The Involvement and Manifestations of SARS-CoV-2 Virus in Cardiovascular Pathology DOI Creative Commons

Sofia Teodora Hărșan,

Anca Sin

Medicina, Journal Year: 2025, Volume and Issue: 61(5), P. 773 - 773

Published: April 22, 2025

Although the acute phase of COVID-19 pandemic has subsided, emergence post-COVID-19 condition presents a new and complex public health challenge, characterized by persistent, multisystem symptoms that can endure for weeks or months after initial infection with SARS-CoV-2 virus, significantly affecting survivors’ quality life. Among most concerning sequelae are cardiovascular complications, which encompass broad spectrum conditions, including arrhythmias, myocardial damage, postural orthostatic tachycardia syndrome. This narrative review explores burden on reviewing latest relevant findings in literature highlighting different aspects COVID-19’s involvement. investigates pathophysiological mechanisms underlying involvement condition, focus direct viral invasion via ACE2 receptors, immune-mediated injury, cytokine storm, systemic inflammation, endothelial dysfunction, mitochondrial injury. The interplay between pre-existing diseases, such as hypertension, atherosclerosis, diabetes, atrial fibrillation, is also explored, revealing individuals conditions at heightened risk both severe illness long-term complications. Long-term immune activation persistence antigens increasingly recognized contributors to ongoing even mild asymptomatic infections. As healthcare system continues adapt consequences pandemic, deeper understanding these manifestations essential. knowledge will inform development targeted strategies prevention, clinical management, rehabilitation affected patients. Furthermore, insights gained from intersection be instrumental shaping responses future epidemics, necessity multidisciplinary approaches patient care preparedness.

Language: Английский

Pathophysiological, immunological, and inflammatory features of long COVID DOI Creative Commons
Karen Böhmwald, Benjamín Diethelm‐Varela,

Linmar Rodríguez-Guilarte

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 28, 2024

The COVID-19 pandemic continues to cause severe global disruption, resulting in significant excess mortality, overwhelming healthcare systems, and imposing substantial social economic burdens on nations. While most of the attention therapeutic efforts have concentrated acute phase disease, a notable proportion survivors experience persistent symptoms post-infection clearance. This diverse set symptoms, loosely categorized as long COVID, presents potential additional public health crisis. It is estimated that 1 5 exhibit clinical manifestations consistent with COVID. Despite this prevalence, mechanisms pathophysiology COVID remain poorly understood. Alarmingly, evidence suggests cases within condition develop debilitating or disabling symptoms. Hence, urgent priority should be given further studies equip systems for its management. review provides an overview available information emerging condition, focusing affected individuals’ epidemiology, pathophysiological mechanisms, immunological inflammatory profiles.

Language: Английский

Citations

21
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation DOI Creative Commons
T. Küchler, Roman Günthner,

Andrea Ribeiro

et al.

Angiogenesis, Journal Year: 2023, Volume and Issue: 26(4), P. 547 - 563

Published: July 28, 2023

Post-COVID-19 syndrome (PCS) is a lingering disease with ongoing symptoms such as fatigue and cognitive impairment resulting in high impact on the daily life of patients. Understanding pathophysiology PCS public health priority, it still poses diagnostic treatment challenge for physicians.In this prospective observational cohort study, we analyzed retinal microcirculation using Retinal Vessel Analysis (RVA) patients compared to an age- gender-matched healthy (n = 41, matched out n 204).PCS exhibit persistent endothelial dysfunction (ED), indicated by significantly lower venular flicker-induced dilation (vFID; 3.42% ± 1.77% vs. 4.64% 2.59%; p 0.02), narrower central artery equivalent (CRAE; 178.1 [167.5-190.2] 189.1 [179.4-197.2], 0.01) arteriolar-venular ratio (AVR; (0.84 [0.8-0.9] 0.88 [0.8-0.9], 0.007). When combining AVR vFID, predicted scores reached good ability discriminate groups (area under curve: 0.75). Higher severity correlated (R - 0.37 0.017). The association microvascular changes were amplified exhibiting higher levels inflammatory parameters.Our results demonstrate that prolonged hallmark PCS, impairments seem explain As potential therapies emerge, RVA parameters may become relevant clinical biomarkers diagnosis therapy management.This study was previously registered at ClinicalTrials ("All Eyes PCS-Analysis Microvasculature Patients Syndrome". NCT05635552. https://clinicaltrials.gov/ct2/show/NCT05635552 ). Persistent post-COVID-19 syndrome. Acute SARS-CoV-2 infection indirectly or directly causes endotheliitis N 41 recruited vessel analysis performed assess function. Images SVA DVA are illustrative data analysis. For each patient cohort, diameter three measurement cycles calculated plotted diameter-time curve. exhibited reduced veins (vFID) measured dynamic (DVA) arteriolar (CRAE) (AVR) tendency towards (CRVE) when naïve participants. Created BioRender.com.

Language: Английский

Citations

29
Hematological alterations associated with long COVID-19 DOI Creative Commons
Guilherme C. Lechuga, Carlos Morel, Salvatore G. De-Simone

et al.

Frontiers in Physiology, Journal Year: 2023, Volume and Issue: 14

Published: July 24, 2023

Long COVID-19 is a condition characterized by persistent symptoms lasting beyond the acute phase of COVID-19. produces diverse symptomatology and can impact organs systems, including hematological system. Several studies have reported, in patients, abnormalities. Most these alterations are associated with higher risk severe disease poor outcomes. This literature review identified reporting parameters individuals Findings suggest that range sustained alterations, red blood cells, anemia, lymphopenia, elevated levels inflammatory markers such as ferritin, D-dimer, IL-6. These may contribute to better understanding pathophysiology its symptoms. However, further research needed elucidate underlying mechanisms potential treatments for changes

Language: Английский

Citations

26
People with Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Exhibit Similarly Impaired Vascular Function DOI
Marie Mclaughlin, Nilihan E. M. Sanal‐Hayes, Lawrence D. Hayes

et al.

The American Journal of Medicine, Journal Year: 2023, Volume and Issue: unknown

Published: Oct. 1, 2023

Language: Английский

Citations

24
Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19 DOI Creative Commons
Cameron D. Owens, Camila Bonin Pinto,

Sam Detwiler

et al.

Brain Communications, Journal Year: 2024, Volume and Issue: 6(2)

Published: Jan. 1, 2024

Abstract Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds infection) alter cellular physiologic processes within the neurovascular unit contribute cognitive dysfunction. COVID-19 has posed significant complications during acute convalescent stages in multiple organ systems, including brain. Cognitive impairment is prevalent complication patients, irrespective of severity SARS-CoV-2 infection. Moreover, overwhelming evidence from vitro, preclinical clinical studies reported SARS-CoV-2-induced pathologies components are associated with impairment. Neurovascular disruption alters coupling response, critical mechanism regulates cerebromicrovascular blood flow meet energetic demands locally active neurons. Normal processing achieved through response involves coordinated action cells (i.e. neurons glia) cell types endothelia, smooth muscle pericytes). However, current work on COVID-19-induced yet investigate as causal factor. Hence, this review, we aim describe SARS-CoV-2's effects how they can impact decline disease. Additionally, explore potential therapeutic interventions mitigate Given great both individuals public health, necessity effort fundamental scientific research application becomes imperative. This integrated endeavour crucial mitigating deficits induced by its subsequent burden especially vulnerable population.

Language: Английский

Citations

11
Tracking Persistent Symptoms in Scotland (TraPSS): a longitudinal prospective cohort study of COVID-19 recovery after mild acute infection DOI Creative Commons
Nicholas Sculthorpe, Marie Mclaughlin, Luke Cerexhe

et al.

BMJ Open, Journal Year: 2025, Volume and Issue: 15(1), P. e086646 - e086646

Published: Jan. 1, 2025

Background COVID-19 disease results in disparate responses between individuals and has led to the emergence of long coronavirus (Long-COVID), characterised by persistent cyclical symptomology. To understand complexity Long-COVID, importance symptom surveillance prospective longitudinal studies is evident. Methods A 9-month cohort study was conducted within Scotland (n=287), using a mobile app determine proportion recovered those with symptoms common symptoms, associations gender age. Results 3.1% participants experienced at month 9, meeting criteria for as defined National Institute Health Care Excellence terminology. The random effects model revealed significant time (month) effect infection recovery (p<0.001, estimate=0.07). Fatigue, cough muscle pain were most baseline, fatigue persisting longest, while like improved rapidly. Older age increased likelihood reporting (p=0.028, estimate=0.07) cognitive impairment estimate=0.93). Female headaches (p=0.024, estimate=0.53) post-exertional malaise (PEM) frequency (p=0.05, estimate=137.68), x PEM (p=0.033, estimate=18.96). Conclusions majority people fully recover from acute COVID-19, although often slowly. Age play role burden rates, emphasising need tailored approaches Long-COVID management. Further analysis required characteristics still ongoing months after initial identify risk factors potential predictors development Long-COVID.

Language: Английский

Citations

1
Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement DOI Open Access
Evgeni Gusev, Alexey Sarapultsev

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6389 - 6389

Published: June 9, 2024

Long COVID (LC), also referred to as Post COVID-19 Condition, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and other terms, represents a complex multisystem disease persisting after the acute phase COVID-19. Characterized by myriad symptoms across different organ systems, LC presents significant diagnostic management challenges. Central disorder is role low-grade inflammation, non-classical inflammatory response that contributes chronicity diversity observed. This review explores pathophysiological underpinnings LC, emphasizing importance inflammation core component. By delineating pathogenetic relationships clinical manifestations this article highlights necessity for an integrated approach employs both personalized medicine standardized protocols aimed at mitigating long-term consequences. The insights gained not only enhance our understanding but inform development therapeutic strategies could be applicable chronic conditions with similar features.

Language: Английский

Citations

8
SARS-CoV-2 induced vascular endothelial dysfunction: direct or indirect effects? DOI Open Access
Kathy O. Lui, Zhangjing Ma, Stefanie Dimmeler

et al.

Cardiovascular Research, Journal Year: 2023, Volume and Issue: 120(1), P. 34 - 43

Published: Dec. 29, 2023

Clinical evidence reveals that manifestations of endothelial dysfunction are widely observed in COVID-19 and long-COVID patients. However, whether these detrimental effects caused by direct infection the endothelium or indirectly mediated systemic inflammation has been a matter debate. It well acknowledged cells (ECs) cardiovascular system ubiquitously express SARS-CoV-2 entry receptor angiotensin-converting enzyme 2 (ACE2), yet accumulating suggests it is more predominantly expressed pericytes vascular smooth muscle mammalian blood vessel. Besides, replicative ECs to be demonstrated both vitro vivo. In this study, we review latest research on ACE2 expression different beds, heterogeneity various EC subsets with differential response SARS-CoV-2. We also discuss ACE2-independent alternative mechanisms underlying activation COVID-19, clinical SARS-CoV-2-induced dysfunction. Altogether, understanding ACE2-dependent driving would shed light strategies effective therapies targeting complications associated COVID-19.

Language: Английский

Citations

16
SARS-CoV-2 Spike Proteins and Cell–Cell Communication Induce P-Selectin and Markers of Endothelial Injury, NETosis, and Inflammation in Human Lung Microvascular Endothelial Cells and Neutrophils: Implications for the Pathogenesis of COVID-19 Coagulopathy DOI Open Access

Biju Bhargavan,

Georgette D. Kanmogne

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(16), P. 12585 - 12585

Published: Aug. 9, 2023

COVID-19 progression often involves severe lung injury, inflammation, coagulopathy, and leukocyte infiltration into pulmonary tissues. The pathogenesis of these complications is unknown. Because vascular endothelium neutrophils express angiotensin-converting enzyme-2 spike (S)-proteins, which are present in bodily fluids tissues SARS-CoV-2-infected patients, we investigated the effect S-proteins cell-cell communication on human microvascular endothelial cells expression P-selectin, markers NETosis, inflammation. Exposure or to endothelial-neutrophils co-culture induced P-selectin transcription expression, significantly increased expression/secretion IL-6, von Willebrand factor (vWF, pro-coagulant), citrullinated histone H3 (cit-H3, NETosis marker). Compared SARS-CoV-2 Wuhan variant, Delta variant 1.4-15-fold higher IL-6 vWF. Recombinant tissue pathway inhibitor (rTFPI), 5,5'-dithio-bis-(2-nitrobenzoic acid) (thiol blocker), thrombomodulin (anticoagulant) blocked S-protein-induced vWF, cit-H3. This suggests that following contact with endothelial-neutrophil interactions, increase adhesion molecules, induce coagulopathy via pathway, mechanisms involving functional thiol groups, and/or fibrinolysis system. Using rTFPI, effectors system thiol-based drugs could be viable therapeutic strategies against SARS-CoV-2-induced coagulopathy.

Language: Английский

Citations

15
Four years into the pandemic, managing COVID-19 patients with acute coagulopathy: what have we learned? DOI
Toshiaki Iba, Jerrold H. Levy, Cheryl L. Maier

et al.

Journal of Thrombosis and Haemostasis, Journal Year: 2024, Volume and Issue: 22(6), P. 1541 - 1549

Published: Feb. 29, 2024

Language: Английский

Citations

6