6 november 2021: Zie ook dit artikel hoe  ozontherapie patiënten besmet geweest met het coronavirus en daarmee schade hebben opgelopen kan helpen te herstellen: https://kanker-actueel.nl/ozontherapie-is-een-goedkope-en-veilige-manier-om-de-kwetsbaarheid-bij-veel-virussen-de-overvloedige-zwavel-bevattende-aminozuren-zoals-het-corona-virus-sars-cov-2-aan-te-pakken-en-te-elimineren.html

4 november 2021: Volkskrant

Nieuw Nederlands onderzoek bij topsporters op Papendal van sportcardioloog en onderzoeksleider Harald Jørstad (Amsterdam UMC) laat zien dat 1 jaar na besmet te zijn geweest met het coronavirus - Covid-19 nog altijd 4 procent van de 100 onderzochte topsporters sporen hebben van een ontstoken hartspier (myocarditis) en dat zou een risico inhouden dat deze topsporters bij grote inspanningen een hartstilstand zouden kunnen krijgen. Denk bv aan Christian Eriksen tijdens de EK van afgelopen zomer. En natuurlijk geldt dit ook voor de miljoenen amateursporters die regelmatig over hun grenzen gaan in hun sport om of conditie op te bouwen of te presteren in een wedstrijd. Wat ik me ook afvraag is of de vaccins hier tegen beschermen. Want bij het Lareb zijn relatief behoorlijk wat meldingen gedaan van myocarditis na vaccinatie. En in Wuhan bleken relatief veel mensen die waren overleden aan de gevolgen van het coronavirus overleden aan een hartstilstand. Het abstract van de nieuwe studie is nog niet vrijgegeven, maar zal vandaag worden gepresenteerd.

Hier nog wat meer studies naar myocarditis). 


Zo werd bij een onderzoek vorig jaar juli:

Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19)

bij 100 willekeurig uitgekozen Duitse patiënten die onlangs hersteld waren van een COVID-19-infectie, gevonden dat op een CMR = cardiale magnetische resonantie scan hartafwijkingen werden gezien bij 78 patiënten (78%) en een aanhoudende myocardontsteking bij 60 patiënten (60%). En die afwijkingen werden gezien onafhankelijk van reeds bestaande aandoeningen, ernst en algemeen beloop van de acute ziekte en de tijd vanaf de oorspronkelijke diagnose van corona - Covid-19.

Afgelopen zomer werd deze studie:Prevalence of Clinical and Subclinical Myocarditis in Competitive Athletes With Recent SARS-CoV-2 InfectionResults From the Big Ten COVID-19 Cardiac Registry gepubliceerd in JAMA.

In deze cohortstudie van 1597 Amerikaanse competitieve collegiale atleten die uitgebreide cardiovasculaire tests ondergingen, was de prevalentie van klinische myocarditis op basis van een op symptomen gebaseerde screeningstrategie slechts 0,31%. Screening met cardiovasculaire magnetische resonantie beeldvorming verhoogde de prevalentie van klinische en subklinische myocarditis met een factor 7,4 tot 2,3%. De Volkskrant schreef hierover: Onderzoek onder bijna 1.600 Amerikaanse topsporters geeft voor het eerst een betrouwbare schatting over de schade die het coronavirus kan toebrengen aan het hart en die schade is minder ernstig dan aanvankelijk werd gedacht. Bij ruim 2 procent van de onderzochte sporters werden na een corona-infectie op MRI-scans sporen gevonden van een ontsteking van de hartspier, bij ongeveer de helft verdwenen die in de maanden daarna.

Ook deze studie is interessant waarin myocarditis optrad na vaccinatieFulminant myocarditis and systemic hyperinflammation temporally associated with BNT162b2 mRNA COVID-19 vaccination in two patients

Een recente studie: One-year Risks and Burdens of Incident Cardiovascular Disease in COVID-19: Cardiovascular Manifestations of Long COVID

laat zien dat hartschade door Covid-19 veel verder gaat dan de beginfase van de ziekte. Uit dit onderzoek bleek dat zelfs mensen die nooit ziek genoeg waren om in het ziekenhuis te worden opgenomen, een jaar later het risico lopen hartfalen en dodelijke bloedstolsels te ontwikkelen. Hartaandoeningen en beroertes zijn wereldwijd al de belangrijkste doodsoorzaken. De verhoogde kans op dodelijke hartcomplicaties bij Covid-overlevenden is zorgwekkend te noemen. Aldus de onderzoekers van deze studie


Hier een uitgebreide conclusie van deze grote studie:

In this work involving 151,195 people with COVID-19, 3,670,087 contemporary controls, and 3,656,337 historical controls — which altogether correspond to 6,633,341 person years of follow up, we provide evidence that beyond the first 30 days of infection, people with COVID-19 exhibited increased risks and 12-month burdens of incident cardiovascular disease including cerebrovascular disorders, dysrhythmias, inflammatory heart disease, ischemic heart disease, heart failure, thromboembolic disease, and other cardiac disorders. Our analyses of the risks and burdens of cardiovascular outcomes across care settings of the acute infection reveal two key findings: (1) that the risks and associated burdens were evident among those who were not hospitalized during the acute phase of the disease — this group represents the majority of people with COVID-19 and (2) that the risks and associated burdens exhibited a graded increase across the severity spectrum of the acute COVID-19 infection (from non-hospitalized to hospitalized individuals, to those admitted to intensive care). The risks and associated burdens were consistent in analyses considering the contemporary control group and — separately — the historical control group as the referent category. The results were robust to challenge in multiple sensitivity analyses. Application of a positive outcome control yielded results consistent with established knowledge; and testing of a battery of negative outcome controls yielded results consistent with a priori expectations. Taken together, our results suggest that one-year risk and burden of cardiovascular disease among those who survive the acute phase of COVID-19 are substantial and span several cardiovascular disorders. Care strategies of people who survived the acute episode of COVID-19 should include attention to cardiovascular health and disease.

The broader implications of the findings are clear. Cardiovascular complications have been described in the acute phase of COVID-196-8. Our studies suggest that the risk of incident cardiovascular disease extends well beyond the acute phase of COVID-19. Given the large and growing number of people infected with COVID-19 (more than 43 million people in the US, nearly 8 million people in the UK, and more than 231 million people globally), the risks and 12-month burdens cardiovascular disease reported here may translate in large number of potentially affected people around the world. Governments and health systems around the world should be prepared to deal with the likely significant contribution of the COVID-19 pandemic to a rise in the burden of cardiovascular diseases.

The mechanism or mechanisms that underlie the association between COVID-19 and development of cardiovascular diseases in the post-acute phase of the disease are not entirely clear9,10. Putative mechanisms include lingering damage from direct viral invasion of cardiomyocytes and/or endothelial cells and subsequent cell death, transcriptional alteration of multiple cell types in heart tissue, downregulation of ACE2 and dysregulation of the renin–angiotensin–aldosterone system, autonomic dysfunction, pro-coagulant state, elevated levels of pro-inflammatory cytokines, and subsequent fibrosis and scarring of cardiac tissue9,11-13. An aberrant persistent hyperactivated immune response, autoimmunity, or persistence of the virus in immune privileged sites has also been cited as putative explanations of extrapulmonary (including cardiovascular) post-acute sequelae of COVID-199,11,12,14. Insight developed from prior natural disasters and previous pandemics also suggest the putative presence of indirect effects including changes in the broader contextual environment, social (e.g. isolation, quarantine, reduced social contact and loneliness), economic (e.g. financial distress due to complete loss or reduced income), and behavioral conditions (e.g. changes in dietary habits and physical activity), lived experiences of trauma and grief (from pandemic related happenings) that may be differentially experienced by people with COVID-19 may also shape their cardiovascular outcomes15-20. These putative direct and indirect mechanistic pathways may accelerate the progression pre-existing subclinical disease and/or lead to development of de novo disease. A deeper understanding of the direct biologic mechanisms and the putative contribution of indirect contextual drivers will be needed to inform development of prevention and treatment strategies of the cardiovascular manifestations among people with COVID-19.

This study has several strengths. We used the vast and rich national healthcare databases of the US Department of Veterans Affairs to build a large cohort of people with COVID-19. We designed the study cohort to investigate incident cardiovascular disease in the post-acute phase of the disease. We pre-specified a comprehensive list of cardiovascular outcomes. We examined the associations using two large control groups – a contemporary and a historical control; this approach allowed us to deduce that the associations between COVID-19 and risks of cardiovascular outcomes are not related to the broader temporal changes between the pre-pandemic and the pandemic eras, but rather related (possibly through both a direct and indirect pathway) to exposure to COVID-19 itself. Our modeling approach included specification of 19 predefined variables selected based on established knowledge and 100 algorithmically selected variables from VA high dimensional data domains including diagnostic codes, prescription records, and laboratory test results. We evaluated the associations across care settings of the acute infection. We challenged robustness of results in multiple sensitivity analyses, and successfully tested positive and negative outcome controls. We provided estimates of risk on both the ratio scale (hazard ratios) and the absolute scale (burden per 1000 persons at 12 months); the latter also reflects the contribution of baseline risk and provides an estimate of potential harm that is more easily explainable to the general public than risk reported on the ratio scale (e.g., hazard ratio).

This study has several limitations. The demographic composition of our cohort (majority White and male) may limit generalizability of study findings. We used the electronic healthcare databases of the US Department of Veterans Affairs to conduct this study, and although we used validated outcome definitions, and took care to adjust the analyses for a large set of predefined and algorithmically selected variables, we cannot completely rule out misclassification bias and residual confounding. The associations should not be interpreted as causal effects of COVID-19 exposure; our approach does not allow us to disentangle the direct effects of the viral infection and the immune response to it from the putative contribution of indirect contextual exposure (differentially experienced by people with COVID-19) to cardiovascular outcomes; however, regardless of relative contribution of a direct and indirect pathway, the excess burden experienced by people with COVID-19 represents the additional burden of disease that health systems will encounter as a result of this pandemic. Finally, as the pandemic with all its dynamic features continues to progress, as the virus continues to mutate and as new variants emerge, as treatment strategies of the acute and post-acute COVID-19 evolve, as vaccine uptake improves, it is possible that the epidemiology of cardiovascular manifestations in COVID-19 may also change over time21.

In sum, using a national cohort of people with COVID-19, we show that at risk and 12-month burden of incident cardiovascular disease are substantial and span several cardiovascular disease categories (ischemic and non-ischemic heart disease, dysrhythmias, and others). The risk and burden of cardiovascular disease were evident even among those whose acute COVID-19 did not necessitate hospitalization. Care pathways of people who survived the acute episode of COVID-19 should include attention to cardiovascular health and disease.

References:

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