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Count of studies: 98
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Myocardial fibrosis occurs in non-hospitalised patients with chronic symptoms after COVID-19 1/26/2022https://doi.org/10.1016%2Fj.ijcha.2022.100964PMC8789662A. Krishnanhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789662/In our cohort of recovering patients, managed in the community for initial COVID-19 infection and complaining of persistent symptoms, there is a larger than expected burden of myocardial injury demonstrated by presence of scar on LGE imaging by 12 months.
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Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered from Coronavirus Disease 2019 (COVID-19) 11/1/2020https://doi.org/10.1001/jamacardio.2020.355732730619Puntmann, V.O.https://www.scopus.com/record/display.uri?eid=2-s2.0-85089103970&origin=inward&txGid=fc726298163e320d0cac8957f532349cIn this study of a cohort of German patients recently recovered from COVID-19 infection, CMR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity and overall course of the acute illness, and time from the original diagnosis.
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Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19) 7/27/2020https://doi.org/10.1001%2Fjamacardio.2020.3557PMC7385689Valentina O. Puntmannhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7385689/In this study of a cohort of German patients recently recovered from COVID-19 infection, CMR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity and overall course of the acute illness, and time from the original diagnosis.
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Cardiac Involvement in Patients Recovered From COVID-2019 Identified Using Magnetic Resonance Imaging5/12/2020https://doi.org/10.1016%2Fj.jcmg.2020.05.004PMC7214335Lu Huanghttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214335/Fifteen patients (58%) had abnormal CMR findings on conventional CMR sequences: myocardial edema was found in 14 (54%) patients and LGE was found in 8 (31%) patients
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Long-term cardiovascular outcomes of COVID-192/7/2022https://doi.org/10.1038/s41591-022-01689-3
Xie, Y.https://www.nature.com/articles/s41591-022-01689-3Individuals with COVID-19 are at increased risk of incident cardiovascular disease spanning several categories, including cerebrovascular disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure and thromboembolic disease. These risks and burdens were evident even among individuals who were not hospitalized during the acute phase of the infection and increased in a graded fashion according to the care setting during the acute phase (non-hospitalized, hospitalized and admitted to intensive care).
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Cardiac Manifestations Of Coronavirus (COVID-19)5/2/2022Basu-Ray Ihttps://www.ncbi.nlm.nih.gov/books/NBK556152/Cardiac damage has been noted even without clinical features of respiratory disease. On the one hand, respiratory symptoms are worse in COVID-19 affected patients with preexisting cardiac ailments; however, new-onset cardiac dysfunction is common in this subset.
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Risks of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19: nationwide self-controlled cases series and matched cohort study 2/22/2022https://doi.org/10.1136/bmj-2021-069590Ioannis Katsoularishttps://www.bmj.com/content/377/bmj-2021-069590Incidence rate ratios were significantly increased 70 days after covid-19 for deep vein thrombosis, 110 days for pulmonary embolism, and 60 days for bleeding.
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SARS-CoV-2 Infection and Increased Risk for Pediatric Stroke11/20/2022https://doi.org/10.1016/j.pediatrneurol.2022.10.003MaryGlen J.VielleuxMDhttps://www.sciencedirect.com/science/article/pii/S0887899422002107Prior COVID-19 infection, but not acute infection, is correlated with a risk for stroke in the pediatric population.
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Excess risk for acute myocardial infarction mortality during the COVID-19 pandemic9/29/2022https://doi.org/10.1002/jmv.28187http://www.ncbi.nlm.nih.gov/pmc/articles/pmc9839603/Yee Hui Yeohttps://onlinelibrary.wiley.com/doi/10.1002/jmv.28187The SAPC (semi-annual percentage change) in the youngest and middle-age group in AMI-associated mortality increased by 5.3% (95% confidence interval [CI]: 1.6%–9.1%) and 3.4% (95% CI: 0.1%–6.8%), respectively. The excess death, defined as the difference between the observed and the predicted mortality rates, was most pronounced for the youngest (25–44 years) aged decedents, ranging from 23% to 34% for the youngest compared to 13%–18% for the oldest age groups.
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Prognosis of Myocarditis Developing After mRNA COVID-19 Vaccination Compared With Viral Myocarditis12/1/2022https://doi.org/10.1016/j.jacc.2022.09.049Lai Fhttps://www.jacc.org/doi/10.1016/j.jacc.2022.09.049This study found a significantly lower rate of mortality among individuals with myocarditis after mRNA vaccination compared with those with viral infection–related myocarditis.Adjusted analysis showed that the postvaccination myocarditis group had a 92% lower mortality risk (adjusted HR: 0.08; 95% CI: 0.01-0.57).
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Increased risk of acute myocardial infarction after COVID-19 recovery: A systematic review and meta-analysis12/16/2022https://doi.org/10.1016/j.ijcard.2022.12.032Marco Zuinhttps://www.internationaljournalofcardiology.com/article/S0167-5273(22)01914-3/fulltextThe risk of acute myocardial infarction was 93% higher in COVID-19 recovered patients compared to the general population. Over a mean follow-up of 8.5 months, among COVID-19 recovered patients AMI occurred in 3.5 cases per 1.000 individuals compared to 2.02 cases per 1.000 individuals in the control cohort, defined as those who did not experience COVID-19 infection in the same period).
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Chronic biopsy proven post-COVID myoendocarditis with SARS-Cov-2 persistence and high level of antiheart antibodies7/19/2022https://doi.org/10.1002/clc.23886Olga Blagova MD, PhDhttps://onlinelibrary.wiley.com/doi/10.1002/clc.23886COVID-19 can lead to long-term severe post-COVID myoendocarditis, that is characterized by prolonged persistence of coronavirus in cardiomyocytes, endothelium, and macrophages (up to 18 months) in combination with high immune activity.
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Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank10/24/2022https://doi.org/10.1136/heartjnl-2022-321492Zahra Raisi-Estabraghhttps://heart.bmj.com/content/109/2/119Individuals hospitalised (either with a primary or secondary daignoses of COVID-19) have increased risk of incident cardiovascular events across a range of disease and mortality outcomes. The risk of most events is highest in the early postinfection period. Individuals not requiring hospitalisation have increased risk of VTE, but not of other cardiovascular-specific outcomes.
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Mid- and Long-Term Atrio-Ventricular Functional Changes in Children after Recovery from COVID-19
12/26/2022https://doi.org/10.3390/jcm12010186Jolanda Sabatinohttps://www.mdpi.com/2077-0383/12/1/186Our study demonstrated for the first time the persistence of LV (left ventricular) myocardial deformation abnormalities in previously healthy children with an asymptomatic or mildly symptomatic (WHO stages 0 or 1) COVID-19 course. These findings imply that subclinical LV dysfunction may also be a typical characteristic of COVID-19 infection in children and are concerning given the predictive value of LV longitudinal strain in the general population. (Note: Studies find longitudinal strain is associated with long-term risk of cardiovascular morbidity and mortality.)
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One-year cardiovascular outcomes after coronavirus disease 2019: The cardiovascular COVID-19 registry12/30/2022https://doi.org/10.1371/journal.pone.0279333Luis Ortega-Pazhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0279333At one year, there were no significant differences in the primary endpoint of CV death between the COVID-19 and control cohorts (1.4% vs. 0.8%; HRadj 1.28 [0.56–2.91]; p = 0.555), but there was a higher risk of all-cause death (17.8% vs. 4.0%; HRadj 2.82 [1.99–4.0]; p = 0.001). COVID-19 cohort had higher rates of ATE (arterial thrombotic events) (2.5% vs. 0.8%, HRadj 2.26 [1.02–4.99]; p = 0.044), VTE (venous thromboembolism) (3.7% vs. 0.4%, HRadj 9.33 [2.93–29.70]; p = 0.001), and serious cardiac arrhythmias (2.5% vs. 0.6%, HRadj 3.37 [1.35–8.46]; p = 0.010).
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Risk of incident heart failure after COVID-19 recovery: a systematic review and meta-analysis12/27/2022https://doi.org/10.1007/s10741-022-10292-0Marco Zuinhttps://link.springer.com/article/10.1007/s10741-022-10292-0COVID-19 survivors had an additional 90% risk of developing HF (Heart Failure) after COVID-19 infection in the long-term period.
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Analysis of thrombogenicity under flow reveals new insights into the prothrombotic state of patients with post-COVID syndrome 1/1/2023https://doi.org/10.1016/j.jtha.2022.10.013Adela Constantinescu-Bercuhttps://www.jthjournal.org/article/S1538-7836(22)07182-3/fulltextPost-COVID syndrome can lead to increased platelet recruitment and larger thrombi under flow. The median time of 23 months from symptom onset suggests potential long-term thrombogenicity. Our data show a significant increase in platelet binding on both collagen and anti-VWF A3 in patients with PCS compared with that in controls.
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Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank1/19/2023https://doi.org/10.1093/cvr/cvac195Eric Yuk Fai Wanhttps://academic.oup.com/cardiovascres/advance-article/doi/10.1093/cvr/cvac195/6987834In the acute phase, patients with COVID-19 (n = 7584) were associated with a significantly higher short-term risk of CVD (cardiovascular disease) {hazard ratio (HR): 4.3} and all-cause mortality [HR: 81.1] than the contemporary (n = 75 790) controls (n = 75 774). Regarding the post-acute phase, patients with COVID-19 (n = 7139) persisted with a significantly higher risk of CVD in the long-term [HR: 1.4] and all-cause mortality [HR: 5.0] compared to the contemporary (n = 71 296) controls (n = 71 314).
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Risks and burdens of incident dyslipidaemia in long COVID: a cohort study1/6/2023https://doi.org/10.1016/S2213-8587(22)00355-2Evan Xu, BAhttps://www.thelancet.com/journals/landia/article/PIIS2213-8587(22)00355-2/fulltextCompared with the non-infected contemporary control group, those in the COVID-19 group had higher risks and burdens of incident dyslipidaemia, including total cholesterol greater than 200 mg/dL (hazard ratio [HR] 1·26), triglycerides greater than 150 mg/dL (1·27), LDL cholesterol greater than 130 mg/dL (1·24), and HDL cholesterol lower than 40 mg/dL (1·20). The risk of a composite of these abnormal lipid laboratory outcomes was 1·24 (95% CI 1·21–1·27).
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Clinical presentation and management strategies of cardiovascular autonomic dysfunction following a COVID-19 infection – a systematic review1/24/2023https://doi.org/10.1111/ene.15714Diogo Reis Carneirohttps://onlinelibrary.wiley.com/doi/10.1111/ene.15714There is evidence from the scientific literature about different types of cardiovascular autonomic dysfunction developing during and after COVID-19. Reflex syncope was the most common cardiovascular autonomic disorder in the acute phase (p=0.008), postural orthostatic tachycardia syndrome (POTS) the most frequent diagnosis in people with post-COVID-19 orthostatic complaints (p<0.001). Full recovery was more frequent in people with acute versus post-COVID-19 onset of cardiovascular autonomic disturbances (43% vs. 15%, p=0.002).
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Long COVID Syndrome and Cardiovascular Manifestations: A Systematic Review and Meta-Analysis1/29/2023https://doi.org/10.3390/diagnostics13030491Abhigan Babu Shresthahttps://www.mdpi.com/2075-4418/13/3/491In our meta-analysis, the odds of developing myocarditis were around 5-fold, pericarditis was 1.5-fold, and cardiomyopathy was 2-fold in the post-COVID-19 phase... The odds of developing coronary vessel diseases such as angina (OR 1.6) and myocardial infarction (OR 1.6) were also significantly higher in long-COVID cases... the odds of developing thromboembolic changes such as deep vein thrombosis (OR 1.98), pulmonary embolism (OR 2.76), TIA (1.49), and stroke (OR 1.39) are also higher in post-COVID syndrome.
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Clinical outcomes of myocarditis after SARS-CoV-2 mRNA vaccination in four Nordic countries: population based cohort study2/1/202310.1136/bmjmed-2022-000373Anders Husbyhttps://bmjmedicine.bmj.com/content/2/1/e000373The relative risk of heart failure within 90 days was 0.56 (95% confidence interval 0.37 to 0.85) and 1.48 (0.86 to 2.54) for myocarditis associated with vaccination and covid-19 disease, respectively, compared with conventional myocarditis; the relative risk of death was 0.48 (0.21 to 1.09) and 2.35 (1.06 to 5.19), respectively. Among patients aged 12-39 years with no predisposing comorbidities, the relative risk of heart failure or death was markedly higher for myocarditis associated with covid-19 disease than for myocarditis associated with vaccination (relative risk 5.78, 1.84 to 18.20).
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Abnormal right ventricular echocardiographic findings in recovered patients associated with severe acute respiratory syndrome in COVID-19 2/17/2023https://doi.org/10.1111/echo.15538Leandro S. A. Barros MDhttps://onlinelibrary.wiley.com/doi/10.1111/echo.15538SARS is a risk factor for abnormal RV echocardiographic findings in patients recovered from COVID-19. The frequency of RV echocardiographic changes in patients who had recovered from COVID-19 was 44.3%. RV systolic dysfunction was identified in 31.1%, followed by ventricular dilation in 14.7% and pulmonary hypertension in 9.8%. An association was observed between SARS and RV echocardiographic changes in recovered patients during outpatient follow-up (OR: 4.96; 95% CI: 1.37–17.9; p = 0.015).
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Cardiac manifestations in children with the multisystem inflammatory syndrome (MIS-C) associated with SARS-CoV-2 infection: Systematic review and meta-analysis2/18/2023https://doi.org/10.1002/rmv.2432Márcio Antonio Ferreira Arantes Juniorhttps://onlinelibrary.wiley.com/doi/10.1002/rmv.2432Study of children hospitalized with MIS-C: these children will have an increased cardiovascular risk with a greater chance of acute myocardial infarction, arrhythmias, or thrombosis will be essential for healthcare planning. The combined prevalence of myocarditis or pericarditis was 34.3% (95% CI: 25.0%–44.2%). The combined prevalence for echocardiogram anomalies was 40.8% (95% CI: 30.5%–51.5%), that of Kawasaki disease presentation was 14.8% (95% CI: 7.5%–23.7%), and that of coronary dilation was 15.2% (95% CI: 11.0%–19.8%).
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Orthostatic tachycardia after covid-19 2/24/2023https://doi.org/10.1136/bmj-2022-073488Ana B Espinosa-Gonzalezhttps://www.bmj.com/content/380/bmj-2022-073488About 25% of long covid patients may have dysautonomia and 2-14% will develop orthostatic tachycardia (postural orthostatic tachycardia syndrome) six to eight months after infection. Dysautonomia in long covid typically affects young, previously healthy individuals (aged 15-45), with a female sex predominance (80%).
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Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage9/15/2022https://doi.org/10.1111/imm.13577Arutha Kulasinghehttps://onlinelibrary.wiley.com/doi/10.1111/imm.13577#.ZAmL4C-VzGI.twitterHost transcriptomics showed upregulation of genes associated with DNA damage and repair, heat shock, and M1-like macrophage infiltration in the cardiac tissues of COVID-19 patients. These data demonstrate the emergence of distinct transcriptomic profiles in cardiac tissues of SARS-CoV-2 and pH1N1 influenza infection supporting the need for a greater understanding of the effects on extra-pulmonary organs.
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One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database3/3/2023doi:10.1001/jamahealthforum.2023.0010Andrea DeVries, PhDhttps://jamanetwork.com/journals/jama-health-forum/fullarticle/2802095Adults with PCC (post–COVID-19 condition) experienced increased risks for a number of cardiovascular outcomes, such as ischemic stroke. During the 12-month follow-up period, 2.8% of the individuals with PCC vs 1.2% of the individuals without COVID-19 died, implying an excess death rate of 16.4 per 1000 individuals.
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Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks8/11/2022https://doi.org/10.1016/j.eclinm.2022.101619Weijie Wanghttps://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00349-2/fulltextCOVID-19 survivors were associated with increased risks of cerebrovascular diseases, such as stroke (HR [95% CI] = 1.618 [1.545-1.694]), arrhythmia related disorders, such as atrial fibrillation (HR [95% CI] = 2.407 [2.296-2.523]), inflammatory heart disease, such as myocarditis (HR [95% CI] =4.406 [2.890-6.716]), ischemic heart disease(IHD), like ischemic cardiomyopathy (HR [95% CI] = 2.811 [2.477-3.190]), other cardiac disorders, such as heart failure (HR [95% CI] =2.296 [2.200-2.396]) and thromboembolic disorders (e.g. pulmonary embolism: HR [95% CI] =2.648 [2.443-2.870]). The risks of two composite endpoints, major adverse cardiovascular event (HR [95% CI] = 1.871 [1.816–1.927]) and any cardiovascular outcome (HR [95% CI] = 1.552 [1.526–1.578]), were also higher in the COVID-19 survivors than in the controls. Moreover, the survival probability of the COVID-19 survivors dramatically decreased in all the cardiovascular outcomes.
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Ectopic expression of SARS-CoV-2 S and ORF-9B proteins alters metabolic profiles and impairs contractile function in cardiomyocytes 2/22/2023https://doi.org/10.3389/fcell.2023.1110271Peng Zhanghttps://www.frontiersin.org/articles/10.3389/fcell.2023.1110271/fullWe found that the ectopic expression of S and ORF-9B subunits significantly impaired the contractile function and altered the metabolic profiles in human cardiomyocytes... Based on the transcriptomic analysis, both S and ORF-9B subunits dysregulated signaling pathways associated with metabolism and cardiomyopathy, including upregulated genes involved in HIF-signaling and downregulated genes involved in cholesterol biosynthetic processes. The ORF-9B subunit also enhanced glycolysis in the CMs.
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Left ventricular global longitudinal strain as a parameter of mild myocardial dysfunction in athletes after COVID-193/15/2023https://doi.org/10.1101/2023.03.14.23287258Jana Schellenberghttps://www.medrxiv.org/content/10.1101/2023.03.14.23287258v1 In a cohort of athletes at a median two months after COVID-19, significantly lower GLS (global longitudinal strain) and diastolic function were observed, suggesting mild myocardial dysfunction. There was a trend toward lower GLS in PCAt (positive COVID-19 test group) with subjectively perceived performance limitation (p=0.054).
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SARS-CoV-2 spike protein-mediated cardiomyocyte fusion may contribute to increased arrhythmic risk in COVID-193/8/2023https://doi.org/10.1371/journal.pone.0282151Daniel J. Clemenshttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0282151The SARS-CoV-2 spike protein can directly perturb both the cardiomyocyte’s repolarization reserve and intracellular calcium handling that may confer the intrinsic, mechanistic substrate for the increased risk of SCD observed during this COVID-19 pandemic.
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The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread3/17/2023https://doi.org/10.1002/iid3.798Aseel Awad Alsaidanhttps://onlinelibrary.wiley.com/doi/10.1002/iid3.798SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS (acute coronary syndrome) or cause new-onset T2MI (Secondary or type 2 myocardial infarction). As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.
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How Does COVID-19 Affect the Heart?3/10/2023https://doi.org/10.1007/s11886-023-01841-6Lorenzo R. Sewananhttps://link.springer.com/article/10.1007/s11886-023-01841-6The high prevalences of microthrombi and inflammatory infiltrates in fatal COVID-19 raise the concern that recovered COVID-19 patients may have similar but subclinical cardiac pathology. Imaging and epidemiologic studies of recovered COVID-19 patients suggest that even mild illness confers increased risks of cardiac inflammation, cardiovascular disorders, and cardiovascular death. The ongoing evolution of SARS-CoV-2 variants and vast numbers of recovered COVID-19 patients portend a burgeoning global cardiovascular disease burden.
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CARDIAC COMPLICATIONS AMONG LONG COVID PATIENTS: A SYSTEMATIC REVIEW AND META-ANALYSIS3/1/2023https://doi.org/10.1016/S0735-1097(23)02559-7Joanna Leehttps://www.jacc.org/doi/10.1016/S0735-1097%2823%2902559-7Patients with long COVID have significantly higher odds of developing cardiac complications compared to those who do not. The unadjusted odds of cardiac complications in long COVID-19 were significantly higher (OR 2.35, p=0.01) with high heterogeneity (I2=91%). We performed sensitivity analysis by excluding study by Galloway et al to reduce the heterogeneity and the odds of cardiac complications remained same with moderate heterogeneity (OR 2.57, p=<0.001, I2=51%).
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Cardiovascular and Cerebral Vascular Health in Females with Post-Acute Sequelae of COVID-19 (PASC) 3/31/2023https://doi.org/10.1152/ajpheart.00018.2023Damsara Nandadevahttps://journals.physiology.org/doi/abs/10.1152/ajpheart.00018.2023BP and central arterial stiffness are elevated in females with PASC, whereas peripheral and cerebral vascular function appear to be unaffected; effects that appear independent of symptom burden.
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Cardiac impairment in Long Covid 1-year post SARS-CoV-2 infection10/3/2022https://doi.org/10.1093/eurheartj/ehac544.219A Roca-Fernandezhttps://academic.oup.com/eurheartj/article/43/Supplement_2/ehac544.219/6744392?login=falseCardiac impairment, other than myocarditis, is present in 1 in 5 individuals with Long Covid at 6 months, persisting in over half of those at 12 months.
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Longitudinal Trends in Cardiovascular Risk Factor Profiles and Complications Among Patients Hospitalized for COVID-19 Infection: Results From the American Heart Association COVID-19 Cardiovascular Disease Registry4/5/2023https://doi.org/10.1161/CIRCOUTCOMES.122.009652Eric J. Hallhttps://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.122.009652Despite a shifting risk factor profile toward a younger population with lower rates of established CVD (cardiovascular disease), the incidence of diagnosed cardiovascular complications of COVID increased from the onset of the pandemic through December 2021. All-cause mortality decreased during the initial months of the pandemic and thereafter remained consistently high through December 2021.
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Incidence of myocarditis among patients recovered from COVID-19 infection identified using cardiac magnetic resonance imaging1/25/2023https://doi.org/10.1093/eurheartj/ehac779.008R Tugadehttps://academic.oup.com/eurheartj/article/44/Supplement_1/ehac779.008/7000570?login=falseMyocarditis is one of the cardiovascular complications among patients who recovered from COVID-19... Fifty-four percent (54%) of patients had positive conventional MRI findings indicative of myocarditis. Dyspnea, palpitations and chest discomfort were the most commonly reported symptoms in 29 (54%), 24 (44%) and 21 (39%) patients, respectively. Twenty-nine patients (54%) were observed with increased T2 signal or positive LGE (Late gadolinium enhancement, a predictor of adverse cardiovascular outcomes).
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Major adverse cardiovascular events are associated with necroptosis during severe COVID-19 4/20/2023https://doi.org/10.1186/s13054-023-04423-8Rosana Wiscovitch-Russohttps://ccforum.biomedcentral.com/articles/10.1186/s13054-023-04423-8SARS-CoV-2 identification in the systemic circulation is associated with MACE (major adverse cardiac events ) and necroptosis activity. The increased pMLKL and Troponin-I indicated the occurrence of necroptosis in the heart.
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SARS-CoV-2 infection is associated with anti-desmoglein 2 autoantibody detection4/24/2023https://doi.org/10.1093/cei/uxad046Kerensa E Ward, MSchttps://academic.oup.com/cei/advance-article/doi/10.1093/cei/uxad046/7140487We find increased levels of DSG2 protein in sera from acute COVID-19 patients. Furthermore, we find that DSG2 (anti-desmoglein) autoantibody levels are increased significantly in convalescent sera following severe COVID-19 but not in hospitalised patients recovering from influenza infection or healthy controls. Levels of autoantibody in sera from patients with severe COVID-19 were comparable to levels in patients with non-COVID-19-associated cardiac disease.
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Long-term prognostic impact of subclinical myocardial dysfunction in patients recovered from COVID-194/26/2023https://doi.org/10.1111/echo.15575Francesco Cannata MDhttps://onlinelibrary.wiley.com/doi/10.1111/echo.15575In patients recovered from COVID-19 pneumonia, a subclinical myocardial dysfunction is present in one-third of the whole population at 7-month follow-up and is associated with a higher risk of MACE (major adverse cardiovascular events) at long-term follow-up.
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Long-Term Adverse Effects of Mild COVID-19 Disease on Arterial Stiffness, and Systemic and Central Hemodynamics: A Pre-Post Study3/8/2023https://doi.org/10.3390/jcm12062123Mario Podrug https://www.mdpi.com/2077-0383/12/6/2123We found that various parameters of arterial stiffness and central hemodynamics respond simultaneously to the mild COVID-19 disease in predominantly healthy individuals. The detected responses to COVID-19 disease are not straightforward but rather deteriorate with the time since the onset of COVID-19 infection and age. Within the period of 2–3 months following infection, our models demonstrated a clinically significant progression of vascular impairment.
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Changes in blood flow vortices inside the left ventricle in COVID-19 patients with intraventricular clot despite a normal coronary and myocardial motion5/23/2023https://doi.org/10.1007/s12574-023-00603-1

Mersedeh Karvandihttps://link.springer.com/article/10.1007/s12574-023-00603-1Our results suggest that in some COVID-19 patients, cardiac wall motion is not satisfactorily able to circulate the blood fluid in normal directions and that, despite normal myocardium, changes in the directions of blood flow inside the left ventricle might lead to clots in different zones. This phenomenon may be related to changes in blood properties, such as viscosity.
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Prevalence of coronary artery disease among COVID-19 patients: a systematic review and meta-analysis 6/1/2023https://doi.org/10.1101/2023.06.01.23290768Naushaba Akhtarhttps://www.medrxiv.org/content/10.1101/2023.06.01.23290768v1The burden of coronary artery disease has been considerable, varying with geography. The prevalence of coronary artery disease among COVID-19 patients was 15.24% (95% CI: 11.41% - 20.06%). The studies were highly heterogeneous... Europe reported the highest prevalence [21.70% (14.80% - 30.65%)], and Asia has the least prevalence [10.07% (6.55% - 15.19%)].
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Coronary microvascular health in symptomatic patients with prior COVID-19 infection: an updated analysis5/31/2023https://doi.org/10.1093/ehjci/jead118Ahmed Ibrahim Ahmedhttps://academic.oup.com/ehjcimaging/advance-article-abstract/doi/10.1093/ehjci/jead118/7186983?redirectedFrom=fulltext&login=falsePatients with prior COVID-19 had a statistically significant higher odds of Myocardial flow reserve (MFR) <2 (adjusted odds ratio 3.1, 95% confidence interval 2.8–4.25 P < 0.001). The proportion of cases with MFR <2 peaked 6–9 months from imaging with a statistically non-significant downtrend afterwards and was comparable across SARS-CoV-2 variants but increased with increasing severity of infection.
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SARS-CoV-2 reinfection: Adding insult to dysfunctional endothelium in patients with atherosclerotic cardiovascular disease 9/1/2023https://doi.org/10.1016/j.athplu.2023.06.002Petri T. Kovanenhttps://www.sciencedirect.com/science/article/pii/S266708952300010X?via%3DihubBoth the first infection and reinfection with SARS-CoV-2 increase cardiac event risk, particularly in vulnerable patients with cardiovascular risk factors and the accompanying systemic endothelial dysfunction. By worsening pre-existing endothelial dysfunction, both the first infection and reinfection with ensuing COVID-19 may turn the endothelium procoagulative and prothrombotic, and ultimately lead to local thrombus formation.
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Incidence and predictors of development of new onset hypertension post COVID-19 disease6/14/2023https://doi.org/10.1016/j.ihj.2023.06.002Pooja Vyas Ahttps://www.sciencedirect.com/science/article/pii/S0019483223001037We found that 32.3% of the population had new onset of hypertension at 1 year follow-up post-COVID-19 disease recovery.
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Risk of ischemic stroke in patients recovered from COVID-19 infection: A systematic review and meta-analysis7/25/2023https://doi.org/10.1177/23969873231190432Marco Zuin https://journals.sagepub.com/doi/10.1177/23969873231190432Recovered COVID-19 patients presented a higher risk of ischemic stroke ((HR: 2.06, 95% CI: 1.75–2.41, p < 0.0001, I2 = 63.7%) compared to people who did not have COVID-19. COVID-19 patients hospitalized at the time of the infection have a subsequent higher risk of stroke during the follow-up compared to those non-hospitalized.
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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels8/15/2023https://doi.org/10.1101/2023.08.14.553245Natalia Eberhardthttps://www.biorxiv.org/content/10.1101/2023.08.14.553245v1Our data establish that SARS-CoV-2 infects macrophages in coronary atherosclerotic lesions, resulting in plaque inflammation that may promote acute CV complications and long-term risk for CV events.
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Echocardiographic Assessment in Patients Recovered from Acute COVID-19 Illness8/15/2023https://doi.org/10.3390/jcdd10080349Luke Stefanihttps://www.mdpi.com/2308-3425/10/8/349Alterations in LV (left ventricular) and RV (right ventricular) strain were observed in both hospitalized and non-hospitalized patients. In the subset of COVID-19 patients without any co-morbidities (n = 30), LV GLS remained reduced compared to controls. Abnormal LV strain was evident in both hospitalized and non-hospitalized patients, suggesting that these changes are independent of the severity of COVID-19 infection at presentation.
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Effects of COVID-19 Infection in Healthy Subjects on Cardiac Function and Biomarkers of Oxygen Transport, Blood Coagulation and Inflammation 7/25/2023https://doi.org/10.3390/v15081623Nadezhda Gumanovahttps://www.mdpi.com/1999-4915/15/8/1623LV filling, inflammation, blood coagulation, and hemoglobin appear to be influenced by COVID-19 infection in healthy participants. The left ventricular mass index, mitral ratio of peak early to late diastolic filling velocity or flow velocity across the mitral valve, and deceleration time of early mitral inflow were decreased (p < 0.05) in IgG-SARS-positive participants versus those in IgG-SARS-negative participants according to multivariate logistic regression analysis.
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Incidence of New-Onset Hypertension Post–COVID-19: Comparison With Influenza 8/21/2023https://doi.org/10.1161/HYPERTENSIONAHA.123.21174Vincent Zhanghttps://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.123.21174Incidence of new-onset persistent hypertension in patients with COVID-19 is higher than those with influenza, likely constituting a major health burden given the sheer number of patients with COVID-19. Hospitalized patients with COVID-19 were 2.23 ([95% CI, 1.48–3.54]; P<0.001) times and nonhospitalized patients with COVID-19 were 1.52 ([95% CI, 1.22–1.90]; P<0.01) times more likely to develop persistent hypertension than influenza counterparts.
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Myocardial injury and related mortality in hospitalized patients with COVID-19 during the Omicron pandemic: new perspectives and insights10/13/2023https://doi.org/10.1016/j.virs.2023.10.005Wu Hehttps://www.sciencedirect.com/science/article/pii/S1995820X23001281?via%3DihubMyocardial injury accounted for 30.8% of the total patients with SARS-CoV-2 infection and was associated with higher in-hospital mortality than those without injury... our results showed that the proportion of cardiac muscle injuries was higher in patients infected with the Omicron variant.
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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels9/28/2023https://doi.org/10.1038/s44161-023-00336-5
Natalia Eberhardthttps://www.nature.com/articles/s44161-023-00336-5Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection... Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk.
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Autonomic dysregulation in long-term patients suffering from Post-COVID-19 Syndrome assessed by heart rate variability 9/22/2023https://doi.org/10.1038/s41598-023-42615-y
Frank C. Moorenhttps://www.nature.com/articles/s41598-023-42615-yPCS (Post COVID Syndrome) patients showed disturbed diurnal adjustment of HRV (heart rate variability), with impaired parasympathetic activity at night. Our data demonstrate persistent HRV alterations in PCS patients with long-term symptom duration, suggesting a sustained impairment of sympathovagal balance. Moreover, sympathetic overstimulation and diminished parasympathetic response in long-term PCS patients are comparable to findings in CAD (Coronary Artery Disease) patients.
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Baroreflex sensitivity is impaired in survivors of mild COVID-19 at 3–6 months of clinical recovery; association with carotid artery stiffness10/31/2023https://doi.org/10.14814/phy2.15845Prachi Srivastavahttps://physoc.onlinelibrary.wiley.com/doi/10.14814/phy2.15845Fifty-seven survivors of mild COVID-19, with an age range of 22–66 years (27 females) participated at 3–6 months of recovering from the acute phase of RT-PCR positive COVID-19BRS (baroreflex sensitivity) was found to be significantly lower in the COVID survivor group for the systolic blood pressure-based sequences. The COVID survivor group showed significantly higher carotid β stiffness index, and pulse wave velocity. Impairment of BRS in the male survivors of mild COVID-19 at 3–6 months of clinical recovery shows association with carotid artery stiffness.
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Prolonged platelet hyperactivity after COVID-19 infection10/11/2023https://doi.org/10.1111/bjh.19125Noriko Narahttps://onlinelibrary.wiley.com/doi/10.1111/bjh.19125Our results showed that platelet hyperactivity persisted for at least 40 days even after acute inflammation subsided in most patients with COVID-19, regardless of disease severity. Persistent platelet hyperactivity may contribute to thromboembolic complications in post-COVID-19 patients.
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Risk of arrhythmias following COVID-19: nationwide self-controlled case series and matched cohort study11/21/2023https://doi.org/10.1093/ehjopen/oead120Ioannis Katsoularishttps://academic.oup.com/ehjopen/advance-article/doi/10.1093/ehjopen/oead120/7439882?login=falseThe incidence rate ratio of atrial tachycardias, paroxysmal supraventricular tachycardias and bradyarrhythmias was significantly increased up to 60, 180 and 14 days after COVID-19, respectively. There is an increased risk of cardiac arrhythmias following COVID-19, and particularly increased in elderly vulnerable individuals, as well as in individuals with severe COVID-19.
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Cardiovascular Follow-up of Patients Treated for MIS-C 11/15/2023https://doi.org/10.1542/peds.2023-063002
Dayna Zimmerman
https://publications.aap.org/pediatrics/article/doi/10.1542/peds.2023-063002/195462/Cardiovascular-Follow-up-of-Patients-Treated-for?autologincheck=redirectedThe high prevalence of abnormal findings on follow-up cardiac studies and lack of significant difference between patients with and without apparent myocardial injury during hospitalization suggests that all patients treated for MIS-C warrant cardiology follow-up.
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Pooled rates and demographics of POTS following SARS-CoV-2 infection versus COVID-19 vaccination: Systematic review and meta-analysis12/1/2023https://doi.org/10.1016/j.autneu.2023.103132Shin Jie Yonghttps://www.sciencedirect.com/science/article/abs/pii/S1566070223000619POTS (postural orthostatic tachycardia syndrome) was 2.12-fold more likely to occur in infected than uninfected individuals (RR = 2.12, 95 % CI: 1.71 to 2.62, P < 0.001).
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The effect of mild to moderate COVID-19 infection on the cardiorespiratory fitness of firefighters 11/30/2023https://doi.org/10.3389/fpubh.2023.1308605Susanne D'Isabelhttps://www.frontiersin.org/articles/10.3389/fpubh.2023.1308605/fullPeak VO2 (maximum volume of oxygen consumption attainable during physical exertion) (ml·kg−1·min−1) declined 7.3% among firefighters an average of 110 days past reporting mild to moderate COVID-19 infection. This decrease has implications for the operational readiness and safety of firefighters.
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Clinical and electrocardiographic correlates of myocardial dysfunction after COVID-19 in nonhospitalised patients in long-term follow-up. Data from the polish long-covid cardiovascular study 12/19/2023https://doi.org/10.1002/jmv.29331Joanna Kapustahttps://onlinelibrary.wiley.com/doi/10.1002/jmv.29331The study showed that myocardial damage after COVID-19 affects men more often and is independent of typical clinical factors and the severity of the disease course. The QRS fragmentation and arrhythmias observed in the ECG indicate the possibility of myocardial dysfunction in patients after COVID-19.
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Predicted risk of heart failure pandemic due to persistent SARS-CoV-2 infection using a three-dimensional cardiac model 12/22/2023https://doi.org/10.1016/j.isci.2023.108641Kozue Muratahttps://www.sciencedirect.com/science/article/pii/S2589004223027189?via%3DihubMild infections sustained viral presence without significant dysfunction for a month, indicating persistent infection. However, when exposed to hypoxic conditions mimicking ischemic heart diseases, cardiac function deteriorated alongside intracellular SARS-CoV-2 reactivation in cardiomyocytes and disrupted vascular network formation. This study demonstrates that SARS-CoV-2 persistently infects the heart opportunistically causing cardiac dysfunction triggered by detrimental stimuli such as ischemia, potentially predicting a post COVID-19 era heart failure pandemic.
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High Cardiac Troponin Levels in Infants with Acute SARS-CoV-2 Infection: A Prospective Comparative study12/21/2023https://doi.org/10.1016/j.jpeds.2023.113876Andrea Lo Vecchiohttps://www.sciencedirect.com/science/article/abs/pii/S0022347623007400Infants with acute SARS-CoV-2 infection may show a subclinical and transient alteration of myocardial injury markers, especially in the first months of life. hs-cTn levels normalized during follow-up and were not associated with cardiac functional impairment; nevertheless, long-term consequences are unknown and should be carefully followed.
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Association between Cardiovascular Disease Risk and long COVID-19: A Systematic Review and Meta-analysis12/31/2023https://doi.org/10.1101/2023.12.30.23300656Yunxia Huanghttps://www.medrxiv.org/content/10.1101/2023.12.30.23300656v1Our meta-analysis revealed a pooled OR of 1.68 (95% CI 1.55-1.81) (I2 = 69.1%, p= 0.000) for the overall risk of cardiovascular outcomes, indicating an elevated risk of cardiovascular diseases in individuals affected by long COVID-19. Our meta-analysis substantiates that individuals afflicted with long COVID-19 face an elevated risk of developing cardiovascular diseases.
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Cardiovascular autonomic dysfunction in post-COVID-19 syndrome: a major health-care burden1/2/2024https://doi.org/10.1038/s41569-023-00962-3

Artur Fedorowskihttps://www.nature.com/articles/s41569-023-00962-3Cardiovascular autonomic dysfunction (CVAD), in particular postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia, are among the most frequent and distinct phenotypes of post-COVID-19 syndrome; one-third of highly symptomatic patients can be affected. As well as global circulatory disturbances, CVAD in post-COVID-19 syndrome can manifest as microvascular and endothelial dysfunction, with local symptoms such as headache, brain fog, chest pain, dyspnoea and peripheral circulatory symptoms, including skin discolouration, oedema, Raynaud-like phenomena, and heat and cold intolerance.
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Longitudinal strain and myocardial work in symptomatic patients having recovered from COVID-19 and possible associations with the severity of the disease1/26/2024https://doi.org/10.1007/s10554-023-03042-2Luciana Bartolomei Orru D’Ávilahttps://link.springer.com/article/10.1007/s10554-023-03042-2In our study with long COVID-19 individuals, despite having a similar LVGLS (left ventricle global longitudinal strain), patients had subclinical LV (left ventricular) dysfunction, demonstrated only by an increase in GWW (Global wasted work) and a decrease in GWE (global work efficiency).
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Increased risk of new-onset cardiovascular disease after COVID-19: A systematic review and meta-analysis of 14 cohorts2/1/2024https://doi.org/10.1002/rmv.2518Mingyao Sunhttps://onlinelibrary.wiley.com/doi/10.1002/rmv.2518The results showed a 2.42 times higher risk of any CVD (cardiovascular disease), a 95% higher risk of MACE (major adverse cardiovascular events), a 61% higher risk of arrhythmias, a 71% higher risk of heart failure, a 5 times higher risk of myocarditis, and a 2.49 times higher risk of thrombotic events associated with COVID-19.
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Risks of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19: nationwide self-controlled cases series and matched cohort study 4/6/2022https://doi.org/10.1136/bmj-2021-069590Ioannis Katsoularishttps://www.bmj.com/content/377/bmj-2021-069590Compared with the control period, incidence rate ratios were significantly increased 70 days after covid-19 for deep vein thrombosis, 110 days for pulmonary embolism, and 60 days for bleeding. The risk ratios during days 1-30 after covid-19 were 4.98 (4.96 to 5.01) for deep vein thrombosis, 33.05 (32.8 to 33.3) for pulmonary embolism, and 1.88 (1.71 to 2.07) for bleeding, after adjusting for the effect of potential confounders.
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Cardiac damage and tropism of severe acute respiratory syndrome coronavirus 2 4/1/2024https://doi.org/10.1016/j.mib.2024.102437Melina Tangoshttps://www.sciencedirect.com/science/article/pii/S1369527424000134An infection with SARS-CoV-2 has the potential to manifest a diverse set of cardiovascular health problems, including myocardial tissue damage, arrhythmia, myocarditis, and pericarditis. Evidence is pointing toward prolonged COVID symptoms with cardiac involvement in some individuals, independent of infection severity.
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3D Holo-tomographic Mapping of COVID-19 Microclots in Blood to Assess Disease Severity1/9/2024https://doi.org/10.1021/cbmi.3c00126Talia Bergagliohttps://pubs.acs.org/doi/full/10.1021/cbmi.3c00126#Fewer microclots and platelet aggregates were detected in the plasma of healthy controls compared to COVID-19 patients. We observed microclots in all COVID-19 plasma samples. However, only a few microclots were detected in plasma from healthy donors, suggesting that microclotting is a salient feature of COVID-19.
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Autonomic cardiac function in children and adolescents with long COVID: a case-controlled study 3/6/2024https://doi.org/10.1007/s00431-024-05503-9A. B. Deloguhttps://link.springer.com/article/10.1007/s00431-024-05503-9Data analysis showed that pediatric patients with long COVID had significant changes in HRV (Heart rate variability) variables compared to healthy controls.These findings suggest that pediatric patients with long COVID have an imbalance of cardiac autonomic function toward a relative predominance of parasympathetic tone, as already reported in adult patients with long COVID.
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The role of COVID-19 vaccines in preventing post-COVID-19 thromboembolic and cardiovascular complications3/12/2024https://doi.org/10.1136/heartjnl-2023-323483Núria Mercadé-Besorahttps://heart.bmj.com/content/early/2024/01/24/heartjnl-2023-323483COVID-19 vaccination reduced the risk of post-COVID-19 cardiac and thromboembolic outcomes. These effects were more pronounced for acute COVID-19 outcomes, consistent with known reductions in disease severity following breakthrough versus unvaccinated SARS-CoV-2 infection. Vaccination was associated with reduced risks of acute (30-day) and post-acute COVID-19 VTE, ATE and HF: for example, meta-analytic sHR of 0.22 (95% CI 0.17 to 0.29), 0.53 (0.44 to 0.63) and 0.45 (0.38 to 0.53), respectively, for 0–30 days after SARS-CoV-2 infection, while in the 91–180 days sHR were 0.53 (0.40 to 0.70), 0.72 (0.58 to 0.88) and 0.61 (0.51 to 0.73), respectively.
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Echocardiographic Strain Evaluation Shows Persistent Echocardiographic Changes at 1 Year after Diagnosis of Multisystem Inflammatory Syndrome in Children3/5/2024https://doi.org/10.3390/children11030308Jihye Youhttps://www.mdpi.com/2227-9067/11/3/308#Persistent cardiac alterations were observed in patients with MIS-C, particularly in both ventricular functions. At 1-year follow-up, the reduced LVEF in the apical 4-chamber, overall longitudinal strain in the apical 4-chamber, and GLS persisted. However, the right ventricular free wall and global strain remained diminished compared with those in the control group.
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Patients with COVID-19 Infection and Stroke have Higher than Expected Mortality, Regardless of the Primary Presentation 3/30/2024https://doi.org/10.1101/2024.03.29.24305101 Jintong Liuhttps://www.medrxiv.org/content/10.1101/2024.03.29.24305101v1We retrospectively reviewed and characterized all patients who presented to a single, quaternary medical center between March and December 2020. In the early pandemic, patients with COVID-19 infection and stroke had a higher mortality rate compared to COVID-19 negative patients with stroke. Among patients with both COVID-19 and stroke, patients presenting with COVID-19 first had worse outcomes than patients presenting with stroke first.
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Right heart overload – possible long-term sequelae of Covid-19: a narrative review
3/27/2024https://doi.org/10.34119/bjhrv7n2-210Mariana da Costa Rochahttps://ojs.brazilianjournals.com.br/ojs/index.php/BJHR/article/view/68387SARS-CoV2 creates a pro-thrombotic state through direct endothelial damage and a cytokine storm, affecting the lung, among other organs, leading to hypoxia and a rise in vascular resistance. Increased vascular resistance makes patients prone to cardiac stress, with a known association with right heart failure, among other insults to the heart. This condition affects both outpatients and inpatients, hypertension being a significant risk factor.
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Predictors and Clinical Significance of Myocardial Injury in Elderly Patients Under the COVID-19 Pandemic3/27/2024https://doi.org/10.2147/IJGM.S458365You Zhouhttps://www.dovepress.com/predictors-and-clinical-significance-of-myocardial-injury-in-elderly-p-peer-reviewed-fulltext-article-IJGMMyocardial injury was a common phenomenon and prognostic predictor in elder patients after SARS-CoV-2 infection. Predictors of myocardial injury included age (per 5-year increase), hypertension, vaccination, creatine, and neutrophil-to-lymphocyte ratio.Vaccination was shown to be the only protective factor of myocardial injury in older patients infected by the omicron variant of SARS-Cov-2.
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High prevalence of cardiac post-acute sequelae in patients recovered from Covid-19. Results from the ARCA post-COVID study4/5/2024https://doi.org/10.1016/j.ijcrp.2024.200267Valeria Antoncecchihttps://www.sciencedirect.com/science/article/pii/S2772487524000321NCA (new cardiac alterations) were found in 138 patients (27.49%): among them 60 cases (11.95%) of pericardial effusion. the prevalence of NCA in patients who recovered from COVID-19 is high and constant since the beginning of the pandemic. More than 6 months after the SARS-CoV2 infection, 77% of patients were still symptomatic, regardless of hospitalization or home treatment. The most frequent symptoms were dyspnoea, weakness, palpitations, fatigue, and anxiety/depression, with a prevalence greater than 10%.
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Incidence of New-Onset Hypertension Post–COVID-19: Comparison With Influenza 8/21/2023https://doi.org/10.1161/HYPERTENSIONAHA.123.21174Vincent Zhanghttps://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.123.21174Incidence of new-onset persistent hypertension in patients with COVID-19 is higher than those with influenza, likely constituting a major health burden given the sheer number of patients with COVID-19. Hospitalized patients with COVID-19 were 2.23 ([95% CI, 1.48–3.54]; P<0.001) times and nonhospitalized patients with COVID-19 were 1.52 ([95% CI, 1.22–1.90]; P<0.01) times more likely to develop persistent hypertension than influenza counterparts.
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Risk of major adverse cardiovascular events after SARS-CoV-2 infection in British Columbia: a population-based study4/24/2024https://doi.org/10.1016/j.amjmed.2024.04.010Héctor Alexander Velásquez Garcíahttps://www.sciencedirect.com/science/article/abs/pii/S0002934324002377SARS-CoV-2 infection was associated with higher cardiovascular risk with graded increase across the acute COVID-19 severity. The risk of major adverse cardiovascular events was higher in the exposed (adjusted HR [aHR]:1·34; 95%CI:1·22-1·46), with greater risk observed in those who were hospitalized (aHR:3·81; 95%CI:3·12-4·65) or required ICU admission (aHR:6·25; 95%CI:4·59-8·52) compared to the unexposed group. The fraction of cardiovascular events attributable to SARS-CoV-2 was 7·04% (95%CI:4·67-9·41%).
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Persistence of SARS-CoV-2 colonization and high expression of inflammatory factors in cardiac tissue 6 months after COVID-19 recovery: a prospective cohort study4/30/2024https://doi.org/10.21037/cdt-23-381Sanjiu Yuhttps://cdt.amegroups.org/article/view/123848/htmlOur research suggests that certain COVID-19-recovered patients have persistent colonization of SARS-CoV-2 in their cardiac tissue, accompanied by a local increase in inflammatory factors. In four of nine patients, SARS-CoV-2 RNA was detected in their LA tissue, indicating viral colonization. Among the four positive cases, the IL-6 and IL-1β relative expression levels in the LA tissue of one patient were increased approximately 55- and 110-fold, respectively, compared to those of SARS-CoV-2 (−) patients.
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Cardiopulmonary Exercise Testing in Children With Long COVID: A Case-controlled Study5/7/2024https://doi.org/10.1097/INF.0000000000004371Baldi, Fabianahttps://journals.lww.com/pidj/fulltext/9900/cardiopulmonary_exercise_testing_in_children_with.849.aspxOverall, 90.2% of LC patients (55 of 61) had a pathologic test vs 10.3% (3/29) of the healthy control. Compared with healthy controls, children with LC have objective impaired functional capacity (expressed by a low VO2 peak), signs of deconditioning and cardiogenic inefficiency when assessed with CPET.
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Evaluation of blood pressure variation in recovered COVID-19 patients at one-year follow-up: a retrospective cohort study5/7/2024https://doi.org/10.1186/s12872-024-03916-wPouria Azamihttps://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-024-03916-w#citeasOur findings suggest a potential association between COVID-19 and increased systolic and diastolic BP in non-hospitalized patients, with a notable proportion of participants experiencing new-onset or exacerbated hypertension. COVID-19 raised systolic and diastolic BP in the long term in non-hospitalized patients, with over one-sixth developing new-onset or exacerbated hypertension.
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Long-term cardiovascular disease outcomes in non-hospitalized medicare beneficiaries diagnosed with COVID-19: Population-based matched cohort study5/14/2024https://doi.org/10.1371/journal.pone.0302593Quanhe Yanghttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0302593COVID-19 showed initial stronger effects on all-cause mortality, hospitalization and 12 incident CVD outcomes with adjusted HRs in 0–3 months ranging from 1.05 (95% CI 1.01–1.09) for mortality to 2.55 (2.26–2.87) for pulmonary embolism. The effects of COVID-19 on outcomes reduced significantly after 3-month follow-up. Risk of mortality, acute myocardial infarction, cardiomyopathy, deep vein thrombosis, and pulmonary embolism returned to baseline after 6-month follow-up.
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Persistent increase of cardiovascular and cerebrovascular events in COVID-19 patients: a 3-year population-based analysis3/19/0202https://doi.org/10.1093/cvr/cvae049Allegra Battistonihttps://academic.oup.com/cardiovascres/article-abstract/120/6/623/7631430?login=falseThe proportion of individuals with a new diagnosis of major adverse cardiovascular and cerebrovascular events was higher in the 2020–22 COVID-19 group than in the 2017–19 COMEGEN propensity score-matched comparator, with an odds ratio of 1.73 (95% confidence interval: 1.53–1.94; P < 0.001). All major adverse cardiovascular and cerebrovascular events considered showed a significantly higher risk in COVID-19 individuals. Incidence calculated for each 6-month period after the diagnosis of COVID-19 in our population was the highest in the first year (1.39% and 1.45%, respectively), although it remained significantly higher than in the COVID-19-free patients throughout the 3 years.
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Post-Acute Cardiovascular Outcomes of COVID-19 in Children and Adolescents: An EHR Cohort Study from the RECOVER Project5/15/2024https://doi.org/10.1101/2024.05.14.24307380Bingyu Zhanghttps://www.medrxiv.org/content/10.1101/2024.05.14.24307380v1Patients with CHD (Congenital Heart Defects)) post-SARS-CoV-2 infection showed increased risks of any cardiovascular outcome (RR, 1.63). Those without CHDs also experienced heightened cardiovascular risks after SARS-CoV-2 infection (RR, 1.63), covering 14 of 18 conditions in hypertension, arrhythmias, inflammatory heart disease, other cardiac disorders, thrombotic disorders, and cardiovascular-related symptoms. Both children with and without CHDs showed increased risks for a variety of cardiovascular outcomes after SARS-CoV-2 infection, underscoring the need for targeted monitoring and management in the post-acute phase.
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Post-Covid Conditions and their Effects on the Cardiovascular System5/1/2024https://doi.org/10.7417/ct.2024.5056M Osadchukhttps://pubmed.ncbi.nlm.nih.gov/38767072/Cardiac screening results in individuals with COVID-19 reveal a significant prevalence of serious heart problems, affecting over half of the patients. By the 60th day, a reduction in symptoms by 5-10% was noted, and by the 90th day, a decrease in activity by 25-35% was observed. Patients aged 40-60 years exhibited the highest percentage of cardiovascular diseases (75%).
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Long COVID and cardiovascular disease: a prospective cohort study5/27/2024https://doi.org/10.1136/openhrt-2024-002662Claire Alexandra Lawsonhttps://openheart.bmj.com/content/11/1/e002662Full recovery was significantly lower at 12 months in patients with CVD (cardiovasular disease) (adjusted OR (aOR) 0.62, 95% CI 0.43 to 0.89) and cardiovascular risk factors (aOR 0.66, 95% CI 0.50 to 0.86). Patients with CVD or cardiovascular risk factors had a delayed recovery at 12 months following hospitalisation with COVID-19.
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Endothelial dysfunction and cardiovascular risk in post-COVID-19 patients after 6- and 12-months SARS-CoV-2 infection2/7/2024https://doi.org/10.1007/s15010-024-02173-5Paula Poyatoshttps://link.springer.com/article/10.1007/s15010-024-02173-5These findings highlight the presence of vascular sequela that last up to 6- and 12-months post-infection and point out the need for preventive measures and patient follow-up. Post-COVID-19 patients showed a significant downregulation of angiogenesis-related proteins compared to controls indicating a clear endothelial injury. Troponin, NT-proBNP and ferritin levels, markers of cardiovascular risk and inflammation, remained elevated up to 12-months post-infection.
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The Effect of COVID-19 on Cardiovascular Diseases and the Need for Beta-Blocker Dose Modification6/12/2024https://doi.org/10.12775/JEHS.2024.74.51789Tomasz Jędrasekhttps://apcz.umk.pl/JEHS/article/view/51789Patients with coronary artery diseases, who suffered from COVID-19, need to start or intensify treatment with beta-blockers and are more likely to develop long-term complications after recovery. Patients with preexisting CVD should be closely monitored during and after recovery from SARS-CoV-2 infection due to the higher risk of complications and the potential need for modifications in the treatment of chronic diseases.
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Pro-inflammatory cytokines are elevated two-years after acute severe COVID-19: a pre-vaccine, two-years, five-point longitudinal assessment of individuals with Long COVID6/13/2024https://doi.org/10.1093/eurjpc/zwae175.289C Luz Goularthttps://academic.oup.com/eurjpc/article/31/Supplement_1/zwae175.289/7692407?login=falseEven after more two years of COVID-19 infection the cytokine profile from this evaluation showed substantially elevated levels of IL-1β and TNF-α in participants with PASC, which could ultimately lead to new or worsening cardiovascular problems in this population. Regarding the prevalence of Long covid after 2 years of primary infection, 51/80 (63%) reported having remained with one or more symptoms.The longitudinal assessment of cytokine levels among participants showed significantly higher levels of IL-1β between D1 and D120 (p<0.0001); D1 and D720 (p<0.0001). In relation to TNF-α on D7 and D720 (p<0.001).
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Pathogenic mechanisms of cardiovascular damage in COVID-196/19/2024https://doi.org/10.1186/s10020-024-00855-2Hong-Hua Shaohttps://molmed.biomedcentral.com/articles/10.1186/s10020-024-00855-2Cardiovascular damage in COVID-19 patients is common and portends a worse prognosis. The most common cardiovascular damage was myocarditis and pericarditis, hypertension, arrhythmia, myocardial injury and heart failure, coronary heart disease, stress cardiomyopathy, ischemic stroke, blood coagulation abnormalities, and dyslipidemia.
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Evidence Circulating Microclots and Activated Platelets Contribute to Hyperinflammation Within Pediatric Post Acute Sequala of COVID5/1/2024https://doi.org/10.1164/ajrccm-conference.2024.209.1_MeetingAbstracts.A2247Y.K. Okuducuhttps://www.atsjournals.org/doi/10.1164/ajrccm-conference.2024.209.1_MeetingAbstracts.A2247We discovered evidence that children with PASC generate circulating microclots, activated platelets, and increased levels of clotting-related proteins. We showed that children with MIS-C and Long COVID contained many microclots within their plasma, a finding absent in healthy children.
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Increased risk of arrhythmias, heart failure, and thrombosis in SARS-CoV-2 positive individuals persists at one year post-infection6/20/2024https://doi.org/10.1016/j.csbj.2024.06.024C Tintorehttps://www.sciencedirect.com/science/article/pii/S2001037024002125In the first 3 months of follow-up, SARS-CoV-2 positive individuals had a higher risk of mortality and of all cardiovascular events. From 4-12 months, there was increased risk of mortality in SARS-CoV-2 positive individuals overall, of heart failure in SARS-CoV-2 positive females (HR= 1.26 [1.11-1.42]), and of arrhythmias and thrombosis in SARS-CoV-2 positive males (HR= 1.29 [1.14-1.47] and HR= 1.35 [1.03-1.77], respectively).
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THE ELECTROCARDIOGRAPHIC CHANGES IN PATIENTS WITH VIRAL RESPIRATORY INFECTION IN SARS COV 19 VERSUS OTHER RESPIRATORY VIRUSES A SINGLE CENTER RETROSPECTIVE COHORT4/5/2024https://doi.org/10.1016/S0735-1097(24)02110-7Reihaneh C. Moghadamhttps://www.jacc.org/doi/full/10.1016/S0735-1097%2824%2902110-7This comparative study of 553 patients with RVI showed a statistically significant increase in ischemic findings and arrhythmias in patients with COV vs. non-COV infections. Pertinent EKG findings included 38.6% new ischemic ABNLs in COV-G (positive for SARS-CoV-2) vs. 25.6% in non-COV-G (non-COV-G including Flu-A, Flu-B, Corona OC43, Corona HKU1, Corona NL63, hMPV, RSV, or RVs) in Pts with no underlying ischemic EKG ABNLs, 38.7% new rhythm ABNLs in COV-G vs. 25.9% in non-CoV-G in Pts without underlying rhythm abnormality in prior EKGs.
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Cardiovascular complications in the course of COVID-19 - lessons learned and implications for the future care of patients with viral respiratory diseases: Data from a single center retrospective observational study6/29/2024https://doi.org/10.1016/j.hrtlng.2024.06.009Dominika Krogulechttps://www.sciencedirect.com/science/article/pii/S0147956324001171Cardiovascular events are common and can cause significant clinical deterioration during the course of COVID-19. The risk of cardiovascular complications was especially pronounced in patients with older age, pre-existing cardiovascular disease and more sever pneumonia at presentation to care.
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Trends in Sudden Cardiac Death in Pilots: A Post COVID-19 Challenging Crisis of Global Perspectives (2011-2023)7/1/2024https://doi.org/10.1101/2024.06.29.24309708Julian Yin Vieira Borgeshttps://www.medrxiv.org/content/10.1101/2024.06.29.24309708v1Pilots who had been infected with COVID-19 had a 1.8 times higher risk of SCD (Sudden Cardiac Death) compared to those who had not been infected (RR: 1.8, 95% CI: 1.3-2.5) (16). Three studies examined the association between COVID-19 vaccination and the risk of myocarditis, a condition linked to SCD. The pooled analysis found no significant increase in the risk of myocarditis among vaccinated pilots compared to unvaccinated pilots (RR: 1.2, 95% CI: 0.8-1.8)
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Cardiovascular disease risk after a SARS-CoV-2 infection: a systematic review and meta-analysis7/4/2024https://doi.org/10.1016/j.jinf.2024.106215Karla Romero Starkehttps://www.sciencedirect.com/science/article/pii/S016344532400149XPooled analysis show that for PE (pulmonary embolism), the risks were still doubled up to 4.5 months post-infection, and were still increased six to seven months after infection. For MI (myocardial infarction), a doubling of the risk was observed one month after infection, and an increasedrisk was still observed at least three months after infection. Results for IS (ischemic stroke) depict a doubling of the risk 1.5 months post-infection. After nine months, the risk remained and was still statistically significant.