Covid19-Sources

In this randomized, open-label, positive-controlled trial, eligible participants were allocated to four cohorts: Cohort #1, Cohort #2, Cohort #3, and Cohort #4. Prior to allocation, participants in Cohort #1 and Cohort #2 had received two doses of the inactivated vaccine BBIBP-CorV; those in Cohort #3 had received three doses of the inactivated vaccine BBIBP-CorV; and those in Cohort #4 had received three doses of the recombinant protein vaccine ZF2001. During the trial, participants in Cohort #1 were administered a single dose of the inactivated vaccine BBIBP-CorV, whereas participants in the other cohorts received a single dose of the bivalent recombinant protein vaccine ZF2202. Immunogenicity against Delta, BA.2, and BA.5 subvariants was assessed on day 14 post-vaccination. Results A total of 272 participants were enrolled and allocated to Cohort #1 (N=61), Cohort #2 (N=61), Cohort #3 (N=75), and Cohort #4 (N=75). On day 14 post-vaccination, the geometric mean titers (GMTs) of neutralizing antibodies against the Delta variant increased 14.9-fold, 98.8-fold, 25.8-fold, and 62.8-fold, respectively, across these cohorts. For the BA.2 subvariant, the GMTs increased 6.1, 38.5, 32.7, and 100.1 times, respectively. For the BA.5 subvariant, the GMTs increased 2.7, 14.2, 15.2, and 28.1 times, respectively. Within 28 days after vaccination, the incidences of adverse reactions were 41.7%, 31.2%, 37.3%, and 57.3%, respectively. No serious adverse event and adverse event resulted in withdrawal or death occurred.

This study aimed to explore variations of brain functional connectivity patterns among post-COVID-19 patients with different outcomes of sleep quality. Methods Post-COVID-19 patients were prospectively enrolled and categorized into improvement or deterioration groups based on changes in sleep quality after a three-month follow-up. Functional MRI and blood samples were collected, while a battery of assessments was administered to evaluate sleep quality, mental status, and cognition. Baseline and follow-up data were compared to identify post-infection alterations. Brain functional networks and graph theory analysis were employed to derive network properties, with subsequent investigation into the correlation between these properties, sleep and psychological assessment scores, and blood test outcomes. Results The graph theory analysis revealed a significantly increase in global efficiency (Eglob) and local efficiency (Eloc), and a decrease in λ, in the improvement group. A notable enhancement of frontoparietal network (FPN) were observed. The deterioration group exhibited a significant increase in Eloc and λ, along with a decrease in Eglob. Furthermore, the deterioration group demonstrated a lower level of Eglob at follow-up. With respect to network strength, all networks except FPN showed significantly higher values in the improvement group. Pittsburgh Sleep Quality Index and Self-Rating Anxiety Scale scores differed between two groups. Conclusion Changes in sleep quality following COVID-19 infection are associated with brain functional connectivity patterns. Decreased Eglob is related to worsened sleep quality. The normalized strength of FPN serves as a key indicator for improved sleep quality, while other networks also play roles in regulating sleep quality.

Aims This study aimed to explore the epidemiological circumstances, long-term clinical outcomes, and perceived impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on elite athletes’ sports performance. A secondary objective was to determine the sports-specific (contact vs. noncontact) prevalence of SARS-CoV‑2 among 65 SARS-CoV-2-positive athletes from the Olympic Training Center Rhineland (OSP; n = 599). Methods In all, 65 SARS-CoV-2-positive athletes from the German Olympic Training Center (OSP; 66% males—age: 23 ± 4 years; 34% females—age: 23 ± 5 years) participated in the panel study. Data collection occurred between June 2020 and October 2021 at two test times (t0: after a negative polymerase chain reaction [PCR] test, t1: 16 weeks after t0) through questionnaires and clinical assessments. Results The SARS-CoV‑2 prevalence was nearly identical in noncontact and contact-sport athletes (10.8% vs. 11.3%); 37% experienced symptoms lasting  4 weeks. Over 50% of athletes paused their training for 4–8 weeks. At t1, 40% still experienced reduced perceived performance capacity (PPC) compared to their pre-COVID-19 level, while 64% reported ongoing limitations in sports participation, with mental and physical fatigue as the most prominent limiting factor, followed by shortness of breath and joint and muscle pain. Conclusion The long-term management of SARS-CoV-2-positive elite athletes should involve a comprehensive, multidimensional psychophysiological approach to address persistent sport-restricting symptoms. This approach will assist in developing tailored training protocols that allow a gradual increase in intensity and volume.

This case-control study among US children estimates the association of mRNA COVID-19 vaccination with likelihood of post–COVID-19 condition.

Increased risks of death and hospitalisation for organ disorders after discharge for COVID-19 hospitalisation have been reported but their persistence is unknown. Methods We conducted a nationwide cohort study using the French claims database; subjects hospitalised for COVID-19 between 2020/01/01 and 2020/08/30 were followed up to 30-months and matched to controls from the general population (GP) not hospitalised for COVID-19 during this period. Outcomes were all-cause mortality and organ disorders-related hospitalisation identified using ICD-10 codes. Cumulative incidences were estimated using the Kaplan-Meier method. Incidence rate ratios (IRR) were estimated such as the adjusted sub-distribution hazard ratio on 6-month periods during the follow-up using Cox regressions. Results 63,990 COVID-19 subjects (mean age (SD) 65 years (18), 53.1% male) were matched to 319,891 controls. The weighted cumulative incidences of all-cause mortality and all-cause hospitalisation were 5,218/105 person-years (PY) [95%CI 5,127; 5,305] and 16,334/105 PY [16,162; 16,664] among COVID-19 subjects and 4,013/105 [3,960; 4,047] and 12,095/105 PY [12,024; 12,197] among controls, respectively. COVID-19 subjects were more likely to be hospitalised for cardiovascular (IRR 1.22 [1.15; 1.29]), psychiatric (IRR 1.41 [1.29; 1.53]), neurological (IRR 1.50 [1.41; 1.61]), and respiratory events (IRR 1.99 [1.87; 2.12]). The excess risk strongly decreased after the first 6 months for all outcomes but remained significantly increased up to 30-month for neurological, respiratory disorders, chronic renal failure and diabetes. Conclusions COVID-19 hospitalised subjects were at increased risk of death or hospitalisation for various organ disorders up to 30 months after discharge, reflecting the multi-organ consequences of the disease.

The SARS-CoV-2 pandemic has taught important lessons about the central role of virus-specific CD8+ T cells in mediating antiviral immunity, both during natural infection and following vaccination. In contrast to antibodies, which primarily prevent viral entry, CD8+ T cells exert antiviral functions by recognizing viral peptides presented on infected cells, allowing them to directly kill the virus-infected cells and prevent further viral spread. This is particularly important for individuals with reduced or absent humoral responses. Indeed, virus-specific CD8+ T cell responses induced by infection are associated with improved survival and thus, with a protective role, in immunosuppressed individuals, who have deficient humoral and B cell immunity (1). The protective role of CD8+ T cells during viral infection has further been demonstrated in preclinical models where depletion of CD8+ T cells abrogated viral control and CD8+ T cell transfer improved viral control (2). Moreover, CD8+ T cells have been suggested to play a significant role in the control of emerging viral variants. CD8+ T cells target a broad range of epitopes from both structural and nonstructural proteins of the virus, which are often conserved across different strains (3–5). The breadth of the CD8+ T cell response together with the high level of conservation enables virus-specific CD8+ T cells to cross-recognize various viral variants (4–7), thereby mitigating the impact of mutations that may arise over time. Consequently, a robust CD8+ T cell response can be crucial in maintaining immunity and preventing severe disease, even in the face of viral evolution. Infection- and vaccine-induced CD8+ T cell responses are stable over time and are rapidly reactivated in case of reinfection, hence exhibiting robust memory responses that contribute to long-lasting immunity (8, 9). However, despite these beneficial effects, CD8+ T cells have also been implicated in the pathogenesis of severe COVID-19. They may be involved indirectly by an insufficient ability to limit viral replication and spread or directly through nonspecific effector functions that lead to the killing of uninfected cells and tissue damage. In this minireview, we highlight some of the key features of SARS-CoV-2-specific CD8+ T cell immunity during natural infection and after vaccination that contribute to both viral control and disease pathogenesis.

Localized surface plasmon resonance (LSPR) is an optical phenomenon derived from the dielectric properties of noble metals, resulting in a highly change-sensitive spectrum that can be used on a sensor platform. We have used gold nanorods to develop a diagnostic assay to detect antibodies against the nucleocapsid (N) protein of SARS-CoV-2. This approach is particularly valuable, considering the limited role of serology in recognizing acute infections. Gold nanoparticles were coated with the recombinant N protein and characterized by spectroscopy, fluorometry, and electron microscopy. Positive and negative COVID-19 sera samples were initially categorized through qRT-PCR and further validated using an anti-IgG ELISA. The nanosensor was accurate and able to detect very low levels of anti-SARS-CoV-2 antibodies derived from different virus variants early in infection (before 10 days post-infection). The nanoplatform exhibited high sensitivity and specificity, is suitable for mass production, and has easy implementation and automatic read-out.

COVID19 presented an unprecedented challenge for modern science/medicine. Faced with a novel infectious disease, doctors, scientists, and health officials rose to the challenge in remarkable speed.…

medRxiv - The Preprint Server for Health Sciences

Among participants followed up to 3 years after initial infection, those with current Long COVID had worse physical and mental health outcomes. The majority of those with Long COVID did not resolve, with less than 2% having resolved Long COVID. The resolved Long COVID cohort had moderately worse physical and mental health compared with those never-having-Long COVID. COVID-19 vaccination was associated with better outcomes.

This cohort study assesses the severity and long-term mortality of COVID-19, influenza, and respiratory syncytial virus in a large cohort of nonhospitalized veterans.

Among 5 899 170 individuals, COVID-19 admissions (n=24 400) were more frequent than influenza admissions (n=8385; aIRR 2·04 [95% CI 1·38–3·02]), particularly during the first year (May, 2022, to May, 2023) versus the second year (May, 2023, to June, 2024; p=0·0096), in the summer versus the winter (p0·0001), and among people aged 65 years or older versus younger than 65 years (p0·0001). The number of deaths was also higher for patients with COVID-19 (n=2361) than patients with influenza (n=489, aIRR 3·19 [95% CI 2·24–4·53]). Among patients admitted in the winter (n=19 286), the risk of mortality from COVID-19 was higher than for influenza (aRR 1·23 [95% CI 1·08–1·37]), particularly among those without COVID-19 and influenza vaccination (1·36 [1·05–1·67]), with comorbidities (1·27 [1·11–1·43]), and who were male (1·36 [1·14–1·59]).

Medical News: A team of researchers from the University of Iowa-USA has made significant discoveries about how certain lung cells survive acute SARS-CoV-2 infection and play a role in both inflammation and lung regeneration. Their findings provide a new understanding of the aftermath of severe COVID-19 cases, particularly how the body recovers and why some patients experience long-term symptoms. T...

DMZ – POLITIK / WISSEN / GESUNDHEIT ¦ AA ¦ Der Beitrag im "Pandemic Accountability Index" (Pandemie-Verantwortlichkeitsindex) vom letzten November, in dem über hundert Studien und Artikel zu den Auswirkungen des SARS-CoV-2-Virus auf den Körper berichtet wurde, ist mittlerweile über sechs Monate alt. Seitdem wurden weitere Forschungsergebnisse veröffentlicht. Es ist daher an der Zeit, unser Verständnis dafür zu aktualisieren, warum es so wichtig ist, Infektionen mit diesem gefährlichen und behindernden Virus zu verhindern. Laut der Weltgesundheitsorganisation (WHO) leiden allein in Europa über 36 Millionen Menschen an Langzeitfolgen von COVID, einem Oberbegriff für zahlreiche medizinische Komplikationen. Diejenigen, die behauptet haben, dass SARS-CoV-2 relativ harmlos oder "mild" sei und COVID-19 "nur eine Erkältung/Grippe" sei, müssen sich mit der ständig wachsenden Anzahl wissenschaftlicher Forschungsergebnisse auseinandersetzen, die seitdem veröffentlicht wurden. Kinder und COVID: COVID-19 ist eine der häufigsten Todesursachen bei Kindern und Jugendlichen in den USA (University of Oxford). Anstieg von Diabetes bei Kindern und Jugendlichen (Jama Network). Auch milde Infektionen können zu langfristigen Folgen führen, einschließlich Long-COVID (University of Minnesota). Mehr als 70% der Haushaltsübertragungen von COVID in den USA gehen von Kindern aus (CIDRAP). Kinder können nach einer asymptomatischen oder milden COVID-19-Erkrankung langfristige Herzmuskeldeformationen entwickeln (MDPI Open Access Journals). Langzeitfolgen bei Jugendlichen und jungen Erwachsenen nach mildem COVID-19 (Frontiers in Immunology). Einige Kinder zeigen nach einer COVID-19-Infektion Symptome wie Fieber, Erbrechen und Augenschmerzen (NHK). COVID-19 kann bei Kindern autoimmune Reaktionen auslösen (HCPLive). Erhöhte Raten von Asthma, Myokarditis, Diabetes und anderen Erkrankungen bei Kindern mit bestätigtem COVID-19 (Medical Journal of Australia). Über 30% der Kinder zeigen auch nach 2 Monaten noch Symptome, und 2,3% haben nach 6 Monaten immer noch anhaltende Symptome (Frontiers in Pediatrics). Das Immunsystem von Kindern entwickelt keine "adaptiven" Erinnerungen, die vor einer erneuten SARS-CoV-2-Infektion schützen (Garvan Institute of Medical Research). Die Prävalenz von Langzeitfolgen bei COVID-19 liegt bei 23,36% (ScienceDirect). Die Omikron-Variante verursacht siebenmal mehr Todesfälle bei hospitalisierten Kindern als die Influenza (South China Morning Post). In Ohio haben zwischen 30.000 und 70.000 Kinder Long COVID (US News). COVID-19 kann zu Herzerkrankungen bei Kindern führen (MDPI Open Access Journals). Entzündliche Erkrankungen bei Kindern nach COVID-19 (ScienceDirect). Neurologische Komplikationen nach COVID-19 bei Kindern (American Academy of Pediatrics). Augenmanifestationen von COVID-19 bei Kindern (SageJournals). Beeinträchtigungen der Gesundheit bei Kindern und Jugendlichen nach einer COVID-19-Erkrankung (American Academy of Pediatrics). Nahezu alle mit COVID-19 infizierten Kinder zeigen Anzeichen von Schädigung der Blutgefäße (Blood Advances). Eine Studie zeigt, dass vorherige COVID-19-Infektionen mit einem signifikant erhöhten Risiko für RSV-Infektionen bei Kindern in Verbindung gebracht werden (medRxiv). Zwischen 12 und 16% der Kinder und Jugendlichen, die mit Omikron infiziert waren, erfüllen die Definition von Long COVID (Journal of Pediatrics). Diabetes-Typ-1-Inzidenz und -Risiko bei Kindern mit einer COVID-19-Diagnose (Jama Network). Prävalenz von Long COVID bei Kindern und Jugendlichen beträgt 25,24%, am häufigsten mit Stimmungssymptomen (Nature). Ungewöhnlicher Anstieg von Hirnabszessen bei amerikanischen Kindern (CDC). Veränderte Verformung der roten Blutkörperchen bei Kindern und Jugendlichen nach SARS-CoV-2-Infektion (Nature). Kinder haben ein ähnliches Risiko für Langzeitfolgen von Long COVID bei einer erneuten Infektion wie bei der Erstinfektion (Journal of Pediatrics). SARS-CoV-2 kann sich über Wochen bis Monate systemisch ausbreiten und persistieren, unabhängig von der Schwere der Erkrankung (Lancet). Originallinks: COVID-19 is a leading cause of death in children and young people in the US (University of Oxford) Surge in child and teen diabetes (Jama Network) “Two US studies describe pediatric COVID...7.0% of hospitalized children developed neurologic complications such as seizures...even mild infections can lead to long COVID.” (University of Minnesota) More than 70% of US household COVID spread started with a child (CIDRAP) "Persistence of LV myocardial deformation abnormalities in previously healthy children with an asymptomatic or mildly symptomatic COVID-19 course after an average follow-up of 148 ± 68 days.” (MDPI Open Access Journals) “Inflammatory markers and pulmonary function in adolescents and young adults 6 months after mild COVID-19” (Frontiers in Immunology) “Fever, vomiting, and eye pain are a few of the symptoms afflicting a small number of children after they have been infected with COVID-19.” (NHK) COVID-19 May Trigger Autoimmune Responses in Children (HCPLive) “…increased rates of asthma, myocarditis and cardiomyopathy, cardiac dysrhythmias, diabetes, renal failure, venous thromboembolism, and coagulation disorders in children with laboratory‐confirmed COVID‐19 compared with children without COVID‐19.” (Medical Journal of Australia) “32.6% of the children had persistent symptoms at 2 months, 9.3% at 4 months, and 2.3% at 6 months” (Frontiers in Pediatrics) Children’s immune systems do not develop ‘adaptive’ memory to protect against second time SARS-CoV-2 infection (Garvan Institute of Medical Research) Based on 40 studies with 12,424 individuals, the pooled prevalence of any long COVID was 23.36 % (ScienceDirect) “Omicron strain causes 7 times more deaths among hospitalised children than influenza” (South China Morning Post) “In Ohio, between 30,000 and 70,000 children have long COVID.” (US News) COVID-19 Heart Lesions in Children: Clinical, Diagnostic and Immunological Changes (MDPI Open Access Journals) Multisystem inflammatory syndrome in children: A dysregulated autoimmune disorder following COVID-19 (ScienceDirect) COVID-19 and Acute Neurologic Complications in Children (American Academy of Pediatrics) Ocular manifestations of COVID-19 in pediatric patients (SageJournals) Health Impairments in Children and Adolescents After Hospitalization for Acute COVID-19 or MIS-C (American Academy of Pediatrics) "Virtually all children infected with COVID-19 show signs of blood vessel damage" (Blood Advances) "Findings from our study support that prior COVID-19 infection was associated with a significantly increased risk for RSV infection and was a driving force for the 2022 surge of severe pediatric RSV cases in the US." (medRxiv) “12-16% children and youth infected with Omicron met the research definition of #LongCovid at 3 and 6 months after infection, with no evidence of difference between cases of first-positive and reinfection” (Journal of Pediatrics) Type 1 Diabetes Incidence and Risk in Children With a Diagnosis of COVID-19 (Jama Network) Long-COVID in children and adolescents: prevalence of long-COVID was 25.24%, most prevalent clinical: mood symptoms (16.50%) - (Nature) Abnormal Surge of Brain Abscesses in American Children, CDC Says (ScienceAlert) Increased red blood cell deformation in children and adolescents after SARS-CoV-2 infection (Nature) Children are at as much risk of Long COVID disability from reinfection as they are from primary infection (Journal of Pediatrics) “in children, independent from disease severity, SARS-CoV-2 can spread systemically and persist for weeks to months.” (Lancet) NEUROLOGISCHE BEEINTRÄCHTIGUNGEN: Geruchs- und Geschmacksstörungen nach COVID-19 (BMJ). Neuropsychologische Defizite bei Patienten mit anhaltenden COVID-19-Symptomen (Nature). Neuroinflammation nach COVID-19 mit anhaltenden depressiven und kognitiven Symptomen (JAMA Psychiatry). SARS-CoV-2 fördert die Beseitigung synaptischer Verbindungen durch Mikrogliazellen im menschlichen Gehirn (Nature). Langfristige Auswirkungen von COVID-19 auf kognitive Funktionen bis zu 6 Monate nach der Entlassung: Rolle von Depressionen und Auswirkungen auf die Lebensqualität (Springer Link). SARS-CoV-2 ist mit Veränderungen der Gehirnstruktur verbunden (Nature). Jeder vierte Patient zeigt kognitive Defizite nach einem milden COVID-19-Verlauf (NIH). Neurokognitive und psychiatrische Symptome nach COVID-19-Infektion: Nachweise aus Labor- und Bevölkerungsstudien (ScienceDirect). COVID-19 und kognitive Beeinträchtigungen: Neuroinvasive und Blut-Hirn-Schrankenstörungen (Journal of Neuroinflammation). COVID-19 kann dazu führen, dass Gehirnzellen abnormal fusionieren und Beeinträchtigungen der Gehirnfunktion verursachen, bei 10% der untersuchten Fälle kommt die neuronale Aktivität vollständig zum Stillstand (ScienceAdvances). COVID-19 kann auch durch Hyperaktivierung der Immunantwort, Zelltod oder Entzündungen verschiedene Hirnregionen beeinträchtigen und zu Gedächtnisstörungen führen (CIDRAP). Rasche Verschlechterung der Demenz nach COVID-19 (NIH). Originallinks: Smell and taste dysfunction after covid-19 (BMJ) Neuropsychological deficits in patients with persistent COVID-19 symptoms (Nature) Neuroinflammation After COVID-19 With Persistent Depressive and Cognitive Symptoms (JAMA Psychiatry) SARS-CoV-2 promotes microglial synapse elimination in human brain organoids (Nature) Long-term consequences of COVID-19 on cognitive functioning up to 6 months after discharge: role of depression and impact on quality of life (Springer Link) SARS-CoV-2 is associated with changes in brain structure (Nature) 1 in 4 Showing Cognitive Deficits After Mild Case (NIH) Neurocognitive and psychiatric symptoms following infection with COVID-19: Evidence from laboratory and population studies (ScienceDirect) COVID-19 and cognitive impairment: neuroinvasive and blood‒brain barrier dysfunction (Journal of Neuroinflammation) Covid cause...

Ibargüen-González, Heller et al. analyze plasma levels of pancreatic enzymes and inflammatory markers in a retrospective cohort study of 120 COVID-19 patients. Host factor PLAC8 is found to be required for SARS-CoV-2 pancreatic infection.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shown diverse life-threatening effects, most of which are considered short-term. In addition to its short-term effects, which has claimed many millions of lives since 2019, the long-term complications of this virus are still under investigation. Similar to many oncogenic viruses, it has been hypothesized that SARS-CoV-2 employs various strategies to cause cancer in different organs. These include leveraging the renin angiotensin system, altering tumor suppressing pathways by means of its nonstructural proteins, and triggering inflammatory cascades by enhancing cytokine production in the form of a “cytokine storm” paving the way for the emergence of cancer stem cells in target organs. Since infection with SARS-CoV-2 occurs in several organs either directly or indirectly, it is expected that cancer stem cells may develop in multiple organs. Thus, we have reviewed the impact of coronavirus disease 2019 (COVID-19) on the vulnerability and susceptibility of specific organs to cancer development. It is important to note that the cancer-related effects of SARS-CoV-2 proposed in this article are based on the ability of the virus and its proteins to cause cancer but that the long-term consequences of this infection will only be illustrated in the long run.

Blood biomarkers in a middle-aged population suggest that SARS-CoV-2 infection is associated with greater brain β-amyloid plaque accumulation.

COVID-19, even in mild cases, is linked to changes in Alzheimer’s disease-related brain biomarkers comparable to four years of aging. This study raises concerns about long-term neurological risks and cognitive decline post-COVID.

Two distinct patterns in the protective effect of natural infection against reinfection in the Omicron variant versus pre-Omicron eras show that SARS-CoV-2 immune protection is shaped by dynamic interaction between host immunity and viral evolution.

Medical News: In the ongoing exploration of COVID-19’s far-reaching impacts on human health, researchers have uncovered a significant connection between the virus and reversible cerebral vasoconstriction syndrome (RCVS), a condition marked by temporary constriction of blood vessels in the brain. While RCVS is not a new medical phenomenon, its association with COVID-19 infection has only rece...

Medical News: Understanding the Threat of Nontuberculous Mycobacteria Nontuberculous mycobacteria (NTM) infections have been increasingly recognized as a major health concern, particularly in developed countries such as the United States. Unlike Mycobacterium tuberculosis, which causes tuberculosis (TB), NTM is commonly found in natural environments like soil, water, and food. While most people a...

One lingering effect of the COVID-19 pandemic created by SARS-CoV-2 is the emergence of Long COVID (LC), characterized by enduring neurological sequelae affecting a significant portion of survivors. This review provides a thorough analysis of these neurological disruptions with respect to cognitive dysfunction, which broadly manifest as chronic insomnia, fatigue, mood dysregulation, and cognitive impairments with respect to cognitive dysfunction. Furthermore, we characterize how diagnostic tools such as PET, MRI, EEG, and ultrasonography provide critical insight into subtle neurological anomalies that may mechanistically explain the Long COVID disease phenotype. In this review, we explore the mechanistic hypotheses of these neurological changes, which describe CNS invasion, neuroinflammation, blood-brain barrier disruption, and gut-brain axis dysregulation, along with the novel vascular disruption hypothesis that highlights endothelial dysfunction and hypoperfusion as a core underlying mechanism. We lastly evaluate the clinical treatment landscape, scrutinizing the efficacy of various therapeutic strategies ranging from antivirals to anti-inflammatory agents in mitigating the multifaceted symptoms of LC.

The COVID-19 pandemic has caused numerous deaths worldwide. Despite the mitigation of infection manifestations in recent months, the possible conseque…

Background COVID-19 is a disease that affects multiple organs and is believed to have an impact on the function of the heart muscle. Initial findings from hospitalized COVID-19 patients indicate the presence of myocardial injury characterized by increased levels of high-sensitive troponin. The causes of myocardial damage are diverse and not completely comprehended. Methods A three-dimensional echocardiogram (3DE) accurately measures the volume of the left ventricle (LV) and its function, both globally and regionally. It eliminates the subjective nature of two-dimensional echocardiography (2DE) when evaluating irregularities in the movement of the LV walls. This study sought to assess the left ventricular systolic function in 150 individuals who had recovered from COVID-19 and were experiencing post-COVID symptoms such as dyspnea, palpitation, or chest discomfort using 3DE. Results Our investigation revealed a notable statistical correlation (p-value of  0.001) between patients who had post-COVID-19 syndrome and reported enduring symptoms such as shortness of breath, or chest discomfort, and various 3D echocardiographic strain patterns (the mean GLS% in the cases group was − 16.06 ± 4.36, whereas in the control group it was − 17.9 ± 2.57). Subclinical myocardial dysfunction, as shown by a decrease in left ventricular global longitudinal strain (LV-GLS), is common in over 85% of patients with post-COVID-19 syndrome. However, more commonly observed indicators of left ventricular (LV) function, such as lower ejection fraction (EF) and anomalies in wall motion, were less frequently found. Conclusion Our study findings suggest that persons who developed symptoms such as difficulty breathing, rapid heartbeat, or chest pain following their recovery from COVID-19 exhibited a reduction in left ventricular global longitudinal strain (LV-GLS) as measured by three-dimensional echocardiography (3DE). Ongoing research is focused on determining the mechanism of heart damage in COVID-19 infection.

Now 6 Ongoing Clinical Trials in the United States