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      Atrial Fibrillation and Cardiovascular Risk Assessment among COVID-19 Patients Using Different Scores

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          Abstract

          Atrial fibrillation is a common arrhythmic complication of coronavirus disease 2019 (COVID-19) patients. Cardiovascular complications of this viral infection need to be identified with different means to detect adverse events early. This is particularly true for hospitalized COVID-19 patients who have severe illness. This review provides a comprehensive overview about the different scores used to predict atrial fibrillation as well as cardiovascular morbidity and mortality among COVID-19 patients.

          Abstract

          Since the advent of severe acute respiratory syndrome-coronavirus-2 in December 2019, millions of people have been infected and succumbed to death because of this deadly virus. Cardiovascular complications such as thromboembolism and arrhythmia are predominant causes of morbidity and mortality. Different scores previously used for atrial fibrillation (AF) identification or prediction of its complications were investigated by physicians to understand whether those scores can predict in-hospital mortality or AF among patients infected with the severe acute respiratory syndromecoronavirus-2 virus. Using such scores gives hope for early prediction of atrial arrhythmia and in-hospital mortality among coronavirus disease 2019–infected patients. We have discussed the mechanisms of AF and cardiovascular damage in coronavirus disease 2019 patients, different methods of AF prediction, and compared different scores for prediction of in-hospital mortality after this viral infection.

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          Most cited references35

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          Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation.

          Contemporary clinical risk stratification schemata for predicting stroke and thromboembolism (TE) in patients with atrial fibrillation (AF) are largely derived from risk factors identified from trial cohorts. Thus, many potential risk factors have not been included. We refined the 2006 Birmingham/National Institute for Health and Clinical Excellence (NICE) stroke risk stratification schema into a risk factor-based approach by reclassifying and/or incorporating additional new risk factors where relevant. This schema was then compared with existing stroke risk stratification schema in a real-world cohort of patients with AF (n = 1,084) from the Euro Heart Survey for AF. Risk categorization differed widely between the different schemes compared. Patients classified as high risk ranged from 10.2% with the Framingham schema to 75.7% with the Birmingham 2009 schema. The classic CHADS(2) (Congestive heart failure, Hypertension, Age > 75, Diabetes, prior Stroke/transient ischemic attack) schema categorized the largest proportion (61.9%) into the intermediate-risk strata, whereas the Birmingham 2009 schema classified 15.1% into this category. The Birmingham 2009 schema classified only 9.2% as low risk, whereas the Framingham scheme categorized 48.3% as low risk. Calculated C-statistics suggested modest predictive value of all schema for TE. The Birmingham 2009 schema fared marginally better (C-statistic, 0.606) than CHADS(2). However, those classified as low risk by the Birmingham 2009 and NICE schema were truly low risk with no TE events recorded, whereas TE events occurred in 1.4% of low-risk CHADS(2) subjects. When expressed as a scoring system, the Birmingham 2009 schema (CHA(2)DS(2)-VASc acronym) showed an increase in TE rate with increasing scores (P value for trend = .003). Our novel, simple stroke risk stratification schema, based on a risk factor approach, provides some improvement in predictive value for TE over the CHADS(2) schema, with low event rates in low-risk subjects and the classification of only a small proportion of subjects into the intermediate-risk category. This schema could improve our approach to stroke risk stratification in patients with AF.
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            COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options

            Abstract The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) —a homologue of ACE—to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use. Moreover, renin–angiotensin–aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures (social distancing and social isolation) also increase cardiovascular risk. Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed.
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              Estimates of current and future incidence and prevalence of atrial fibrillation in the U.S. adult population.

              Estimates and projections of diagnosed incidence and prevalence of atrial fibrillation (AF) in the United States have been highly inconsistent across published studies. Although it is generally acknowledged that AF incidence and prevalence are increasing due to growing numbers of older people in the U.S. population, estimates of the rate of expected growth have varied widely. Reasons for these variations include differences in study design, covered time period, birth cohort, and temporal effects, as well as improvements in AF diagnosis due to increased use of diagnostic tools and health care awareness. The objective of this study was to estimate and project the incidence and prevalence of diagnosed AF in the United States out to 2030. A large health insurance claims database for the years 2001 to 2008, representing a geographically diverse 5% of the U.S. population, was used in this study. The trend and growth rate in AF incidence and prevalence was projected by a dynamic age-period cohort simulation progression model that included all diagnosed AF cases in future prevalence projections regardless of follow-up treatment, as well as those cases expected to be chronic in nature. Results from the model showed that AF incidence will double, from 1.2 million cases in 2010 to 2.6 million cases in 2030. Given this increase in incidence, AF prevalence is projected to increase from 5.2 million in 2010 to 12.1 million cases in 2030. The effect of uncertainty in model parameters was explored in deterministic and probabilistic sensitivity analyses. Variability in future trends in AF incidence and recurrence rates has the greatest impact on the projected estimates of chronic AF prevalence. It can be concluded that both incidence and prevalence of AF are likely to rise from 2010 to 2030, but there exists a wide range of uncertainty around the magnitude of future trends.
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                Author and article information

                Contributors
                Journal
                South Med J
                South Med J
                SMJ
                Southern Medical Journal
                Lippincott Williams & Wilkins
                0038-4348
                1541-8243
                December 2022
                1 December 2022
                1 December 2022
                : 115
                : 12
                : 921-925
                Affiliations
                [1]From Bridgeport Hospital/Yale New Haven Health, Bridgeport, Connecticut, the University of Tennessee College of Medicine, Memphis, the Department of Neurology, National Institute of Neurosciences and Hospital, Dhaka, Bangladesh, and Department of Cardiology, National Institute of Cardiovascular Diseases and Hospital, Dhaka, Bangladesh.
                Author notes
                [*]Correspondence to Dr Md. Mashiul Alam, Bridgeport Hospital/Yale New Haven Health, 267 Grant St, Bridgeport, CT 06610. E-mail: mashiull@ 123456gmail.com . To purchase a single copy of this article, visit sma.org/smj. To purchase larger reprint quantities, please contact reprintsolutions@ 123456wolterskluwer.com .
                Article
                SMJ_220275 00012
                10.14423/SMJ.0000000000001477
                9696680
                c330476f-960a-40e7-9d77-c40231013d62
                Copyright © 2022 by The Southern Medical Association

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                History
                : 20 May 2022
                Categories
                Medicine & Medical Specialties

                atrial fibrillation,cha2ds2vasc score,covid-19,in-hospital mortality,thromboembolism

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