Atrial inflammation and microvascular thrombogenicity are increased in deceased COVID-19 patients

Wu, Linghe; Jiang, Zhu; Meulendijks, Eva R.; Baylan, Umit; Waas, Ingeborg S. E.; Bugiani, Marianna; Tuinman, Pieter R.; Fronczek, Judith; Heunks, Leo; Groot, Joris R. de; Rossum, Albert C. van; Niessen, H.W.M.; Krijnen, Paul A J

doi:10.1016/j.carpath.2023.107524

Cited by 5 publications

(4 citation statements)

References 34 publications

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“…Furthermore, it could be parallelism with community-acquired pneumonia (CAP) patients, as reported in other meta-analyses [18]. The key mechanisms and potential predictors of the incidence of AF are inflammatory responses in the atrial myocardium as well as adipose-tissue inflammation [19,20]. On the other hand, new-onset AF in patients with COVID-19 may be a factor that predicates other adverse cardiovascular diseases rather than an independent factor of mortality [21].…”

Section: Introductionmentioning

confidence: 92%

New-Onset Atrial Fibrillation in the Setting of COVID-19 Infection Is a Predictor of Mortality in Hospitalized Patients: CovAF-Study

Parahuleva

Harbaum

Patsalis

et al. 2023

JCM

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Recent studies show that hospitalized COVID-19 patients have an increased incidence of arrhythmia, especially atrial fibrillation (AF). This single-center study included 383 hospitalized patients with positive polymerase chain reaction tests for COVID-19 from March 2020 to April 2021. Patient characteristics were documented, and data were analyzed for episodes of AF on admission or during the hospital stay, intrahospital mortality, need for intensive care and/or invasive ventilation, inflammatory parameters (hs-CRP, IL-6, and procalcitonin), and differential blood count. We demonstrated that in the setting of hospitalized cases of COVID-19 infection, there is an incidence of 9.8% (n = 36) for the occurrence of new-onset AF. Furthermore, it was shown that a total of 21% (n = 77) had a history of episodes of paroxysmal/persistent AF. However, only about one-third of patients with pre-existing AF had relevant documented tachycardic episodes during the hospital stay. Patients with new-onset AF had a significantly increased intrahospital mortality compared to the control and the pre-existing AF without rapid ventricular rate (RVR) group. Patients with new-onset AF required intensive care and invasive ventilation more frequently. Further analysis examined patients with episodes of RVR and demonstrated that they had significantly elevated CRP (p < 0.05) and PCT (p < 0.05) levels on the day of hospital admission compared to patients without RVR.

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Section: Introductionmentioning

confidence: 92%

New-Onset Atrial Fibrillation in the Setting of COVID-19 Infection Is a Predictor of Mortality in Hospitalized Patients: CovAF-Study

Parahuleva

Harbaum

Patsalis

et al. 2023

JCM

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“…• AF is a common occurrence following infection with SARS-CoV-2 (COVID-19) [257][258][259][260][261][262][263][264][265][266][267]. • The Odds Ratio (OR) for AF 365 days after COVID-19 compared to a well-established control group was 1.83 in a large study [268].…”

Section: Examples In Which We Know That Infection Can Lead To Atrial ...mentioning

confidence: 99%

Fibrinaloid Microclots and Atrial Fibrillation

Kell,

Lip,

Pretorius

2024

Biomedicines

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Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well-known consequence of atrial fibrillation. We here ask the question whether the fibrinaloid microclots seen in plasma or serum may in fact also be a cause of (or contributor to) the development of AF. We consider known ‘risk factors’ for AF, and in particular, exogenous stimuli such as infection and air pollution by particulates, both of which are known to cause AF. The external accompaniments of both bacterial (lipopolysaccharide and lipoteichoic acids) and viral (SARS-CoV-2 spike protein) infections are known to stimulate fibrinaloid microclots when added in vitro, and fibrinaloid microclots, as with other amyloid proteins, can be cytotoxic, both by inducing hypoxia/reperfusion and by other means. Strokes and thromboembolisms are also common consequences of AF. Consequently, taking a systems approach, we review the considerable evidence in detail, which leads us to suggest that it is likely that microclots may well have an aetiological role in the development of AF. This has significant mechanistic and therapeutic implications.

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“…Severe infection often results in overactivation of certain innate immune subsets [ 8 – 15 ] while additional studies have reported suppression of adaptive immune subsets that are necessary for antiviral immunity and memory responses [ 16 – 18 ]. These highly dysregulated immune responses not only represent their own form of infection-induced pathology but also drive vascular pathology, including coagulopathies, myocarditis, and tissue damage particularly in the lung following infection [ 10 , 19 , 20 ]. Immune-independent mechanisms underlying COVID-19-induced vascular damage, including changes in essential vitamins and platelet aggregation, have also been reported [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Health disparities in COVID-19: immune and vascular changes are linked to disease severity and persist in a high-risk population in Riverside County, California

Bergersen,

Pham,

et al. 2023

BMC Public Health

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Background Health disparities in underserved communities, such as inadequate healthcare access, impact COVID-19 disease outcomes. These disparities are evident in Hispanic populations nationwide, with disproportionately high infection and mortality rates. Furthermore, infected individuals can develop long COVID with sustained impacts on quality of life. The goal of this study was to identify immune and endothelial factors that are associated with COVID-19 outcomes in Riverside County, a high-risk and predominantly Hispanic community, and investigate the long-term impacts of COVID-19 infection. Methods 112 participants in Riverside County, California, were recruited according to the following criteria: healthy control (n = 23), outpatients with moderate infection (outpatient, n = 33), ICU patients with severe infection (hospitalized, n = 33), and individuals recovered from moderate infection (n = 23). Differences in outcomes between Hispanic and non-Hispanic individuals and presence/absence of co-morbidities were evaluated. Circulating immune and vascular biomarkers were measured by ELISA, multiplex analyte assays, and flow cytometry. Follow-up assessments for long COVID, lung health, and immune and vascular changes were conducted after recovery (n = 23) including paired analyses of the same participants. Results Compared to uninfected controls, the severe infection group had a higher proportion of Hispanic individuals (n = 23, p = 0.012) than moderate infection (n = 8, p = 0.550). Disease severity was associated with changes in innate monocytes and neutrophils, lymphopenia, disrupted cytokine production (increased IL-8 and IP-10/CXCL10 but reduced IFNλ2/3 and IFNγ), and increased endothelial injury (myoglobin, VCAM-1). In the severe infection group, a machine learning model identified LCN2/NGAL, IL-6, and monocyte activation as parameters associated with fatality while anti-coagulant therapy was associated with survival. Recovery from moderate COVID infection resulted in long-term immune changes including increased monocytes/lymphocytes and decreased neutrophils and endothelial markers. This group had a lower proportion of co-morbidities (n = 8, p = 1.0) but still reported symptoms associated with long COVID despite recovered pulmonary function. Conclusion This study indicates increased severity of COVID-19 infection in Hispanic individuals of Riverside County, California. Infection resulted in immunological and vascular changes and long COVID symptoms that were sustained for up to 11 months, however, lung volume and airflow resistance was recovered. Given the immune and behavioral impacts of long COVID, the potential for increased susceptibility to infections and decreased quality of life in high-risk populations warrants further investigation.

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Atrial inflammation and microvascular thrombogenicity are increased in deceased COVID-19 patients

Cited by 5 publications

References 34 publications

New-Onset Atrial Fibrillation in the Setting of COVID-19 Infection Is a Predictor of Mortality in Hospitalized Patients: CovAF-Study

New-Onset Atrial Fibrillation in the Setting of COVID-19 Infection Is a Predictor of Mortality in Hospitalized Patients: CovAF-Study

Fibrinaloid Microclots and Atrial Fibrillation

Health disparities in COVID-19: immune and vascular changes are linked to disease severity and persist in a high-risk population in Riverside County, California

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