Abstract 10712: Mrna COVID Vaccines Dramatically Increase Endothelial Inflammatory Markers and ACS Risk as Measured by the PULS Cardiac Test: a Warning

Authors: Steven R Gundry Originally published 8 Nov 2021Circulation. 2021;144:A10712

Abstract

Our group has been using the PLUS Cardiac Test (GD Biosciences, Inc, Irvine, CA) a clinically validated measurement of multiple protein biomarkers which generates a score predicting the 5 yr risk (percentage chance) of a new Acute Coronary Syndrome (ACS). The score is based on changes from the norm of multiple protein biomarkers including IL-16, a proinflammatory cytokine, soluble Fas, an inducer of apoptosis, and Hepatocyte Growth Factor (HGF)which serves as a marker for chemotaxis of T-cells into epithelium and cardiac tissue, among other markers. Elevation above the norm increases the PULS score, while decreases below the norm lowers the PULS score.The score has been measured every 3-6 months in our patient population for 8 years. Recently, with the advent of the mRNA COVID 19 vaccines (vac) by Moderna and Pfizer, dramatic changes in the PULS score became apparent in most patients.This report summarizes those results. A total of 566 pts, aged 28 to 97, M:F ratio 1:1 seen in a preventive cardiology practice had a new PULS test drawn from 2 to 10 weeks following the 2nd COVID shot and was compared to the previous PULS score drawn 3 to 5 months previously pre- shot. Baseline IL-16 increased from 35=/-20 above the norm to 82 =/- 75 above the norm post-vac; sFas increased from 22+/- 15 above the norm to 46=/-24 above the norm post-vac; HGF increased from 42+/-12 above the norm to 86+/-31 above the norm post-vac. These changes resulted in an increase of the PULS score from 11% 5 yr ACS risk to 25% 5 yr ACS risk. At the time of this report, these changes persist for at least 2.5 months post second dose of vac.We conclude that the mRNA vacs dramatically increase inflammation on the endothelium and T cell infiltration of cardiac muscle and may account for the observations of increased thrombosis, cardiomyopathy, and other vascular events following vaccination.

Footnotes

Author Disclosures: For author disclosure information, please visit the AHA Scientific Sessions 2021 Online Program Planner and search for the abstract title.

Study Finds Teenage Boys Six Times More Likely To Suffer Heart Problems From Vaccine Than Be Hospitalized by COVID

Authors; Paul Joseph Watson via Summit News,

Research conducted by the University of California has found that teenage boys are six times more likely to suffer from heart problems caused by the COVID-19 vaccine than to be hospitalized as a result of COVID-19 itself.

“A team led by Dr Tracy Hoeg at the University of California investigated the rate of cardiac myocarditis – heart inflammation – and chest pain in children aged 12-17 following their second dose of the vaccine,” reports the Telegraph.

“They then compared this with the likelihood of children needing hospital treatment owing to Covid-19, at times of low, moderate and high rates of hospitalisation.”

Researchers found that the risk of heart complications for boys aged 12-15 following the vaccine was 162.2 per million, which was the highest out of all the groups they looked at.

This compares to the risk of a healthy boy being hospitalized as a result of a COVID infection, which is around 26.7 per million, meaning the risk they face from the vaccine is 6.1 times higher.

Even during high risk rates of COVID, such as in January this year, the threat posed by the vaccine is 4.3 times higher, while during low risk rates, the risk of teenage boys suffering a “cardiac adverse event” from the vaccine is a whopping 22.8 times higher.

The research data was based on a study of adverse reactions suffered by teens between January and June this year.

In a sane world, such data should represent the nail in the coffin for the argument that teenagers and children should be mandated to take the coronavirus vaccine, but it obviously won’t.

In the UK, the government is pushing to vaccinate 12-15-year-olds, even without parental consent, despite the Joint Committee on Vaccination and Immunisation (JCVI) advising against it.

Meanwhile, in America, Los Angeles County school officials voted unanimously to mandate COVID shots for all

Covid-19 Vaccine Analysis: The most common adverse events reported so far

Authors: DATED: AUGUST 6, 2021 BY SHARYL ATTKISSON 

As of July 19, 2021 there were 419,513 adverse event reports associated with Covid-19 vaccination in the U.S., with a total of 1,814,326 symptoms reported. That’s according to the federal Vaccine Adverse Event Reporting System (VAERS) database.

Report an adverse event after vaccination online here.

Each symptom reported does not necessarily equal one patient. Adverse event reports often include multiple symptoms for a single patient.

Reporting of illnesses and symptoms that occur after Covid-19 vaccination does not necessarily mean they were caused by the vaccine. The system is designed to collect adverse events that occur after vaccination to uncover any patterns of illnesses that were not captured during vaccine studies.

Read CDC info on Covid-19 vaccine here.

Scientists have estimated that adverse events occur at a rate many fold higher than what is reported in VAERS, since it is assumed that most adverse events are not reported through the tracking system. Reports can be made by doctors, patients or family members and/or acquaintances, or vaccine industry representatives. 

Read: Exclusive summary: Covid-19 vaccine concerns.

Some observers claim Covid-19 vaccine adverse events are not as likely to be underreported as those associated with other medicine, due to close monitoring and widespread publicity surrounding Covid-19 vaccination.

Approximately 340 million doses of Covid-19 vaccine have been given in the U.S. Slightly less than half of the U.S. population is fully vaccinated.

According to the Centers for Disease Control (CDC) and Food and Drug Administration (FDA), the benefits of Covid-19 vaccine outweigh the risks for all groups and age categories authorized to receive it.

Watch: CDC disinformation re: studies on Covid-19 vaccine effectiveness in people who have had Covid-19.

The following is a summary of some of the most frequent adverse events reported to VAERS after Covid-19 vaccination. (It is not the entire list.)

Most common Covid-19 vaccine adverse events reported as of July 19, 2021

Yellow highlighted adverse events are subjects of investigations, warnings or stated concerns by public health officials. For details, click here.

128,370 Muscle, bone, joint pain and swelling including:

  • 39,902 Pain in extremity
  • 37,819 Myalgia, muscle pain, weakness, fatigue, spasms, disorders, related
  • 30,138 Arthralgia, joint pain or arthritis, swelling, joint disease, bone pain, spinal osteoarthritis
  • 14,682 Back pain, neck pain
  • 5,829 Muscle and skeletal pain, stiffness, weakness

119,866 Injection site pain, bleeding, hardening, bruising, etc.

105,332 Skin reddening, at injection site or elsewhere, rash, hives

100,564 Fatigue, lethargy, malaise, asthenia, abnormal weakness, loss of energy

89,302 Headache, incl. migraine, sinus

68,252 Vomiting, nausea

68,064 Fever

63,133 Chills

60,913 Pain

49,574 Dizziness

34,076 Flushing, hot flush, feeling hot, abnormally warm skin

31,785 Lung pain or abnormalities, fluid in lung, respiratory tract or lung congestion or infection, wheezing, acute respiratory failure including:

  • 23,005 Dyspnoea, difficulty breathing
  • 1,398 Pneumonia
  • 1,128 Respiratory arrest, failure, stopped or inefficient breathing, abnormal breathing
  • 563 Covid-19 pneumonia
  • 265 Mechanical ventilation
  • 217 Bronchitis

30,909 Skin swelling, pain, tightness, face swelling, swelling under skin, hives, angioedema including:

  • 7,579 Skin pain, sensitivity, burning, discoloration, tenderness

25,319 Heart failure, heart rhythm and rate abnormalities, atrial fibrillation, palpitations, flutter, murmur, pacemaker added, fluid in heart, abnormal echocardiogram including:

  • 3,105 Heart attack or cardiac arrest, sudden loss of blood flow from failure to pump to heart effectively, cardiac failure, disorder

22,085 Itchiness

29,861 Sensory disturbance including:

  • 8,236 Tinnitus, hearing noise
  • 7,951 Abnormal vision, blindness
  • 6,349 Ageusia, loss of taste, altered taste, disorders
  • 2,249 Anosmia, loss of smell, parosmia (rotten smell)
  • 2,075 Hypersensitivity
  • 1,560 Sensitivity or reaction to light 
  • 890 Hearing loss, deafness

Pathophysiology of COVID-19:

Mechanisms Underlying Disease Severity and Progression

Authors: Mary Kathryn Bohn,1,2, Alexandra Hall,1 Lusia Sepiashvili,1,2, Benjamin Jung,1,2 Shannon, Steele,1 and Khosrow Adeli1,2,3

The global epidemiology of coronavirus disease 2019 (COVID-19) suggests a wide spectrum of clinical severity, ranging from asymptomatic to fatal. Although the clinical and laboratory characteristics of COVID-19 patients have been well characterized, the pathophysiological mechanisms underlying disease severity and progression remain unclear. This review highlights key mechanisms that have been proposed to contribute to COVID-19 progression from viral entry to multisystem organ failure, as well as the central role of the immune response in successful viral clearance or progression to death.

Introduction

Coronavirus disease 2019 (COVID-19) is caused by a novel beta-coronavirus known as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). As of June 15, 2020, the number of global confirmed cases has surpassed 8 million, with over 400,000 reported mortalities. The unparalleled pathogenicity and global impact of this pandemic has rapidly engaged the scientific community in urgently needed research. Preliminary reports from the Chinese Center for Disease Control and Prevention have estimated that the large majority of confirmed SARS-CoV-2 cases are mild (81%), with ~14% progressing to severe pneumonia and 5% developing acute respiratory distress syndrome (ARDS), sepsis, and/or multisystem organ failure (MOF) (144). Although more data is urgently needed to elucidate the global epidemiology of COVID-19 (80), a wide spectrum of clinical severity is evident, with most patients able to mount a sufficient and appropriate immune response, ultimately leading to viral clearance and case resolution. However, a significant subset of patients present with severe clinical manifestations, requiring life-supporting treatment (51). The pathophysiological mechanisms behind key events in the progression from mild to severe disease remain unclear, warranting further investigation to inform therapeutic decisions. Here, we review the current literature and summarize key proposed mechanisms of COVID-19 pathophysiological progression (FIGURE 1). Key Pathophysiological Mechanisms: Our Current Understanding Viral Invasion The first step in COVID-19 pathogenesis is viral invasion via its target host cell receptors. SARSCoV-2 viral entry has been described in detail elsewhere (138). In brief, SARS-CoV-2 consists of four main structural glycoproteins: spike (S), membrane (M), envelope (E), and nucleocapsid (N). The M, E, and N proteins are critical for viral particle assembly and release, whereas the S protein is responsible for viral binding and entry into host cells (33, 76, 89, 143, 148). Similar to SARS-CoV, several researchers have identified human angiotensin converting enzyme 2 (ACE2) as an entry receptor for SARS-CoV-2 (75, 99, 148, 156). SARSCoV-2 is mostly transmissible through large respiratory droplets, directly infecting cells of the upper and lower respiratory tract, especially nasal ciliated and alveolar epithelial cells (161). In addition to the lungs, ACE2 is also expressed in various other human tissues, such as the small intestine, kidneys, heart, thyroid, testis, and adipose tissue, indicating the virus may directly infect cells of other organ systems when viremia is present (77). Interestingly, although the S proteins of SARS-CoV-2 and SARSCoV share 72% homology in amino acid sequences, SARS-CoV-2 has been reported to have a higher affinity for the ACE2 receptor (18, 21, 143). Following host cell binding, viral and cell membranes fuse, enabling the virus to enter into the cell (89). For many coronaviruses, including SARS-CoV, host cell binding alone is insufficient to facilitate membrane fusion, requiring S-protein priming or cleavage by host cell proteases or transmembrane serine proteases (9, 10, 90, 94, 108). Indeed, Hoffman and colleagues demonstrated that S-protein priming by transmembrane serine protease 2 (TMPRSS2), which may be substituted by cathepsin B/L, is required to facilitate SARS-CoV-2 entry into host cells (58). In addition, unlike other coronaviruses, SARS-CoV-2 has been reported to possess a furin-like cleavage site in the S-protein domain, located between the S1 and S2 subunits (31, 138). Furin-like proteases are ubiquitously expressed, albeit at low levels, indicating that S-protein priming at this cleavage site may contribute to the widened cell tropism and enhanced transmissibility of SARS-CoV-2 (123). However, whether furin-like protease-mediated cleavage is required for SARS-CoV-2 host entry has yet to be determined. Blocking or inhibiting these processing enzymes may serve as a potential antiviral target (130). Interestingly, SARS-CoV-2 has developed a unique S1/S2 cleavage site in its S protein, characterized by a four-amino acid insertion, which seems to be absent in all other coronaviruses (4). This molecular mimicry has been identified as an efficient evolutionary adaptation that some viruses have acquired for exploiting the host cellular machinery. Once the nucleocapsid is deposited into the cytoplasm of the host cell, the RNA genome is replicated and translated into structural and accessory proteins. Vesicles containing the newly formed viral particles are then transported to and fuse with the plasma membrane, releasing them to infect other host cells in the same fashion (33, 89, 105). Although much progress has been made in our understanding of the mechanisms underlying SARS-CoV-2 invasion, additional research is needed to delineate exactly how cleavage of the S proteins by TMPRSS2 confers viral particle entry as well as how S-protein cleavage by membrane proteases contributes to viral penetration.

For More Information: https://journals.physiology.org/doi/pdf/10.1152/physiol.00019.2020

High sensitivity troponin and COVID-19 outcomes

Authors: Nikolaos Papageorgiou,a,bCatrin Sohrabi,aDavid Prieto Merino,c,dAngelos Tyrlis,aAbed Elfattah Atieh,aBunny Saberwal,aWei-Yao Lim,aAntonio Creta,aMohammed Khanji,aReni Rusinova,aBashistraj Chooneea,aRaj Khiani,d,eNadeev Wijesuriya,e,fAnna Chow,e,fHaroun Butt,e,fStefan Browne,e,fNikhil Joshi,e,fJamie Kay,e,fSyed Ahsan,a and Rui Providenciaa,g

Abstract

Background

Recent reports have demonstrated high troponin levels in patients affected with COVID-19. In the present study, we aimed to determine the association between admission and peak troponin levels and COVID-19 outcomes.

Methods

This was an observational multi-ethnic multi-centre study in a UK cohort of 434 patients admitted and diagnosed COVID-19 positive, across six hospitals in London, UK during the second half of March 2020.

Results

Myocardial injury, defined as positive troponin during admission was observed in 288 (66.4%) patients. Age (OR: 1.68 [1.49–1.88], p < .001), hypertension (OR: 1.81 [1.10–2.99], p = .020) and moderate chronic kidney disease (OR: 9.12 [95% CI: 4.24–19.64], p < .001) independently predicted myocardial injury. After adjustment, patients with positive peak troponin were more likely to need non-invasive and mechanical ventilation (OR: 2.40 [95% CI: 1.27–4.56], p = .007, and OR: 6.81 [95% CI: 3.40–13.62], p < .001, respectively) and urgent renal replacement therapy (OR: 4.14 [95% CI: 1.34–12.78], p = .013). With regards to events, and after adjustment, positive peak troponin levels were independently associated with acute kidney injury (OR: 6.76 [95% CI: 3.40–13.47], p < .001), venous thromboembolism (OR: 11.99 [95% CI: 3.20–44.88], p < .001), development of atrial fibrillation (OR: 10.66 [95% CI: 1.33–85.32], p = .026) and death during admission (OR: 2.40 [95% CI: 1.34–4.29], p = .003). Similar associations were observed for admission troponin. In addition, median length of stay in days was shorter for patients with negative troponin levels: 8 (5–13) negative, 14 (7–23) low-positive levels and 16 (10–23) high-positive (p < .001).

Conclusions

Admission and peak troponin appear to be predictors for cardiovascular and non-cardiovascular events and outcomes in COVID-19 patients, and their utilization may have an impact on patient management.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7970632/

Troponin and BNP Use in COVID-19

Mar 18, 2020 Cardiology Magazine

Authors: James L. Januzzi Jr., MD, FACC

  1. What are the potential mechanisms underlying troponin elevation with COVID-19 infection? Rise and/or fall of troponin indicating myocardial injury is common among patients with acute respiratory infections and correlated with disease severity.  Abnormal troponin values are common among those with COVID-19 infection particularly when testing with a high sensitivity cardiac troponin (hs-cTn) assay. In a recent article summarizing clinical course of patients with COVID-19, detectable hs-cTnI was observed in most patients, and hs-cTnI was significantly elevated in more than half of the patients that died. The mechanisms explaining myocardial injury in those with COVID-19 infection are not fully understood, however in keeping with other severe respiratory illnesses, direct (“non-coronary”) myocardial damage is almost certainly the most common cause. Given presence of abundant distribution of ACE2 – the binding site for the SARS-CoV-2 – in cardiomyocytes, some have postulated that myocarditis might explain rise of hs-cTn in some cases, particularly as acute left ventricular failure has been described in some cases. Lastly, acute myocardial infarction (MI) – either Type 1 MI based plaque rupture triggered by the infection, or Type 2 MI based on supply-demand inequity – is always possible. Importantly, a rise and/or fall of hs-cTn is not sufficient to secure the diagnosis of acute MI, which should be based on clinical judgment, symptoms/signs, and ECG changes. Given the frequency and non-specific nature of abnormal troponin results among patients with COVID-19 infection, clinicians are advised to only measure troponin if the diagnosis of acute MI is being considered on clinical grounds and an abnormal troponin should not be considered evidence for an acute MI without corroborating evidence.
  2. What are the potential mechanisms underlying elevation of natriuretic peptides with COVID-19 infection? Natriuretic peptides are biomarkers of myocardial stress and are frequently elevated among patients with severe respiratory illnesses typically in the absence of elevated filling pressures or clinical heart failure. Much like troponin, elevation of BNP or NT-proBNP is associated with an unfavorable course among patients with ARDS. Patients with COVID-19 often demonstrate significant elevation of BNP or NT-proBNP. The significance of this finding is uncertain and should not necessarily trigger an evaluation or treatment for heart failure unless there is clear clinical evidence for the diagnosis.
  3. What testing should be performed in COVID-19 patients with acute myocardial injury or abnormal natriuretic peptide results?

For More Information: https://www.acc.org/latest-in-cardiology/articles/2020/03/18/15/25/troponin-and-bnp-use-in-covid19

US case series study in children study looking at association of myocarditis with the Pfizer-BioNTech COVID-19 vaccine

Authors: byUK Science Media Centre|Published onAugust 10, 2021: Prof Peter Openshaw

In this case series, 15 cases of myocarditis are described from a single paediatric referral centre in May, June and July 2021.  Each had been given the Pfizer mRNA vaccine between 1 and 6 days prior to diagnosis; children were aged 12-18 years.  In addition to chest pain, most had fever and muscle pain with evidence of inflammation of the heart muscle evident on tests.  All cases were relatively mild and most resolved completely without treatment.  All but one case was male, and most were after the 2nd dose.

The problem with case series of this type is the lack of comparison groups.  How many cases of myocarditis might be seen in normal children, or those given other vaccines (including those that are not for COVID), or in teenagers infected with SARS-CoV-2?

As the authors note, myocarditis does happen after other vaccines.  The estimated rate (62.8 cases per million) makes this a rare event.  To put this in context, the authors point out that COVID-19 vaccination in males aged 12 to 29 years would prevent 11,000 COVID-19 cases, 560 hospitalizations, 138 intensive care unit admissions and 6 deaths compared with 39 to 47 expected case of myocarditis, if the link with the vaccine is causal.

In another recent study that has not yet been peer-reviewed (https://www.medrxiv.org/content/10.1101/2021.07.23.21260998v1), the authors estimated that males aged 12 to 17 were most likely to develop myocarditis within three months of catching covid-19, at a rate of about 450 cases per million infections.  Mendel Singer at Case Western Reserve University in Ohio (an author on this study) said: “If you’re focused on heart inflammation, the safer bet is to take the vaccine.”  The calculations on which this statement is based are still under discussion, but my view that teenagers should be considered for vaccination is not changed by this new publication.

For More Information: https://covidvaccinehub.org/articles/us-case-series-study-in-children-study-looking-at-association-of-myocarditis-with-the-pfizer-biontech-covid-19-vaccine

Long covid: Damage to multiple organs presents in young, low risk patients

Authors: Gareth Iacobucci BMJ 2020; 371 doi: https://doi.org/10.1136/bmj.m4470 (Published 17 November 2020)Cite this as: BMJ 2020;371:m4470

Young, low risk patients with ongoing symptoms of covid-19 had signs of damage to multiple organs four months after initially being infected, a preprint study has suggested.1

Initial data from 201 patients suggest that almost 70% had impairments in one or more organs four months after their initial symptoms of SARS-CoV-2 infection.

The results emerged as the NHS announced plans to establish a network of more than 40 long covid specialist clinics across England this month to help patients with long term symptoms of infection.

The prospective Coverscan study examined the impact of long covid (persistent symptoms three months post infection) across multiple organs in low risk people who are relatively young and had no major underlying health problems. Assessment was done using results from magnetic resonance image scans, blood tests, and online questionnaires.

The research has not yet been peer reviewed and could not establish a causal link between organ impairment and infection. But the authors said the results had “implications not only for [the] burden of long covid but also public health approaches which have assumed low risk in young people with no comorbidities.”

The study enrolled participants at two UK sites in Oxford and London between April and August 2020. Two hundred and one individuals (mean age 44 (standard deviation 11.0) years) completed assessments after SARS-CoV-2 infection a median of 140 days after initial symptoms.

Participants were eligible if they tested positive for SARS-CoV-2 by random polymerase chain reaction swab (n=62), a positive antibody test (n=63), or had typical symptoms and were determined to have covid-19 by two independent clinicians (n=73).

The prevalence of pre-existing conditions was low (obesity: 20%, hypertension: 6%, diabetes: 2%, heart disease: 4%), and less than a fifth (18%) of individuals had been hospitalised with covid-19.

The most commonly reported ongoing symptoms—regardless of hospitalization status—were fatigue (98%), muscle ache (88%), shortness of breath (87%), and headache (83%). There was evidence of mild organ impairment in the heart (32% of patients), lungs (33%), kidneys (12%), liver (10%), pancreas (17%), and spleen (6%).

For More Information: https://www.bmj.com/content/371/bmj.m4470

Pathological findings in organs and tissues of patients with COVID-19: A systematic review

  1. Authors: Sasha Peiris, Hector Mesa, Agnes Aysola, Juan Manivel, Joao Toledo, Marcio Borges-Sa, Sylvain Aldighieri, Ludovic Reveiz

Abstract

Background

Coronavirus disease (COVID-19) is the pandemic caused by SARS-CoV-2 that has caused more than 2.2 million deaths worldwide. We summarize the reported pathologic findings on biopsy and autopsy in patients with severe/fatal COVID-19 and documented the presence and/or effect of SARS-CoV-2 in all organs.

Methods and findings

A systematic search of the PubMed, Embase, MedRxiv, Lilacs and Epistemonikos databases from January to August 2020 for all case reports and case series that reported histopathologic findings of COVID-19 infection at autopsy or tissue biopsy was performed. 603 COVID-19 cases from 75 of 451 screened studies met inclusion criteria. The most common pathologic findings were lungs: diffuse alveolar damage (DAD) (92%) and superimposed acute bronchopneumonia (27%); liver: hepatitis (21%), heart: myocarditis (11.4%). Vasculitis was common only in skin biopsies (25%). Microthrombi were described in the placenta (57.9%), lung (38%), kidney (20%), Central Nervous System (CNS) (18%), and gastrointestinal (GI) tract (2%). Injury of endothelial cells was common in the lung (18%) and heart (4%). Hemodynamic changes such as necrosis due to hypoxia/hypoperfusion, edema and congestion were common in kidney (53%), liver (48%), CNS (31%) and GI tract (18%). SARS-CoV-2 viral particles were demonstrated within organ-specific cells in the trachea, lung, liver, large intestine, kidney, CNS either by electron microscopy, immunofluorescence, or immunohistochemistry. Additional tissues were positive by Polymerase Chain Reaction (PCR) tests only. The included studies were from numerous countries, some were not peer reviewed, and some studies were performed by subspecialists, resulting in variable and inconsistent reporting or over statement of the reported findings.

Conclusions

The main pathologic findings of severe/fatal COVID-19 infection are DAD, changes related to coagulopathy and/or hemodynamic compromise. In addition, according to the observed organ damage myocarditis may be associated with sequelae.

For More Information: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0250708

Late Complications of COVID-19; a Systematic Review of Current Evidence

Authors: SeyedAhmad SeyedAlinaghi,1Amir Masoud Afsahi,2Mehrzad MohsseniPour,1Farzane Behnezhad,3Mohammad Amin Salehi,1Alireza Barzegary,4Pegah Mirzapour,1Esmaeil Mehraeen,5,* and Omid Dadras6

Introduction

Introduction:

COVID-19 is a new rapidly spreading epidemic. The symptoms of this disease could be diverse as the virus can affect any organ in the body of an infected person. This study aimed to investigate the available evidence for long-term complications of COVID-19.

Methods:

This study was a systematic review of current evidence conducted in November 2020 to investigate probable late and long-term complications of COVID-19. We performed a systematic search, using the keywords, in online databases including PubMed, Scopus, Science Direct, Up to Date, and Web of Science, to find papers published from December 2019 to October 2020. Peer-reviewed original papers published in English, which met the eligibility criteria were included in the final report. Addressing non-human studies, unavailability of the full-text document, and duplicated results in databases, were characteristics that led to exclusion of the papers from review.

Results:

The full-texts of 65 articles have been reviewed. We identified 10 potential late complications of COVID-19. A review of studies showed that lung injuries (n=31), venous/arterial thrombosis (n=28), heart injuries (n=26), cardiac/brain stroke (n=23), and neurological injuries (n=20) are the most frequent late complications of COVID-19.

For More Information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7927752/