Post-acute sequelae of COVID-19: understanding and addressing the burden of multisystem manifestations

The Lancet Respiratory Medicine, Journal Year: 2023, Volume and Issue: 11(8), P. 739 - 754

Published: July 17, 2023

Individuals with SARS-CoV-2 infection can develop symptoms that persist well beyond the acute phase of COVID-19 or emerge after phase, lasting for weeks months initial illness. The post-acute sequelae COVID-19, which include physical, cognitive, and mental health impairments, are known collectively as long COVID post-COVID-19 condition. substantial burden this multisystem condition is felt at individual, health-care system, socioeconomic levels, on an unprecedented scale. Survivors COVID-19-related critical illness risk respiratory distress syndrome, sepsis, chronic illness, these multidimensional morbidities might be difficult to differentiate from specific effects COVID-19. We provide overview manifestations in adults. explore various organ systems, describe potential pathophysiological mechanisms, consider challenges providing clinical care support survivors manifestations. Research needed reduce incidence optimise therapeutic rehabilitative patients.

Language: Английский

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Impact of COVID-19 on Cardiovascular Disease

Viruses, Journal Year: 2023, Volume and Issue: 15(2), P. 508 - 508

Published: Feb. 11, 2023

Coronavirus disease 2019 (COVID-19) is a viral infection with the novel severe acute respiratory distress syndrome corona virus 2 (SARS-CoV-2). Until now, more than 670 million people have suffered from COVID-19 worldwide, and roughly 7 death cases were attributed to COVID-19. Recent evidence suggests an interplay between cardiovascular (CVD). may serve as yet underappreciated CVD risk modifier, including factors such diabetes mellitus or arterial hypertension. In addition, recent data suggest that previous increase for many entities of extent similarly observed traditional (CV) factors. Furthermore, increased incidence worse clinical outcomes in individuals preexisting been myocarditis, coronary syndrome, heart failure (HF), thromboembolic complications, arrhythmias. Direct indirect mechanisms proposed by which impact CV risk, entry into tissue induction massive systemic inflammatory response. current review, we provide overview literature reporting interaction CVD, review potential underlying this interaction, discuss preventive treatment strategies their interference evaluated since onset pandemic.

Language: Английский

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Cardiovascular autonomic dysfunction in post-COVID-19 syndrome: a major health-care burden

Nature Reviews Cardiology, Journal Year: 2024, Volume and Issue: 21(6), P. 379 - 395

Published: Jan. 2, 2024

Language: Английский

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New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(5), P. 2973 - 2973

Published: March 4, 2024

The endothelium is a monocellular layer covering the inner surface of blood vessels. It maintains vascular homeostasis regulating tone and permeability exerts anti-inflammatory, antioxidant, anti-proliferative, anti-thrombotic functions. When exposed to detrimental stimuli including hyperglycemia, hyperlipidemia, neurohormonal imbalance, different biological pathways are activated leading oxidative stress, endothelial dysfunction, increased secretion adipokines, cytokines, endothelin-1, fibroblast growth factor, reduced nitric oxide production, eventually loss integrity. Endothelial dysfunction has emerged as hallmark dysmetabolic impairment contributes effects on cardiac metabolism diastolic development cardiovascular diseases heart failure. Different biomarkers have been proposed predict in order identify microvascular macrovascular damage atherosclerosis, particularly metabolic disorders. also plays an important role severe COVID-19 complications patients after SARS-CoV-2 infection. In this review, we will discuss mechanisms involved dysregulation context cardiometabolic well available promising clinical practice.

Language: Английский

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Pathophysiological, immunological, and inflammatory features of long COVID

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

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Cardiovascular disease as part of Long COVID: a systematic review

European Journal of Preventive Cardiology, Journal Year: 2024, Volume and Issue: unknown

Published: Feb. 20, 2024

Long COVID syndrome has had a major impact on million patients' lives worldwide. The cardiovascular system is an important aspect of this multifaceted disease that may manifest in many ways. We have hereby performed narrative review order to identify the extent manifestations syndrome.

Language: Английский

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Early prediction of long COVID-19 syndrome persistence at 12 months after hospitalisation: a prospective observational study from Ukraine

BMJ Open, Journal Year: 2025, Volume and Issue: 15(1), P. e084311 - e084311

Published: Jan. 1, 2025

To identify the early predictors of a self-reported persistence long COVID syndrome (LCS) at 12 months after hospitalisation and to propose prognostic model its development. A combined cross-sectional prospective observational study. tertiary care hospital. 221 patients hospitalised for COVID-19 who have undergone comprehensive clinical, sonographic survey-based evaluation predischarge 1 month with subsequent 12-month follow-up. The final cohort included 166 had completed visit months. LCS discharge. Self-reported was detected in 76% participants 3 43% Patients reported incomplete recovery year were characterised by higher burden comorbidities (Charlson index 0.69±0.96 vs 0.31±0.51, p=0.001) residual pulmonary consolidations (1.56±1.78 0.98±1.56, p=0.034), worse blood pressure (BP) control (systolic BP 138.1±16.2 132.2±15.8 mm Hg, p=0.041), renal (estimated glomerular filtration rate 59.5±14.7 69.8±20.7 mL/min/1.73 m2, p=0.007) endothelial function (flow-mediated dilation brachial artery 10.4±5.4 12.4±5.6%, p=0.048), in-hospital levels liver enzymes (alanine aminotransferase (ALT) 76.3±60.8 46.3±25.3 IU/L, p=0.002) erythrocyte sedimentation (ESR) (34.3±12.1 28.3±12.6 mm/h, p=0.008), slightly indices ventricular longitudinal (left (LV) global strain (GLS) 18.0±2.4 17.0±2.3%, p=0011) Hospital Anxiety Depression Scale anxiety (7.3±4.2 5.6±3.8, p=0.011) depression scores (6.4±3.9 4.9±4.3, p=0.022) EFTER-COVID study physical symptoms score (12.3±3.8 9.2±4.2, p<0.001). At postdischarge, persisting differences marginally LV GLS, mitral E/e' ratio significantly both resting exertional versus complete recovery. Logistic regression machine learning-based binary classification models been developed predict Compared post-COVID-19 completely recovered hospital discharge, those subsequently 'very long' variety more pronounced abnormalities that mostly subsided month, except steady levels. simple artificial neural networks-based using peak ESR, creatinine, ALT weight loss during acute phase, 6-minute walk distance complex assessment as inputs has shown 92% accuracy an area under receiver-operator characteristic curve 0.931 prediction

Language: Английский

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Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 7, 2025

Abstract Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase infection, affecting approximately 10% to over 30% those infected. It presents a significant clinical challenge, notably due pronounced neurocognitive such brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing central role cerebromicrovascular dysfunction. This review investigates key pathophysiological contributing cerebrovascular dysfunction in long and their impacts on health. We discuss how endothelial tropism direct vascular trigger dysfunction, impaired neurovascular coupling, blood–brain barrier disruption, resulting compromised cerebral perfusion. Furthermore, appears induce mitochondrial enhancing oxidative stress inflammation within cells. Autoantibody formation following also potentially exacerbates injury, chronic ongoing compromise. These factors collectively contribute emergence white matter hyperintensities, promote amyloid pathology, may accelerate neurodegenerative processes, including Alzheimer’s disease. emphasizes critical advanced imaging techniques assessing health need for targeted interventions address complications. A deeper understanding essential advance treatments mitigate its long-term consequences.

Language: Английский

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Pathophysiological mechanisms of thrombosis in acute and long COVID-19

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Nov. 16, 2022

COVID-19 patients have a high incidence of thrombosis, and thromboembolic complications are associated with severe mortality. disease is hyper-inflammatory response (cytokine storm) mediated by the immune system. However, role inflammatory in thrombosis remains incompletely understood. In this review, we investigate crosstalk between inflammation context COVID-19, focusing on contributions to pathogenesis propose combined use anti-inflammatory anticoagulant therapeutics. Under conditions, interactions neutrophils platelets, platelet activation, monocyte tissue factor expression, microparticle release, phosphatidylserine (PS) externalization as well complement activation collectively involved immune-thrombosis. Inflammation results apoptosis blood cells, leading release PS cells microparticles, which significantly enhances catalytic efficiency tenase prothrombinase complexes, promotes thrombin-mediated fibrin generation local clot formation. Given risk importance antithrombotic therapies has been generally recognized, but certain deficiencies treatment gaps remain. Antiplatelet drugs not combination treatments, thus fail dampen procoagulant activity. Current treatments also do an optimal time for anticoagulation. The efficacy depends therapy initiation. best early possible after diagnosis, ideally stage disease. We elaborate mechanisms long COVID complications, including persistent inflammation, endothelial injury dysfunction, coagulation abnormalities. above-mentioned contents provide therapeutic strategies further improve patient outcomes.

Language: Английский

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Long COVID-19 Pathophysiology: What Do We Know So Far?

Microorganisms, Journal Year: 2023, Volume and Issue: 11(10), P. 2458 - 2458

Published: Sept. 30, 2023

Long COVID-19 is a recognized entity that affects millions of people worldwide. Its broad clinical symptoms include thrombotic events, brain fog, myocarditis, shortness breath, fatigue, muscle pains, and others. Due to the binding virus with ACE-2 receptors, expressed in many organs, it can potentially affect any system; however, most often cardiovascular, central nervous, respiratory, immune systems. Age, high body mass index, female sex, previous hospitalization, smoking are some its risk factors. Despite great efforts define pathophysiology, gaps remain be explained. The main mechanisms described literature involve viral persistence, hypercoagulopathy, dysregulation, autoimmunity, hyperinflammation, or combination these. exact may differ from system system, but share same pathways. This review aims describe prevalent pathophysiological pathways explaining this syndrome.

Language: Английский

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