SARS–CoV-2 Mediated Hyperferritinemia and Cardiac Arrest: Preliminary Insights

VasanthiDharmalingam, Prakash; Karuppagounder, Vengadeshprabhu; Watanabe, Kenichi; Karmouty‐Quintana, Harry; Palaniyandi, Suresh S.; Guha, Ashrith; Thandavarayan, Rajarajan Amirthalingam

doi:10.1016/j.drudis.2021.01.014

Cited by 8 publications

(5 citation statements)

References 126 publications

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“…This evidence is supported by solid pathophysiological bases: SARS-CoV-2-related myocardial injury can result in ventricular dysfunction and fibrosis, thus promoting new-onset re-entrant arrhythmias, as well as severe hypoxia due to acute respiratory failure and pulmonary embolism, which increase the risk of cardiac arrest [62] . Furthermore, the occurrence of a COVID-19 cytokine release can evoke an unchecked immune response and sub-sequent multiorgan damage that could lead to refractory shock and cardiac arrest [63] . Finally, in a cohort study of 9 autopsy cases of individuals with COVID-19, microscopic examination demonstrated inflammatory infiltrates in subepicardial ganglia in all three patients deceased for ventricular tachyarrhythmias, therefore suggesting neuronal cell death as additional trigger of arrhythmic instability [47] .…”

Section: Pathogenic Effects Of Sars-cov-2 Infection On the Heartmentioning

confidence: 99%

Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

et al. 2022

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Section: Pathogenic Effects Of Sars-cov-2 Infection On the Heartmentioning

confidence: 99%

Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

et al. 2022

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“…People with heart disease before infection tend to have more severe symptoms or develop complications during and after COVID-19, including the development of hypoxemia, coagulopathies, cardiac arrest, and damage ( 289 ). During infection, cardiac cells release troponin, and troponin concentrations have been reported to correlate with disease severity and can be considered a biomarker ( 284 , 290 – 293 ). Synergistically, due to cardiac damage, a decrease in blood pressure occurs, leading to the activation of the RAAS system, which in turn triggers vasoconstriction, vascular inflammation, and an increase in Angiotensin 2 levels, contributing to the pathogenesis and cardiovascular complications of the infected individual.…”

Section: Organ and Body System Complications Upon Sars-cov-2 Infectionmentioning

confidence: 99%

New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

Carvajal,

García-Castillo,

Cuellar

et al. 2024

Front. Immunol.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the respiratory distress condition known as COVID-19. This disease broadly affects several physiological systems, including the gastrointestinal, renal, and central nervous (CNS) systems, significantly influencing the patient’s overall quality of life. Additionally, numerous risk factors have been suggested, including gender, body weight, age, metabolic status, renal health, preexisting cardiomyopathies, and inflammatory conditions. Despite advances in understanding the genome and pathophysiological ramifications of COVID-19, its precise origins remain elusive. SARS-CoV-2 interacts with a receptor-binding domain within angiotensin-converting enzyme 2 (ACE2). This receptor is expressed in various organs of different species, including humans, with different abundance. Although COVID-19 has multiorgan manifestations, the main pathologies occur in the lung, including pulmonary fibrosis, respiratory failure, pulmonary embolism, and secondary bacterial pneumonia. In the post-COVID-19 period, different sequelae may occur, which may have various causes, including the direct action of the virus, alteration of the immune response, and metabolic alterations during infection, among others. Recognizing the serious adverse health effects associated with COVID-19, it becomes imperative to comprehensively elucidate and discuss the existing evidence surrounding this viral infection, including those related to the pathophysiological effects of the disease and the subsequent consequences. This review aims to contribute to a comprehensive understanding of the impact of COVID-19 and its long-term effects on human health.

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“…Hyperferritinemia is often difficult to interpret clinically 7 . Hyperferritinemia can stem from a variety of causes, encompassing liver, renal, and rheumatologic diseases, malignancies, chronic blood transfusions, HIV (human immunodeficiency virus) and other viral infections, diverse hematological disorders, chronic inflammation, or metabolic syndrome 1-3 . Hyperferritinemia is remarkably associated with mortality, regardless of underlying pathology 7 . In a prospective population-based study in Denmark, ferritin emerged as a robust predictor of premature death within the general population.…”

Section: Introductionmentioning

confidence: 99%

Causes of hyperferritinemia: what has changed with the pandemic?

Kılıç,

Tekgöz,

Çolak

et al. 2024

Cukurova Medical Journal

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Purpose: In this study, we aimed to analyze patients with ferritin levels of ≥ 1000 ng/mL based on diagnoses and the wards they received both before the COVID pandemic and during the pandemic periods. Materials and Methods: This retrospective study evaluated the patients who applied to a tertiary hospital and had ferritin onset of the pandemic. The patients' demographic and clinical characteristics and ferritin levels were obtained from the hospital's medical records. Results: There were 2022 patients, 635 (31.4%) female and 1387 (68.6%) male, with a median age of 62 (49-71) years. 554 patients (27.4%) before the pandemic, and 1468 patients (72.6%) during the pandemic had ferritin levels of ≥ 1000 ng/mL. Hyperferritinemia was detected more frequently in males during the pandemic (p

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SARS–CoV-2 Mediated Hyperferritinemia and Cardiac Arrest: Preliminary Insights

Cited by 8 publications

References 126 publications

Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

New insights into the pathogenesis of SARS-CoV-2 during and after the COVID-19 pandemic

Causes of hyperferritinemia: what has changed with the pandemic?

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