Background Myocardial injury is frequent among patients hospitalized with coronavirus disease-2019 (COVID-19) and is associated with a poor prognosis. However, the mechanisms of myocardial injury remain unclear and prior studies have not reported cardiovascular imaging data. Objectives This study sought to characterize the echocardiographic abnormalities associated with myocardial injury and their prognostic impact in patients with COVID-19. Methods We conducted an international, multicenter cohort study including 7 hospitals in New York City and Milan of hospitalized patients with laboratory-confirmed COVID-19 who had undergone transthoracic echocardiographic (TTE) and electrocardiographic evaluation during their index hospitalization. Myocardial injury was defined as any elevation in cardiac troponin at the time of clinical presentation or during the hospitalization. Results A total of 305 patients were included. Mean age was 63 years and 205 patients (67.2%) were male. Overall, myocardial injury was observed in 190 patients (62.3%). Compared with patients without myocardial injury, those with myocardial injury had more electrocardiographic abnormalities, higher inflammatory biomarkers and an increased prevalence of major echocardiographic abnormalities that included left ventricular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysfunction grade II or III, right ventricular dysfunction and pericardial effusions. Rates of in-hospital mortality were 5.2%, 18.6%, and 31.7% in patients without myocardial injury, with myocardial injury without TTE abnormalities, and with myocardial injury and TTE abnormalities. Following multivariable adjustment, myocardial injury with TTE abnormalities was associated with higher risk of death but not myocardial injury without TTE abnormalities. Conclusions Among patients with COVID-19 who underwent TTE, cardiac structural abnormalities were present in nearly two-thirds of patients with myocardial injury. Myocardial injury was associated with increased in-hospital mortality particularly if echocardiographic abnormalities were present.

The Human Disease Ontology (DO) (http://www.disease-ontology.org), database has undergone significant expansion in the past three years. The DO disease classification includes specific formal semantic rules to express meaningful disease models and has expanded from a single asserted classification to include multiple-inferred mechanistic disease classifications, thus providing novel perspectives on related diseases. Expansion of disease terms, alternative anatomy, cell type and genetic disease classifications and workflow automation highlight the updates for the DO since 2015. The enhanced breadth and depth of the DO’s knowledgebase has expanded the DO’s utility for exploring the multi-etiology of human disease, thus improving the capture and communication of health-related data across biomedical databases, bioinformatics tools, genomic and cancer resources and demonstrated by a 6.6× growth in DO’s user community since 2015. The DO’s continual integration of human disease knowledge, evidenced by the more than 200 SVN/GitHub releases/revisions, since previously reported in our DO 2015 NAR paper, includes the addition of 2650 new disease terms, a 30% increase of textual definitions, and an expanding suite of disease classification hierarchies constructed through defined logical axioms.

Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre-including this research content-immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

Background Coronavirus Disease 2019 (COVID-19) results in increased inflammatory markers previously associated with atrial arrhythmias. However, little is known about their incidence or specificity in COVID-19, or their association with outcomes. We determined the incidence, predictors and outcomes of atrial fibrillation or flutter (AF/AFL) in patients hospitalized with COVID-19, or hospitalized with Influenza. Methods This is a retrospective analysis of 3,970 patients admitted with PCR-positive COVID-19 between 2/4/2020-4/22/2020 with manual review performed of 1,110. The comparator arm included 1,420 patients with influenza hospitalized between 1/1/2017-1/1/2020. Results Among 3970 inpatients with COVID-19, the incidence of AF/AFL was 10% (N=375) and in patients without a history of atrial arrhythmias, 4% (N=146). Patients with new-onset AF/AFL were older with increased inflammatory markers including Interleukin-6 (93 vs 68 pg/ml, P<0.01), and more myocardial injury (Troponin-I: 0.2 vs 0.06ng/ml, P<0.01). AF/AFL were associated with increased mortality (46% vs 26%, P<0.01). Manual review captured a somewhat higher incidence of AF/AFL (13%, N=140). Compared to inpatients with COVID-19, patients with Influenza (N=1420) had similar rates of AF/AFL (12%, n=163) but lower mortality. The presence of AF/AFL correlated with similarly increased mortality in both COVID-19 (RR 1.77) and Influenza (RR 1.78). Conclusions AF/AFL occurs in a subset of patients hospitalized with either COVID-19 or Influenza, and is associated with inflammation and disease severity in both infections. The incidence and associated increase in mortality in both cohorts suggests that AF/AFL in not specific to COVID-19, but is rather a generalized response to the systemic inflammation of severe viral illnesses.

Introduction: Recent studies have described several cardiovascular manifestations of COVID-19 including myocardial ischemia, myocarditis, thromboembolism, and malignant arrhythmias. However, to our knowledge, syncope in COVID-19 patients has not been systematically evaluated. We sought to characterize syncope and/or presyncope in COVID-19. Methods: This is a retrospective analysis of consecutive patients hospitalized with laboratory-confirmed COVID-19 with either syncope or presyncope. This "study" group (n = 37) was compared with an age and gender-matched cohort of patients without syncope ("control") (n = 40). Syncope was attributed to various categories. We compared telemetry data, treatments received, and clinical outcomes between the two groups. Results: Among 1000 COVID-19 patients admitted to the Mount Sinai Hospital, the incidence of syncope/presyncope was 3.7%. The median age of the entire cohort was 69 years (range 26-89+ years) and 55% were men. Major comorbidities included hypertension, diabetes, and coronary artery disease. Syncopal episodes were categorized as (a) unspecified in 59.4% patients, (b) neurocardiogenic in 15.6% patients, (c) hypotensive in 12.5% patients, and (d) cardiopulmonary in 3.1% patients with fall versus syncope and seizure versus syncope in 2 of 32 (6.3%) and 1 of 33 (3.1%) patients, respectively. Compared with the "control" group, there were no significant differences in both admission and peak blood levels of d-dimer, troponin-I, and CRP in the "study" group. Additionally, there were no differences in arrhythmias or death between both groups. Conclusions: Syncope/presyncope in patients hospitalized with COVID-19 is uncommon and is infrequently associated with a cardiac etiology or associated with adverse outcomes compared to those who do not present with these symptoms.

Objective Endovascular aortic repair (EVAR) is considered a lower risk option for treating abdominal aortic aneurysms (AAA), and is of particular utility in patients with poor functional status who may be poor candidates for open repair. However, the specific contribution of preoperative functional status EVAR outcomes remains poorly defined. We hypothesized that impaired functional status, based simply on the ability of patients to perform activities of daily living, is associated with worse outcomes after EVAR. Methods Patients undergoing non-emergent EVAR for AAA between 2010 and 2014 were identified in the National Surgical Quality Improvement Program (NSQIP) database. The primary outcomes were 30-day mortality and major operative and systemic complications. Secondary outcomes were inpatient length of stay, need for reoperation, and discharge disposition. Using NSQIP defined preoperative functional status, patients were stratified as Independent or Dependent (either partial or totally dependent), and compared by univariate and multivariable analyses. Results Of 13,432 patients undergoing EVAR between 2010 – 2014, 13,043 were independent (97%) and 389 were dependent (3%) prior to surgery. Dependent patients were older and more frequently minorities; had higher rates of chronic pulmonary, heart, and kidney disease; and were more likely to have an American Society of Anesthesiologists score of 4 or 5. On multivariable analysis, preoperative dependent status was an independently risk factor for operative complications (OR 3.1, 95% CI 2.5 – 3.9), systemic complications (2.8, 2.0 – 3.9), and 30-day mortality (3.4, 2.1 – 5.6). Secondary outcomes were worse among dependent patients. Conclusions Although EVAR is a minimally invasive procedure with substantially less physiologic stress than open aortic repair, preoperative functional status is a critical determinant of adverse outcomes after EVAR, in spite of the minimally invasive nature of the procedure. Functional status, as measured by performance of activities of daily living, can be used as a valuable marker of increased perioperative risk, and may identify patients who may benefit from preoperative conditioning and specialized perioperative care.

Novel functional polymorphisms in 8 candidate genes are associated with HALP in the absence of CHD. Future study is required to examine the extent to which these genes may affect HDL function and serve as potential therapeutic targets for CHD risk reduction.

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