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Study TitleDateDOIPMCIDLead AuthorLinkQuote
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Count of studies: 239
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Endothelial cell infection and endotheliitis in COVID-19
2020-04-20https://doi.org/10.1016/S0140-6736(20)30937-5Zsuzsanna Vargahttps://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30937-5/fulltextHere we demonstrate endothelial cell involvement across vascular beds of different organs in a series of patients with COVID-19. Our findings show the presence of viral elements within endothelial cells and an accumulation of inflammatory cells, with evidence of endothelial and inflammatory cell death. These findings suggest that SARS-CoV-2 infection facilitates the induction of endotheliitis in several organs as a direct consequence of viral involvement (as noted with presence of viral bodies) and of the host inflammatory respons.
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Cardiac Involvement in Patients Recovered From COVID-2019 Identified Using Magnetic Resonance Imaging2020-05-12https://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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Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19)
2020-07-27https://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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Increased risk of acute stroke among patients with severe COVID-19: a multicenter study and meta-analysis2020-09-12https://doi.org/10.1111/ene.14535T. Siepmannhttps://onlinelibrary.wiley.com/doi/full/10.1111/ene.14535Synthesized analysis of data from our multicenter study and previously published cohorts indicates that severity of COVID-19 is associated with an increased risk of acute stroke. Risk of acute stroke was increased for patients with severe compared to non-severe COVID-19 (RR = 4.18, 95% CI: 1.7–10.25; P = 0.002).
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Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered from Coronavirus Disease 2019 (COVID-19)
2020-11-01https://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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Evidence of thrombotic microangiopathy in children with SARS-CoV-2 across the spectrum of clinical presentations
2020-12-08https://doi.org/10.1182/bloodadvances.2020003471Caroline Dioriohttps://ashpublications.org/bloodadvances/article/4/23/6051/474421/Evidence-of-thrombotic-microangiopathy-in-childrenOf the 19 patients for whom complete clinical criteria were available, 17 (89%) met criteria for TMA. A high proportion of tested children with SARS-CoV-2 infection had evidence of complement activation and met clinical and diagnostic criteria for TMA (thrombotic microangiopathy).
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SARS-CoV-2 and Stroke Characteristics: A Report From the Multinational COVID-19 Stroke Study Group
2021-04-21https://doi.org/10.1161%2FSTROKEAHA.120.032927PMC8078130Shima Shahjoueihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8078130/We observed a considerably higher rate of large vessel occlusions, a much lower rate of small vessel occlusion and lacunar infarction, and a considerable number of young stroke when compared with the population studies before the pandemic.
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Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin
2021-08-23https://doi.org/10.1186/s12933-021-01359-7Etheresia Pretoriushttps://cardiab.biomedcentral.com/articles/10.1186/s12933-021-01359-7We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation.
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Cardiac involvement in consecutive unselected hospitalized COVID-19 population: In-hospital evaluation and one-year follow-up
2021-09-15https://doi.org/10.1016/j.ijcard.2021.06.056http://www.ncbi.nlm.nih.gov/pmc/articles/pmc8253670/Viviana Maestrinihttps://pubmed.ncbi.nlm.nih.gov/34224766/Cardiovascular evaluation in COVID-19 patients is crucial since the occurrence of CVD in hospitalized COVID-19 patients is common (28%), requires specific treatment and increases the risk of in-hospital mortality. Persistence or delayed presentation of CVD at 1-month (9%) and persistent symptoms at 1-year follow-up (48%) suggest the need for monitoring COVID-19 survivors.
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Symptom Persistence Despite Improvement in Cardiopulmonary Health – Insights from longitudinal CMR, CPET and lung function testing post-COVID-19
2021-10-20https://doi.org/10.1016/j.eclinm.2021.101159
Mark Philip Cassar
https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(21)00439-9/fulltextAt 2-3 months, 83% of patients had at least one cardiopulmonary symptom versus 33% of controls. By 6 months, 52% of patients remained symptomatic. On CMR (cardiac and lung magnetic resonance imaging), indexed right ventricular (RV) end-diastolic volume (-4·3 mls/m2, P=0·005) decreased and RV ejection fraction (+3·2%, P=0·0003) increased. Lung parenchymal abnormalities and peak V̇O2, although better, were abnormal in patients versus controls.
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Long term effects of mild severity COVID‑19 on right ventricular functions2021-12-01https://doi.org/10.1007/s10554-021-02340-xhttps://pmc.ncbi.nlm.nih.gov/articles/PMC8274467/Fatih Akkayahttps://pubmed.ncbi.nlm.nih.gov/34251551/This results suggested that RV-GLS (RV global longitudinal strain) and RV-FWLS (RV free wall longitudinal strain) decreased in the long term (third month) follow-up of patients treated for mild severity COVID-19 disease. Subclinical RV (Right ventricular) dysfunction may be observed in patients after mild severity COVID-19. RV diamaters, systolic pulmonary artery pressure (sPAP) and RV myocardial performance index (RV MPI) were significantly higher in the COVID-19 patients compared to control group.
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Development of post-COVID-19 cardiovascular events: an analysis of clinical features and risk factors from a single hospital retrospective study2021-12-10https://doi.org/10.53854/liim-2904-6https://pmc.ncbi.nlm.nih.gov/articles/PMC8805477/Gianluca Cuomohttps://pubmed.ncbi.nlm.nih.gov/35146362/In patients with COVID-19, the development of a cardiovascular event occurs quite frequently and is mainly seen in elderly subjects with comorbidities (especially hypertension) in the presence of a severe respiratory picture. A cardiovascular event developed in 15.7% of the subjects. These were mainly pulmonary embolism (9.4%), followed by arrhythmias (3.3%), myocardial infarction (2.3%), and myocarditis (0.8%).
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Myocardial fibrosis occurs in non-hospitalised patients with chronic symptoms after COVID-19
2022-01-26https://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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Long-term cardiovascular outcomes of COVID-192022-02-07https://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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Risks of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19: nationwide self-controlled cases series and matched cohort study
2022-02-22https://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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FOLLOW-UP OF HOSPITALIZED COVID-19 SURVIVORS: ASSESSMENT OF SHORT AND LONG-TERM CARDIOVASCULAR SEQUELAE AFTER SARS-COV-2 INFECTION2022-04-01https://doi.org/10.1016/S0735-1097(22)03148-5Lucia Ilaria Birtolohttps://www.jacc.org/doi/full/10.1016/S0735-1097%2822%2903148-5Our preliminary data showed persistent or delayed onset of cardiovascular involvement (16%) at short-term follow-up and persistent symptoms (45%) at long-term follow-up. 60% of survivors showed persistent chest CT abnormalities and among those 28 % complained of persistent cardiopulmonary symptoms at long term follow-up.
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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
2022-04-06https://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 Manifestations Of Coronavirus (COVID-19)2022-05-02Basu-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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Long-Term Cardiovascular Effects of COVID-19: Emerging Data Relevant to the Cardiovascular Clinician2022-05-04https://doi.org/10.1007/s11883-022-01032-8Diana L. Toblerhttps://link.springer.com/article/10.1007/s11883-022-01032-8Long-term follow-up shows increased incidence of arrhythmia, heart failure, acute coronary syndrome, right ventricular dysfunction, myocardial fibrosis, hypertension, and diabetes mellitus. There is increased mortality in COVID-19 patients after hospital discharge, and initial myocardial injury is associated with increased mortality.
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Post-recovery COVID-19 and incident heart failure in the National COVID Cohort Collaborative (N3C) study
2022-07-15https://doi.org/10.1038/s41467-022-31834-yHusam M. Salahhttps://www.nature.com/articles/s41467-022-31834-yOver a median follow up of 367 days, 10,979 incident heart failure events occurred. After adjustments, COVID-19 hospitalization was associated with a 45% higher hazard of incident heart failure (hazard ratio = 1.45; 95% confidence interval: 1.39–1.51), with more pronounced associations among patients who were younger (P-interaction = 0.003), White (P-interaction = 0.005), or who had established cardiovascular disease (P-interaction = 0.005). In conclusion, COVID-19 hospitalization is associated with increased risk of incident heart failure.
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Chronic biopsy proven post-COVID myoendocarditis with SARS-Cov-2 persistence and high level of antiheart antibodies2022-07-19https://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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Chronic biopsy proven post-COVID myoendocarditis with SARS-Cov-2 persistence and high level of antiheart antibodies2022-07-19https://doi.org/10.1002/clc.23886Olga Blagovahttps://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. The new cardiac symptoms (congestive heart failure 3–4 New York Heart Association class with severe right ventricular involvement, various rhythm, and conduction disturbances) appeared 1–5 months following COVID-19.
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Evolution of right and left ventricle routine and speckle-tracking echocardiography in patients recovering from coronavirus disease 2019: a longitudinal study
2022-07-21https://doi.org/10.1093/ehjci/jeab190https://pmc.ncbi.nlm.nih.gov/articles/PMC8500022/Guy Baruchhttps://pubmed.ncbi.nlm.nih.gov/34542601/A quarter of patients still have LV systolic dysfunction based on STE cut-offs. Moreover, LV STE does not improve significantly, implying subclinical LV dysfunction may be part and parcel of recovering from COVID-19 infection. A significant proportion [36 (45%)] of patients had some deterioration of longitudinal strain at follow-up, and 20 patients (25%) still had abnormal LV STE ∼3 months after COVID-19 acute infection.
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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 networks2022-08-11https://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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Cardiac postacute sequelae symptoms of SARS-CoV-2 in community-dwelling adults: cross-sectional study2022-09-04https://doi.org/10.1136/openhrt-2022-002084Oluwabunmi Ogungbehttps://openheart.bmj.com/content/9/2/e002084More than a third of persons with COVID-19 reported cardiac-related PASC symptoms. Prevalence of cardiac PASC was 43% and newly diagnosed cardiac conditions were 27%. The odds for cardiac-related PASC were higher among persons with underlying pre-existing conditions (adjusted OR (aOR): 2.00, 95% CI: 1.28 to 3.10) and among those who were hospitalised (aOR: 3.03, 95% CI: 1.58 to 5.83).
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Long-term cardiac pathology in individuals with mild initial COVID-19 illness2022-09-05https://doi.org/10.1038/s41591-022-02000-0

Valentina O. Puntmannhttps://www.nature.com/articles/s41591-022-02000-0Symptomatic individuals had higher heart rates and higher imaging values or contrast agent accumulation, denoting inflammatory cardiac involvement, compared to asymptomatic individuals. At follow-up (329 days (IQR, 274–383 days) after infection), 57% of participants had persistent cardiac symptoms. Diffuse myocardial edema was more pronounced in participants who remained symptomatic at follow-up as compared to those who improved.
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Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage2022-09-15https://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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Excess risk for acute myocardial infarction mortality during the COVID-19 pandemic2022-09-29https://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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Cardiac impairment in Long Covid 1-year post SARS-CoV-2 infection2022-10-03https://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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Elevated vascular transformation blood biomarkers in Long-COVID indicate angiogenesis as a key pathophysiological mechanism2022-10-10https://doi.org/10.1186/s10020-022-00548-8Maitray A. Patelhttps://molmed.biomedcentral.com/articles/10.1186/s10020-022-00548-8Long-COVID patients suffer prolonged, diffuse symptoms and poorer health. Vascular transformation blood biomarkers were significantly elevated in Long-COVID. Fourteen vasculature transformation blood biomarkers were significantly elevated in Long-COVID outpatients, versus acutely ill COVID-19 inpatients and healthy controls subjects (P < 0.05).
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Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank2022-10-24https://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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SARS-CoV-2 Infection and Increased Risk for Pediatric Stroke2022-11-20https://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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Prognosis of Myocarditis Developing After mRNA COVID-19 Vaccination Compared With Viral Myocarditis2022-12-01https://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-analysis2022-12-16https://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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Mid- and Long-Term Atrio-Ventricular Functional Changes in Children after Recovery from COVID-19
2022-12-26https://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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Risk of incident heart failure after COVID-19 recovery: a systematic review and meta-analysis2022-12-27https://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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One-year cardiovascular outcomes after coronavirus disease 2019: The cardiovascular COVID-19 registry2022-12-30https://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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Analysis of thrombogenicity under flow reveals new insights into the prothrombotic state of patients with post-COVID syndrome
2023-01-01https://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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Risks and burdens of incident dyslipidaemia in long COVID: a cohort study2023-01-06https://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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Cardiovascular Disease in Post-Acute COVID-19 Syndrome: A Comprehensive Review of Pathophysiology and Diagnosis Approach2023-01-13https://doi.org/10.31083%2Fj.rcm2401028PMC11270463Nuraini Yasmin Kusumawardhanihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11270463/The COVID-19 pandemic is an ongoing catastrophic public health event with dire long-term consequences, as many COVID-19 survivors experience a novel syndrome designated as long COVID syndrome. This novel syndrome also involved the CV system and manifests in coronary artery disease, hypertension, arrhythmia, heart failure, venous thromboembolism, and POTS.
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Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank2023-01-19https://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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Clinical presentation and management strategies of cardiovascular autonomic dysfunction following a COVID-19 infection – a systematic review2023-01-24https://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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Incidence of myocarditis among patients recovered from COVID-19 infection identified using cardiac magnetic resonance imaging2023-01-25https://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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Long COVID Syndrome and Cardiovascular Manifestations: A Systematic Review and Meta-Analysis2023-01-29https://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 study2023-02-0110.1136/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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Cardiac abnormalities in Long COVID 1-year post-SARS-CoV-2 infection2023-02-01https://doi.org/10.1136/openhrt-2022-002241https://pmc.ncbi.nlm.nih.gov/articles/PMC9950586/Adriana Roca-Fernandezhttps://pubmed.ncbi.nlm.nih.gov/36822818/CMR (Cardiac MR) abnormalities (left entricular or right ventricular dysfunction/dilatation and/or abnormal T1mapping), occurred in one in five individuals with Long COVID at 6 months, persisting in over half of those at 12 months. Of individuals with Long COVID, 102/534 (19%) had CMR abnormalities at baseline; 71/102 had complete paired data at 12 months. Of those, 58% presented with ongoing CMR abnormalities at 12 months.
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Cardiopulmonary Long-Term Sequelae in Patients after Severe COVID-19 Disease
2023-02-15https://doi.org/10.3390/jcm12041536https://pmc.ncbi.nlm.nih.gov/articles/PMC9959779/Julia Hanne Niebauerhttps://pubmed.ncbi.nlm.nih.gov/36836071/Even 6 months after discharge, a majority fulfilled criteria for Long-COVID. While no associations between fatigue and cardiopulmonary abnormalities were found, exertional dyspnea correlated with impaired pulmonary function, reduced GLS (global longitudinal strain) and/or diastolic dysfunction. Magnetic resonance imaging revealed traces of pericardial effusion in 18% and signs of former pericarditis or myocarditis in 4%. Pulmonary function was impaired in 11%.
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Abnormal right ventricular echocardiographic findings in recovered patients associated with severe acute respiratory syndrome in COVID-19
2023-02-17https://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-analysis2023-02-18https://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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Ectopic expression of SARS-CoV-2 S and ORF-9B proteins alters metabolic profiles and impairs contractile function in cardiomyocytes
2023-02-22https://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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Orthostatic tachycardia after covid-19
2023-02-24https://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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CARDIAC COMPLICATIONS AMONG LONG COVID PATIENTS: A SYSTEMATIC REVIEW AND META-ANALYSIS2023-03-01https://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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One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database2023-03-03doi: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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SARS-CoV-2 spike protein-mediated cardiomyocyte fusion may contribute to increased arrhythmic risk in COVID-192023-03-08https://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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Long-Term Adverse Effects of Mild COVID-19 Disease on Arterial Stiffness, and Systemic and Central Hemodynamics: A Pre-Post Study2023-03-08https://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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How Does COVID-19 Affect the Heart?2023-03-10https://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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Left ventricular global longitudinal strain as a parameter of mild myocardial dysfunction in athletes after COVID-192023-03-15https://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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The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread2023-03-17https://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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Cardiovascular and Cerebral Vascular Health in Females with Post-Acute Sequelae of COVID-19 (PASC)
2023-03-31https://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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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 Registry2023-04-05https://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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Data-driven analysis to understand long COVID using electronic health records from the RECOVER initiative
2023-04-07https://doi.org/10.1038/s41467-023-37653-zChengxi Zanghttps://www.nature.com/articles/s41467-023-37653-zWe identified a broad list of diagnoses and medications which exhibited significantly higher incidence risk for patients 30–180 days after the laboratory-confirmed SARS-CoV-2 infection compared to non-infected patients. We identified more PASC diagnoses in NYC than in Florida regarding our screening criteria, and conditions including dementia, hair loss, pressure ulcers, pulmonary fibrosis, dyspnea, pulmonary embolism, chest pain, abnormal heartbeat, malaise, and fatigue, were replicated across both cohorts.
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Major adverse cardiovascular events are associated with necroptosis during severe COVID-19
2023-04-20https://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 detection2023-04-24https://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-192023-04-26https://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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COVID-19 HEART unveiling as atrial fibrillation: pathophysiology, management and future directions for research
2023-04-30https://doi.org/10.1186/s43044-023-00359-0

Sri Harsha Kanurihttps://tehj.springeropen.com/articles/10.1186/s43044-023-00359-0COVID-19-induced pathological derangements in the myocardium and systemic circulation in combination are accountable for instigation and persistence of this cardiac arrhythmia. Some patients presented with atrial fibrillation few months later after complete recovery from COVID-19 infections. These long haulers are known to harbor silent COVID-19 infections in the systemic tissues including myocardium.
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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 motion2023-05-23https://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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Coronary microvascular health in symptomatic patients with prior COVID-19 infection: an updated analysis2023-05-31https://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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Prevalence of coronary artery disease among COVID-19 patients: a systematic review and meta-analysis
2023-06-01https://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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Prevalence of probable post-COVID cardiac sequelae and its health seeking behaviour among health care workers: A cross-sectional analytical study
2023-06-14https://doi.org/10.1016/j.ijtb.2023.06.008https://pmc.ncbi.nlm.nih.gov/articles/PMC10264162/Yamini Marimuthuhttps://pubmed.ncbi.nlm.nih.gov/39890371/Around one out of ten individuals had experienced probable post-COVID cardiac sequelae, but only half of them got evaluated for it. The prevalence of probable post-COVID cardiac sequelae among health workers and medical students was 11.9% (95% CI: 8.76-15.7). Females, hypertensive individuals, and those who had moderate-severe disease during acute COVID-19 disease were at higher risk of developing probable post-COVID cardiac sequelae.
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Incidence and predictors of development of new onset hypertension post COVID-19 disease2023-06-14https://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-analysis2023-07-25https://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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Effects of COVID-19 Infection in Healthy Subjects on Cardiac Function and Biomarkers of Oxygen Transport, Blood Coagulation and Inflammation
2023-07-25https://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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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels2023-08-15https://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 Illness2023-08-15https://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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Incidence of New-Onset Hypertension Post–COVID-19: Comparison With Influenza
2023-08-21https://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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SARS-CoV-2 reinfection: Adding insult to dysfunctional endothelium in patients with atherosclerotic cardiovascular disease
2023-09-01https://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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Autonomic dysregulation in long-term patients suffering from Post-COVID-19 Syndrome assessed by heart rate variability
2023-09-22https://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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SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels2023-09-28https://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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Prolonged platelet hyperactivity after COVID-19 infection2023-10-11https://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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Myocardial injury and related mortality in hospitalized patients with COVID-19 during the Omicron pandemic: new perspectives and insights2023-10-13https://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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Baroreflex sensitivity is impaired in survivors of mild COVID-19 at 3–6 months of clinical recovery; association with carotid artery stiffness2023-10-31https://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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Cardiovascular Follow-up of Patients Treated for MIS-C
2023-11-15https://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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Risk of arrhythmias following COVID-19: nationwide self-controlled case series and matched cohort study2023-11-21https://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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The effect of mild to moderate COVID-19 infection on the cardiorespiratory fitness of firefighters
2023-11-30https://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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Pooled rates and demographics of POTS following SARS-CoV-2 infection versus COVID-19 vaccination: Systematic review and meta-analysis2023-12-01https://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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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
2023-12-19https://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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High Cardiac Troponin Levels in Infants with Acute SARS-CoV-2 Infection: A Prospective Comparative study2023-12-21https://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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Predicted risk of heart failure pandemic due to persistent SARS-CoV-2 infection using a three-dimensional cardiac model
2023-12-22https://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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Association between Cardiovascular Disease Risk and long COVID-19: A Systematic Review and Meta-analysis2023-12-31https://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 burden2024-01-02https://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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3D Holo-tomographic Mapping of COVID-19 Microclots in Blood to Assess Disease Severity2024-01-09https://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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Longitudinal strain and myocardial work in symptomatic patients having recovered from COVID-19 and possible associations with the severity of the disease2024-01-26https://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 cohorts2024-02-01https://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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Endothelial dysfunction and cardiovascular risk in post-COVID-19 patients after 6- and 12-months SARS-CoV-2 infection2024-02-07https://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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Echocardiographic Strain Evaluation Shows Persistent Echocardiographic Changes at 1 Year after Diagnosis of Multisystem Inflammatory Syndrome in Children2024-03-05https://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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Autonomic cardiac function in children and adolescents with long COVID: a case-controlled study
2024-03-06https://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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Impact of vaccination on the association of COVID-19 with cardiovascular diseases: An OpenSAFELY cohort study
2024-03-11https://doi.org/10.1038/s41467-024-46497-0Genevieve I. Cezardhttps://www.nature.com/articles/s41467-024-46497-0We showed that the incidence of each arterial thrombotic, venous thrombotic and other cardiovascular outcomes was substantially elevated during weeks 1-4 after COVID-19, compared with before or without COVID-19, but less markedly elevated in time periods beyond week 4.
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The role of COVID-19 vaccines in preventing post-COVID-19 thromboembolic and cardiovascular complications2024-03-12https://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.