these complications of the disease are now well recognized during the acute phase of the infection [12Kucharski A.J. Russell T.W. Diamond C. et al.Early dynamics of transmission and control of COVID-19: a mathematical modelling study.Lancet Infect. Dis. 2020; 20: 553-558Abstract Full Text Full Text PDF PubMed Scopus (1615) Google Scholar, 13Henry B.M. Vikse J. Benoit S. Favaloro E.J. Lippi G. Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: a novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis.Clin. Chim. Acta. 2020; 507: 167-173Crossref PubMed Scopus (281) Google Scholar, 14Ierardi A.M. Angileri S.A. Arrichiello A. Di Meglio L. Gurgitano M. Rodà G.M. Carrafiello G. Pulmonary embolism in COVID-19: ventilation and perfusion computed tomography.IDCases. 2020; 21e00805https://doi.org/10.1016/j.idcr.2020.e00805Crossref Scopus (7) Google Scholar], it is important to notice that this impairment of the microcirculation, we have detected, may affect lung function even in the recovery phase and may last for a long time or even not be healed with time. This evidence should be carefully considered, due to the potential clinical relevance of the problem in the large actual number of patients affected by the SARS-CoV-2 infection worldwide. In summary, the main message from our observation is that in discharged COVID-19 patients still reporting dyspnea, chest CT should be used to quantify the presence of lung perfusion dysfunction. This is important not only for diagnosis, but also to determine the incidence of these complications, whether this damage to the lung microcirculation will resolve with time and the need for specific pharmacological interventions. Deeper knowledge of these pathological processes it is very important for this increasing in size patient population due to the ongoing SARS-CoV-2 outbreak. While extensive investigation with CT in discharged COVID19 patients is in progress by our center and by others, we believe it is urgent to draw attention to these lung complications. Authors declare that they have no competing interests.

BACKGROUND AND AIMS:Brain white matter hyperintensities (WMHs) have been associated with an increased risk of ischemic stroke and considered as markers of brain ischemia. Progression of WMHs in asymptomatic patients with non-hemodynamically significant carotid plaque could represent a putative marker of plaque vulnerability. We prospectively evaluate progression and determinants of WMHs in this population. METHODS:This prospective study included 51 asymptomatic patients with carotid stenosis <70% that underwent brain magnetic resonance imaging scans at baseline and after a median follow up of 595 days (interquartile range 553-641 days). Patients (mean age of 69 years and 45% females) underwent baseline carotid computed tomography angiography, contrast-enhanced ultrasound for carotid plaque characterization and analysis of subsets of circulating lymphocytes and monocytes by flow cytometry. RESULTS:Seventeen subjects (33.3%) had carotid stenoses of 50-70% (Doppler flow velocity) while the rest had stenoses of <50%. In 25 (49.0%) patients, new WMHs, with 5 new lesions on average and a median volume of 134 mm3, were detected at follow-up. None of the plaque characteristics or of the circulating cellular biomarkers investigated were associated with the global and ipsilateral occurrence of new WMHs whereas, at multivariate analysis, female sex, hypercholesterolemia, and lower glomerular filtration rate (GFR) emerged as independent variables associated with new WMHs. CONCLUSIONS:Half of the patients with carotid plaques of intermediate severity had evidence of WMH progression at follow up. Female gender and systemic factors such as hypercholesterolemia, and lower GFR, but not plaque characteristics or circulating cellular biomarkers, are associated with WMH progression.

Background: We explored the relation between blood concentrations of monocyte/lymphocyte subsets and carotid artery plaque macrophage content, measured by positron emission tomography (PET) with C-11-PK11195. Methods and results: In 9 patients with carotid plaques we performed C-11-PK11195-PET/computed tomography angiography imaging and measurement of absolute concentrations and frequencies of circulating monocytes and T-cell subsets. Plaque standardized uptake value (SUV) for C-11-PK11195was negatively correlated with concentrations of total monocytes (r = -0.58, p = 0.05) and CD14(++)CD16(-)HLA-DR+ classical subset (r = -0.82, p = 0.005). These correlations hold true also in relation to plaque target to background ratio. No correlationwas observed between plaque SUV and CD3(+)T lymphocytes, CD4(+)T lymphocytes nor with activated CD3(+)CD4(+)T cells expressing HLA-DR. Conclusions: We first demonstrated a reduction in the absolute concentration of monocytes and particularly in classical monocytes expressing HLA-DR in the presence of an increased uptake of C-11-PK11195 in carotid plaques. The present work, despite being a pilot study comprising only a small number of subjects provides new insights in the search for specific cellular biomarkers with potential diagnostic and prognostic value in patients with a known carotid plaque. (C) 2018 The Authors. Published by Elsevier B.V.

A high prevalence of mitral annular calcium (MAC) is expected in patients undergoing transcatheter aortic valve implantation (TAVI); however, data regarding the prevalence of MAC and impact on risk of cardiovascular events are lacking. To determine the prevalence of MAC and its association with clinical outcomes in patients undergoing TAVI, we retrospectively analyzed 424 patients who underwent transfemoral TAVI from 2007 to 2015 and whose preoperative computed tomography images were available for assessment of MAC. Severe circumferential MAC (SC-MAC) was defined as calcification involving at least the whole posterior annulus alone or with the attachment of the anterior leaflet. Clinical outcomes were examined according to Valve Academic Research Consortium-2 criteria up to 2 years. SC-MAC was found in 17.7% of patients. Patients with SC-MAC were more likely to be female, with a higher prevalence of atrial fibrillation and peripheral artery disease. There were no differences between the groups regarding age, functional class, prevalence of diabetes, kidney disease, and operative risk. Female gender and peripheral artery disease were independent predictors of SC-MAC. SC-MAC did not appear to be associated with periprocedural and 30-day outcomes. At 2 years' follow-up, patients with SC-MAC had significantly higher cardiovascular and all-cause mortality rates. SC-MAC was an independent predictor of cardiovascular mortality during follow-up. In conclusion, SC-MAC is a frequent finding in the TAVI population and appears to be an independent predictor of cardiovascular mortality at 2 years' follow-up. (C) 2017 Elsevier Inc. All rights reserved.

White matter hyperintensities (WMH) can be incidentally found in patients with carotid atherosclerosis on brain magnetic resonance imaging (MRI). We investigated the relationship between WMH and characteristics of carotid plaques in asymptomatic patients without indication for carotid revascularization. We prospectively screened 235 consecutive patients with carotid stenosis <70%. After excluding patients with confounding causes of cerebral damage, 67 asymptomatic patients underwent carotid computed tomography angiography (CTA), contrast-enhanced ultrasound and brain MRI. Number and quantitative measurement of volume of WMH were associated with history of resistant hypertension, degree of stenosis (Doppler) and presence of an ulcerated plaque at CTA (p < 0.05). At multivariate regression analysis, resistant hypertension was independently associated with both number and volume of WMH, presence of an ulcer with number of WMH and degree of stenosis with WMH volume (p < 0.05), although WMH were equally distributed in both hemispheres irrespectively of plaque side. In conclusion, in asymptomatic patients with carotid plaques < 70%, a higher burden of WMHs is associated with history of resistant hypertension that could be the expression of microvascular damage. Stenosis severity and presence of plaque ulceration are also associated with WMH burden although their causative relation is not supported by the bilateral distribution of WMH.

Aim: White matter hyperintensities (WMH) can be incidentally found in patients with carotid atherosclerosis on brain magnetic resonance imaging (MRI). They are believed to reflect cerebral ischemic burden. We investigated the relationship between carotid atherosclerosis and presence and extension of WMH in asymptomatic patients with carotid plaques of intermediate severity.

Congenital coronary-pulmonary fistulas are uncommon coronary anomalies. We present a case of a 63-year-old woman with a tortuous fistula between the proximal left anterior descending and main pulmonary artery which was effectively closed using an AMPLATZER Vascular Plug IV.

AIMS To investigate the feasibility, image quality, and clinical implications of an ultra-low-dose contrast injection computed tomography angiography (CTA) protocol in patients scheduled for transcatheter aortic valve implantation (TAVI). METHODS AND RESULTS Images obtained with 64-slice CT were retrospectively evaluated in 162 TAVI candidates with a body mass index (BMI) of ≤29 kg/m(2). A multiphasic, low iodine dose and BMI-adapted CM protocol was administered in all patients (BMI <22 kg/m(2): 40 mL; BMI 22-29 kg/m(2): 55 mL). All images were evaluated for image quality, vessel attenuation, and estimated radiation dose. The anatomy, diameters, perimeter, and area of the aortic annulus were assessed. Anatomy and diameters of peripheral vessels were also evaluated. Image quality of the aortic root and ilio-femoral vessels was diagnostic in all patients. Vascular attenuation was >200 HU at any vessel level. The mean diameters of the aortic annulus were 22 ± 3 mm (range: 16-28 mm) × 26 ± 3 mm (range: 20-33 mm); the mean perimeter was 77.0 ± 7.1 mm. After CTA, a total of 137 patients (84.6%) underwent TAVI. Mean estimated radiation dose was 20.2 ± 4.6 mSv. CONCLUSION With our protocol, we achieved images of the aortic annulus and aorto-iliac anatomy of sufficient quality to allow patient selection and procedural planning for TAVI, with a substantial reduction of the amount of injected CM.

Poster: ECR 2010 / C-3200 / Correlation between presence and degree of atherosclerosis in the carotideal and coronaric district respectively evalued by doppler US and coronary-CT by: S. Tresoldi , R. Maiolino, N. Ajmone Marsan, F. Besana, G. Manglaviti, G. Cornalba; Milan/IT