A new study out of Europe has revealed that cases of heart inflammation that required hospitalization were much more common among vaccinated individuals compared to the unvaccinated.
A team of researchers from health agencies in Finland, Denmark, Sweden, and Norway found that rates of myocarditis and pericarditis, two forms of potentially life-threatening heart inflammation, were higher in those who had received one or two doses of either mRNA-based vaccine – Pfizer’s or Moderna’s.
In all, researchers studied a total of 23.1 million records on individuals aged 12 or older between December 2020 and October 2021. In addition to the increased rate overall, the massive study confirmed the chances of developing the heart condition increased with a second dose, which mirrors other data that has been uncovered in recent months.
“Results of this large cohort study indicated that both first and second doses of mRNA vaccines were associated with increased risk of myocarditis and pericarditis. For individuals receiving 2 doses of the same vaccine, risk of myocarditis was highest among young males (aged 16-24 years) after the second dose. These findings are compatible with between 4 and 7 excess events in 28 days per 100 000 vaccinees after BNT162b2, and between 9 and 28 excess events per 100 000 vaccinees after mRNA-1273.
The risks of myocarditis and pericarditis were highest within the first 7 days of being vaccinated, were increased for all combinations of mRNA vaccines, and were more pronounced after the second dose.”
Also mirroring other data, the study confirmed that young people, especially young males, are the ones who are suffering the worst effects of the experimental jab. Young men, aged 16-24 were an astounding 5-15X more likely to be hospitalized with heart inflammation than their unvaccinated peers.
But it isn’t just young men, all age groups across both sexes – except for men over 40 and girls aged 12-15 – experienced a higher rate of heart inflammation post-vaccination when compared to the unvaxxed.
From The Epoch Times, who spoke with one of the study’s main researchers, Dr. Rickard Ljung:
“‘These extra cases among men aged 16–24 correspond to a 5 times increased risk after Comirnaty and 15 times increased risk after Spikevax compared to unvaccinated,’ Dr. Rickard Ljung, a professor and physician at the Swedish Medical Products Agency and one of the principal investigators of the study, told The Epoch Times in an email.
Comirnaty is the brand name for Pfizer’s vaccine while Spikevax is the brand name for Moderna’s jab.
Rates were also higher among the age group for those who received any dose of the Pfizer or Moderna vaccines, both of which utilize mRNA technology. And rates were elevated among vaccinated males of all ages after the first or second dose, except for the first dose of Moderna’s shot for those 40 or older, and females 12- to 15-years-old.”
Although the peer-reviewed study found a direct link between mRNA based vaccines and increased incident rate of heart inflammation, the researchers claimed that the “benefits” of the experimental vaccines still “outweigh the risks of side effects,” because cases of heart inflammation are “very rare,” in a press conference about their findings earlier this month.
However, while overall case numbers may be low in comparison to the raw numbers and thus technically “very rare,” the rate at which individuals are developing this serious condition has increased by a whopping amount. When considering the fact that 5-15X more, otherwise healthy, young men will come down with the condition – especially since the chances of Covid-19 killing them at that age are effectively zero (99.995% recovery rate) – it’s downright criminal for governments across the world to continue pushing mass vaccinations for everyone.
Dr. Peter McCullough, a world-renowned Cardiologist who has been warning about the long-term horror show that is vaccine-induced myocarditis in young people, certainly thinks so. In his expert opinion, the study does anything but give confidence that the benefits of the vaccine outweigh the risks. In “no way” is that the case, he says. Actually, it’s quite the opposite.
“In cardiology we spend our entire career trying to save every bit of heart muscle. We put in stents, we do heart catheterization, we do stress tests, we do CT angiograms. The whole game of cardiology is to preserve heart muscle. Under no circumstances would we accept a vaccine that causes even one person to stay sustain heart damage. Not one. And this idea that ‘oh, we’re going to ask a large number of people to sustain heart damage for some other theoretical benefit for a viral infection,’ which for most is less than a common cold, is untenable. The benefits of the vaccines in no way outweigh the risks.”
It’s also worth pointing out that the new study’s findings could be an indicator as to what is driving the massive spike in the excess death rates in the United States and across the world. Correlating exactly with the rollout of the experimental mRNA Covid-19 vaccines, people have been dying at record-breaking rates, especially millennials, who experienced a jaw-dropping 84% increase in excess deaths (compared to pre-pandemic) in the final four months of 2021.
In a recent study posted to the medRxiv* preprint server, researchers assessed the prevalence of organ impairment in long coronavirus disease 2019 (COVID-19) six months and a year post-COVID-19 at London and Oxford.
Multi-organ impairment associated with long COVID-19 is a significant health burden. Standardized multi-organ evaluation is deficient, especially in non-hospitalized patients. Although the symptoms of long COVID-19, also known as post-acute sequelae of COVID-19 (PASC), are well-established, the natural history is poorly classified by symptoms, organ impairment, and function.
About the study
In the present prospective study, researchers assessed organ impairment in long COVID-19 patients six months and a year after the onset of early symptoms and correlated them to their clinical presentation.
The participants were recruited based on specialist referral or the response to advertisements in sites such as Mayo Clinic Healthcare, Perspectum, and Oxford from April 2020 to August 2021, based on their COVID-19 history.
The study was conducted on COVID-19 patients who recovered from the acute phase of the infection. Their health status, symptoms, and organ impairment were assessed. The symptoms assessed comprised cardiopulmonary, severe dyspnoea, and cognitive dysfunction. Biochemical and physiological parameters were analyzed at baseline and post-organ impairment. The radiological investigation comprised multi-organ magnetic resonance imaging (MRI) performed in the long COVID-19 patients and healthy controls.
Over a year, the team prospectively investigated the symptoms, organ impairment, and function, especially dyspnea, cognitive dysfunction, and health-related quality of life (HRQoL). They also evaluated the association between organ impairment and clinical symptoms.
Patients with symptoms of active pulmonary infections (body temperature >37.8°C or ≥3 coughing episodes in a day) and hospital discharges in the previous week or >4 months were excluded from the study. Asymptomatic patients and those with MRI contraindications such as defibrillators, pacemakers, devices with metal implants, and claustrophobia were removed.
Participants with impaired organs, as diagnosed by blood investigations, incidental findings, or MRI, were included in the follow-up assessments. Every visit comprised blood investigations, MRI scanning, and online questionnaire surveys, which were to be filled out beforehand. In addition, a sensitivity analysis was performed that excluded patients at risk of metabolic disorders (including body mass index (BMI) ≥30 kg/m2, diabetes, and hypertension)
Out of 536 participants, the majority were middle-aged (mean age 45 years), female (73%), White (89%), and healthcare workers (32%). About 13% of the COVID-19 patients hospitalized during the acute phase of the infection completed the baseline evaluation. A total of 331 patients (62%) had incidental findings, organ impairment, or reduction in the symptoms from the baseline at both the time points.
Cognitive dysfunction (50% and 38%), poor HRQoL (EuroQOL <0.7 in 55% and 45%), and severe dyspnea (36% and 30%) were observed at six months and one year, respectively. On follow-up, the symptoms were reduced, especially cardiopulmonary and systemic symptoms, whereas fatigue, dyspnea, and cognitive dysfunction were consistently present. The greatest impact on quality of life was related to pain and difficulties performing routine activities. Almost every patient took time off work due to COVID-19. The symptoms were largely associated with obese women, young age, and impairment of a single organ.
At baseline, fibrous inflammation was observed in the pancreas (9%), heart (9%), liver (11%), and kidney (15%). Additionally, increased volumes of the spleen (8%), kidney (9%), and liver (7%) were observed. Moreover, reduced lung capacity (2%), excess adipose deposits in pancreatic tissues (15%) and liver (25%) were observed. High liver fibro-inflammation was associated with cognitive dysfunction at follow-up in 19% and 12% of patients with and without cognitive dysfunction, respectively. Low liver fat was more likely in those without severe dyspnoea at both time points. Increased liver volumes at follow-up were associated with lower HRQoL scores.
The prevalence of multi and single-organ impairment was 23% and 59% at baseline, respectively, and persisted in 27% and 59% of the participants on follow-up assessments. Most of the organ impairments were mild. However, they did not improve substantially between visits. Notably, participants without organ impairment had the lowest symptom burden.
Most biochemical parameters were normal except creatinine kinase (8% and 13%), lactate dehydrogenase (16% and 22%), mean cell hemoglobin concentration (21% and 15%), and cholesterol (46% and 48%), at six months and a year post-COVID-19, respectively. These biochemical markers increased from the baseline on follow-up assessments.
To summarize, organ impairment was detected in 59% of the patients at six months post-COVID-19 and persisted in 59% at one-year follow-up. This has significant implications on the quality of life, symptoms, and long-term health of the patients. These observations highlight the requirement for enhanced preventive measures and integrated patient care to decrease the long COVID-19 burden.
Establishing the rate of post-vaccination cardiac myocarditis in the 12-15 and 16-17-year-old population in the context of their COVID-19 hospitalization risk is critical for developing a vaccination recommendation framework that balances harms with benefits for this patient demographic. Design, Setting and Participants: Using the Vaccine Adverse Event Reporting System (VAERS), this retrospective epidemiological assessment reviewed reports filed between January 1, 2021, and June 18, 2021, among adolescents ages 12-17 who received mRNA vaccination against COVID-19. Symptom search criteria included the words myocarditis, pericarditis, and myopericarditis to identify children with evidence of cardiac injury. The word troponin was a required element in the laboratory findings. Inclusion criteria were aligned with the CDC working case definition for probable myocarditis. Stratified cardiac adverse event (CAE) rates were reported for age, sex and vaccination dose number. A harm-benefit analysis was conducted using existing literature on COVID-19-related hospitalization risks in this demographic. Main outcome measures: 1) Stratified rates of mRNA vaccine-related myocarditis in adolescents age 12-15 and 16-17; and 2) harm-benefit analysis of vaccine-related CAEs in relation to COVID-19 hospitalization risk. Results: A total of 257 CAEs were identified. Rates per million following dose 2 among males were 162.2 (ages 12-15) and 94.0 (ages 16-17); among females, rates were 13.0 and 13.4 per million, respectively. For boys 12-15 without medical comorbidities receiving their second mRNA vaccination dose, the rate of CAE is 3.7-6.1 times higher than their 120-day COVID-19 hospitalization risk as of August 21, 2021 (7-day hospitalizations 1.5/100k population) and 2.6-4.3-fold higher at times of high weekly hospitalization risk (2.1/100k), such as during January 2021. For boys 16-17 without medical comorbidities, the rate of CAE is currently 2.1-3.5 times higher than their 120-day COVID-19 hospitalization risk, and 1.5-2.5 times higher at times of high weekly COVID-19 hospitalization. Conclusions: Post-vaccination CAE rate was highest in young boys aged 12-15 following dose two. For boys 12-17 without medical comorbidities, the likelihood of post vaccination dose two CAE is 162.2 and 94.0/million respectively. This incidence exceeds their expected 120-day COVID-19 hospitalization rate at both moderate (August 21, 2021 rates) and high COVID-19 hospitalization incidence. Further research into the severity and long-term sequelae of post-vaccination CAE is warranted. Quantification of the benefits of the second vaccination dose and vaccination in addition to natural immunity in this demographic may be indicated to minimize harm.
Millennials Experienced the “Worst-Ever Excess Mortality in History” – An 84% Increase In Deaths After Vaccine Mandates
Dowd, with the assistance of an insurance industry expert, compiled data from the CDC showing that, in just the second half of 2021, the total number of excess deaths for millennials was higher than the number of Americans who died in the entirety of the Vietnam War. Between August and December, there were over 61,000 deaths in this age group, compared to 58,000 over the course of 10 years in Vietnam.
In all, excess death among those who are traditionally the healthiest Americans is up by 84%.
Colchicine is an anti-inflammatory drug that is used to treat a variety of conditions, including gout, recurrent pericarditis, and familial Mediterranean fever.1 Recently, the drug has been shown to potentially reduce the risk of cardiovascular events in those with coronary artery disease.2 Colchicine has several potential mechanisms of action, including reducing the chemotaxis of neutrophils, inhibiting inflammasome signaling, and decreasing the production of cytokines, such as interleukin-1 beta.3 When colchicine is administered early in the course of COVID-19, these mechanisms could potentially mitigate or prevent inflammation-associated manifestations of the disease. These anti-inflammatory properties coupled with the drug’s limited immunosuppressive potential, favorable safety profile, and widespread availability have prompted investigation of colchicine for the treatment of COVID-19.
The COVID-19 Treatment Guidelines Panel (the Panel) recommends against the use of colchicine for the treatment of nonhospitalized patients with COVID-19, except in a clinical trial (BIIa).
The Panel recommends against the use of colchicine for the treatment of hospitalized patients with COVID-19 (AI).
For Nonhospitalized Patients With COVID-19
COLCORONA, a large randomized placebo-controlled trial that evaluated colchicine in outpatients with COVID-19, did not reach its primary efficacy endpoint of reducing hospitalizations and death.4 However, in the subset of patients whose diagnosis was confirmed by a positive SARS-CoV-2 polymerase chain reaction (PCR) result from a nasopharyngeal (NP) swab, a slight reduction in hospitalizations was observed among those who received colchicine.
PRINCIPLE, another randomized, open-label, adaptive-platform trial that evaluated colchicine versus usual care, was stopped for futility when no significant difference in time to first self-reported recovery from COVID-19 between the colchicine and usual care recipients was found.5
The PRINCIPLE trial showed no benefit of colchicine, and the larger COLCORONA trial failed to reach its primary endpoint, found only a very modest effect of colchicine in the subgroup of patients with positive SARS-CoV-2 PCR results, and reported more gastrointestinal adverse events in those receiving colchicine. Therefore, the Panel recommends against the use of colchicine for the treatment of COVID-19 in nonhospitalized patients, except in a clinical trial (BIIa).
For Hospitalized Patients With COVID-19
In the RECOVERY trial, a large randomized trial in hospitalized patients with COVID-19, colchicine demonstrated no benefit with regard to 28-day mortality or any secondary outcomes.6 Based on the results from this large trial, the Panel recommends against the use of colchicine for the treatment of COVID-19 in hospitalized patients (AI).
Clinical Data for COVID-19
Colchicine in Nonhospitalized Patients With COVID-19
The COLCORONA Trial
The COLCORONA trial was a contactless, double-blind, placebo-controlled, randomized trial in outpatients who received a diagnosis of COVID-19 within 24 hours of enrollment. Participants were aged ≥70 years or aged ≥40 years with at least 1 of the following risk factors for COVID-19 complications: body mass index ≥30, diabetes mellitus, uncontrolled hypertension, known respiratory disease, heart failure or coronary disease, fever ≥38.4°C within the last 48 hours, dyspnea at presentation, bicytopenia, pancytopenia, or the combination of high neutrophil count and low lymphocyte count. Participants were randomized 1:1 to receive colchicine 0.5 mg twice daily for 3 days and then once daily for 27 days or placebo. The primary endpoint was a composite of death or hospitalization by Day 30; secondary endpoints included components of the primary endpoint, as well as the need for mechanical ventilation by Day 30. Participants reported by telephone the occurrence of any study endpoints at 15 and 30 days after randomization; in some cases, clinical data were confirmed or obtained by medical chart reviews.4
The study enrolled 4,488 participants.
The primary endpoint occurred in 104 of 2,235 participants (4.7%) in the colchicine arm and 131 of 2,253 participants (5.8%) in the placebo arm (OR 0.79; 95% CI, 0.61–1.03; P = 0.08).
There were no statistically significant differences in the secondary outcomes between the arms.
In a prespecified analysis of 4,159 participants who had a SARS-CoV-2 diagnosis confirmed by PCR testing of an NP specimen (93% of those enrolled), those in the colchicine arm were less likely to reach the primary endpoint (96 of 2,075 participants [4.6%]) than those in the placebo arm (126 of 2,084 participants [6.0%]; OR 0.75; 95% CI, 0.57–0.99; P = 0.04). In this subgroup of patients with PCR-confirmed SARS-CoV-2 infection, there were fewer hospitalizations (a secondary outcome) in the colchicine arm (4.5% of patients) than in the placebo arm (5.9% of patients; OR 0.75; 95% CI, 0.57–0.99).
More participants in the colchicine arm experienced gastrointestinal adverse events, including diarrhea which occurred in 13.7% of colchicine recipients versus 7.3% of placebo recipients (P < 0.0001). Unexpectedly, more pulmonary emboli were reported in the colchicine arm than in the placebo arm (11 events [0.5% of patients] vs. 2 events [0.1% of patients]; P= 0.01).
Due to logistical difficulties with staffing, the trial was stopped at approximately 75% of the target enrollment, which may have limited the study’s power to detect differences for the primary outcome.
There was uncertainty as to the accuracy of COVID-19 diagnoses in presumptive cases.
Some patient-reported clinical outcomes were potentially misclassified.
The PRINCIPLE Trial
PRINCIPLE is a randomized, open-label, platform trial that evaluated colchicine in symptomatic, nonhospitalized patients with COVID-19 who were aged ≥65 years or aged ≥18 years with comorbidities or shortness of breath, and who had symptoms for ≤14 days. Participants were randomized to receive colchicine 0.5 mg daily for 14 days or usual care. The coprimary endpoints, which included time to first self-reported recovery or hospitalization or death due to COVID-19 by Day 28, were analyzed using a Bayesian model. Participants were followed through symptom diaries that they completed online daily; those who did not complete the diaries were contacted by telephone on Days 7, 14, and 29. The investigators developed a prespecified criterion for futility, specifying a clinically meaningful benefit in time to first self-reported recovery as a hazard ratio ≥1.2, corresponding to about 1.5 days of faster recovery in the colchicine arm.
The study enrolled 4,997 participants: 212 participants were randomized to receive colchicine; 2,081 to receive usual care alone; and 2,704 to receive other treatments.
The prespecified primary analysis included participants with SARS-CoV-2 positive test results (156 in the colchicine arm; 1,145 in the usual care arm; and 1,454 in the other treatments arm).
The trial was stopped early because the criterion for futility was met; the median time to self-reported recovery was similar in the colchicine arm and the usual care arm (HR 0.92; 95% CrI, 0.72–1.16).
Analyses of self-reported time to recovery and hospitalizations or death due to COVID-19 among concurrent controls also showed no significant differences between the colchicine and usual care arms.
There were no statistically significant differences in the secondary outcomes between the colchicine and usual care arms in both the primary analysis population and in subgroups, including subgroups based on symptom duration, baseline disease severity, age, or comorbidities.
The occurrence of adverse events was similar in the colchicine and usual care arms.
The design of the study was open-label treatment.
The sample size of the colchicine arm was small.
Colchicine in Hospitalized Patients With COVID-19
The RECOVERY Trial
In the RECOVERY trial, hospitalized patients with COVID-19 were randomized to receive colchicine (1 mg loading dose, followed by 0.5 mg 12 hours later, and then 0.5 mg twice daily for 10 days or until discharge) or usual care.6
The study enrolled 11,340 participants.
At randomization, 10,603 patients (94%) were receiving corticosteroids.
The primary endpoint of all-cause mortality at Day 28 occurred in 1,173 of 5,610 participants (21%) in the colchicine arm and 1,190 of 5,730 participants (21%) in the placebo arm (rate ratio 1.01; 95% CI, 0.93–1.10; P = 0.77).
There were no statistically significant differences between the arms for the secondary outcomes of median time to being discharged alive, discharge from the hospital within 28 days, and receipt of mechanical ventilation or death.
The incidence of new cardiac arrhythmias, bleeding events, and thrombotic events was similar in the 2 arms. Two serious adverse events were attributed to colchicine: 1 case of severe acute kidney injury and one case of rhabdomyolysis.
The trial’s open-label design may have introduced bias for assessing some of the secondary endpoints.
The GRECCO-19 Trial
GRECCO-19 was a small, prospective, open-label randomized clinical trial in 105 patients hospitalized with COVID-19 across 16 hospitals in Greece. Patients were assigned 1:1 to receive standard of care with colchicine (1.5 mg loading dose, followed by 0.5 mg after 60 minutes and then 0.5 mg twice daily until hospital discharge or for up to 3 weeks) or standard of care alone.7
Fewer patients in the colchicine arm (1 of 55 patients) than in the standard of care arm (7 of 50 patients) reached the primary clinical endpoint of deterioration in clinical status from baseline by 2 points on a 7-point clinical status scale (OR 0.11; 95% CI, 0.01–0.96).
Participants in the colchicine group were significantly more likely to experience diarrhea (occurred in 45.5% of participants in the colchicine arm vs. 18.0% in the standard of care arm; P = 0.003).
The overall sample size and the number of clinical events reported were small.
The study design was open-label treatment assignment.
The results of several small randomized trials and retrospective cohort studies that have evaluated various doses and durations of colchicine in hospitalized patients with COVID-19 have been published in peer-reviewed journals or made available as preliminary, non-peer-reviewed reports.8-11 Some have shown benefits of colchicine use, including less need for supplemental oxygen, improvements in clinical status on an ordinal clinical scale, and reductions in certain inflammatory markers. In addition, some studies have reported higher discharge rates or fewer deaths among patients who received colchicine than among those who received comparator drugs or placebo. However, the findings of these studies are difficult to interpret due to significant design or methodological limitations, including small sample sizes, open-label designs, and differences in the clinical and demographic characteristics of participants and permitted use of various cotreatments (e.g., remdesivir, corticosteroids) in the treatment arms.
Adverse Effects, Monitoring, and Drug-Drug Interactions
Common adverse effects of colchicine include diarrhea, nausea, vomiting, abdominal cramping and pain, bloating, and loss of appetite. In rare cases, colchicine is associated with serious adverse events, such as neuromyotoxicity and blood dyscrasias. Use of colchicine should be avoided in patients with severe renal insufficiency, and patients with moderate renal insufficiency who receive the drug should be monitored for adverse effects. Caution should be used when colchicine is coadministered with drugs that inhibit cytochrome P450 (CYP) 3A4 and/or P-glycoprotein (P-gp) because such use may increase the risk of colchicine-induced adverse effects due to significant increases in colchicine plasma levels. The risk of myopathy may be increased with the concomitant use of certain HMG-CoA reductase inhibitors (e.g., atorvastatin, lovastatin, simvastatin) due to potential competitive interactions mediated by CYP3A4 and P-gp pathways.12,13 Fatal colchicine toxicity has been reported in individuals with renal or hepatic impairment who received colchicine in conjunction with P-gp inhibitors or strong CYP3A4 inhibitors.
Considerations in Pregnancy
There are limited data on the use of colchicine in pregnancy. Fetal risk cannot be ruled out based on data from animal studies and the drug’s mechanism of action. Colchicine crosses the placenta and has antimitotic properties, which raises a theoretical concern for teratogenicity. However, a recent meta-analysis did not find that colchicine exposure during pregnancy increased the rates of miscarriage or major fetal malformations. There are no data for colchicine use in pregnant women with acute COVID-19. Risks of use should be balanced against potential benefits.12,14
Considerations in Children
Colchicine is most commonly used in children to treat periodic fever syndromes and autoinflammatory conditions. Although colchicine is generally considered safe and well tolerated in children, there are no data on the use of the drug to treat pediatric acute COVID-19 or multisystem inflammatory syndrome in children (MIS-C).
RECOVERY Collaborative Group. Colchicine in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet Respir Med. 2021;Published online ahead of print. Available at: https://www.ncbi.nlm.nih.gov/pubmed/34672950.
Deftereos SG, Giannopoulos G, Vrachatis DA, et al. Effect of colchicine vs standard care on cardiac and inflammatory biomarkers and clinical outcomes in patients hospitalized with coronavirus disease 2019: the GRECCO-19 randomized clinical trial. JAMA Netw Open. 2020;3(6):e2013136. Available at: https://www.ncbi.nlm.nih.gov/pubmed/32579195.
Sandhu T, Tieng A, Chilimuri S, Franchin G. A case control study to evaluate the impact of colchicine on patients admitted to the hospital with moderate to severe COVID-19 infection. Can J Infect Dis Med Microbiol. 2020. Available at: https://www.ncbi.nlm.nih.gov/pubmed/33133323.
Lopes MI, Bonjorno LP, Giannini MC, et al. Beneficial effects of colchicine for moderate to severe COVID-19: a randomised, double-blinded, placebo-controlled clinical trial. RMD Open. 2021;7(1). Available at: https://www.ncbi.nlm.nih.gov/pubmed/33542047.
Background: Colchicine is an old drug originally employed for the treatment of inflammatory disorders such as acute gout and familiar Mediterranean fever.
Methods: In the past few decades, colchicine has been at the forefront of the pharmacotherapy of several cardiac diseases, including acute and recurrent pericarditis, coronary artery disease, prevention of atrial fibrillation and heart failure. In this review, we have summarized the current evidence based medicine and guidelines recommendations in the specific context of pericardial syndromes.
Results: Colchicine has been firstly engaged in the treatment of recurrent pericarditis of viral, idiopathic and autoimmune origin. Shortly thereafter colchicine use has been expanded to the primary prevention of recurrences in patients with a first episode of pericarditis depicting similarly good results. The acquisition of high quality scientific data in the course of time from prospective randomized placebo-controlled trials and metanalyses have established colchicine as first line treatment option in acute and recurrent pericarditis, on top of the conventional treatment. The only concerns related to the use of colchicine are the side effects (mainly gastrointestinal intolerance) which although generally not serious, may account for treatment withdrawal in some cases.
Conclusion: Colchicine has been established as a first line medication in the treatment of acute (first episode) and recurrent pericarditis on top of the conventional treatment as well as for the prevention of postpericardiotomy syndrome. It depicts a good safety profile with gastrointestinal intolerance being the most common side effect.
The COVID-19 pandemic is a highly contagious viral illness which conventionally manifests primarily with respiratory symptoms. We report a case whose first manifestation of COVID-19 was pericarditis, in the absence of respiratory symptoms, without any serious complications. Cardiac involvement in various forms is possible in COVID-19. We present a case where pericarditis, in the absence of the classic COVID-19 signs or symptoms, is the only evident manifestation of the disease. This case highlights an atypical presentation of COVID-19 and the need for a high index of suspicion to allow early diagnosis and limit spread by isolation.
This article is made freely available for use in accordance with BMJ’s website terms and conditions for the duration of the covid-19 pandemic or until otherwise determined by BMJ. You may use, download and print the article for any lawful, non-commercial purpose (including text and data mining) provided that all copyright notices and trade marks are retained.https://bmj.com/coronavirus/usage
The global COVID-19 pandemic is caused by severe acute respiratory syndrome coronavirus 2, an enveloped single-stranded RNA virus of zoonotic origin. Transmission is mainly by aerosolised droplet contact, although surface fomite contact and faecal transmission are reported. Symptoms of coronavirus include high-grade fever, severe cough and breathlessness. Cytokine induction causes heavy neutrophilia in the alveoli, with capillaritis, fibrin deposition and thick mucositis causing respiratory failure, acute lung injury and death. Conversely approximately one in eight patients are estimated to have an entirely benign course, transmitting the virus with no clinical manifestation of the disease.1 2 Chest pain in COVID-19 may have cardiac causes, including acute coronary syndrome, pericarditis and myocarditis.3 We present the first described case of acute pericarditis in the absence of initial respiratory symptoms secondary to COVID-19.
A 66-year-old farmer was admitted with 1-day history of acute-onset severe pleuritic chest pain, with four episodes lasting 10–15 min. The pain was worse when lying flat and relieved by leaning forward. He had no sweating nor fever. His history includes Crohn’s disease, hypertension and benign prostatic hyperplasia. His medications were esomeprazole, ramipril and tamsulosin. He had a 40 pack-year smoking history and a significant familial premature coronary disease. His vaccination schedule was up to date, and he had not travelled recently. On examination his temperature was 36.9°C, blood pressure was 134/83 mm Hg, heart rate was 86 beats/min, respiratory rate was 16 breaths/min and an O2 saturation of 99% on ambient air. His general, cardiovascular and respiratory examinations were normal.
Full blood count, urea and electrolytes, coagulation profile, and liver function tests were normal. His C reactive protein (CRP) was 7 mg/L (normal <5 mg/L). High sensitivity cardiac troponin T (hs-cTnT) on admission and at 6 hours were 10 ng/L and 13 ng/L, respectively (normal <14 ng/L). His ECG showed ST segment elevation in most leads with PR interval depression, and his chest X-ray (CXR) confirmed clear lungs with no abnormality (figure 1). Transthoracic echocardiogram (TTE) confirmed normal structure and function, although his pericardium was echo bright with no pericardial effusion (figure 2). CT of the thorax, abdomen and pelvis was normal.
Transthoracic echocardiogram showing brightened pericardium (white arrows) with no effusion.
Serum, nasopharyngeal and oropharyngeal swab specimen samples were sent for aetiological viruses associated with pericarditis. However, the patient presented in February 2020, which was early in the chronology of COVID-19 in Ireland and he did not have routine COVID-19 screening swabs. Complement levels, erythrocyte sedimentation rate and connective tissue screens were negative. Nucleic acid amplification tests for influenza A and B were negative. Cardiac MRI (cMRI) with adenosine stress perfusion showed a structurally normal heart with no effusion, fibrosis, infarction or infiltration. No inducible perfusion defects were evident during adenosine stress. His pericardium appeared mildly thickened (figure 3).
Cardiac MRI of the patient with perfusion showing normal left ventricle muscle (black arrows). The pericardium, pointed by white arrows, shows mild thickening (bold white) with no effusion.
Differential diagnoses included myocarditis, acute coronary syndrome, pericarditis or pleuritis.
A diagnosis of pericarditis was made based on typical chest pain, ECG presentation and TTE. He was started on oral colchicine two times per day for 2 weeks and was discharged on day 4.
Outcome and follow-up
The patient was readmitted on day 6 with recurrence of intermittent pleuritic chest pain and dry cough. Vital signs, physical examination and blood tests were normal. CXR and ECG remained unchanged. Viral serology was negative for routine viruses associated with pericarditis. A COVID-19 viral PCR nasopharyngeal swab was positive.
The public health team was notified and the patient was isolated. On day 8 he developed upper respiratory tract symptoms with peak temperature of 38.7°C. Lymphopaenia (0.3×109, normal >1×109/L) with normal interleukin-6 (5.77, normal 0.09–7.26 pg/mL), CRP and hs-cTnT were seen. Blood culture showed no growth, and serial CXR remained normal. He recovered with symptomatic treatment and oral colchicines and was discharged on day 12.
COVID-19 has numerous adverse effects on the cardiovascular system. Cardiac injury with troponin leak is associated with increased mortality in COVID-19, and its clinical and radiographic features are difficult to distinguish from those of heart failure.4–6 One reported COVID-19 case with upper respiratory tract symptoms had haemorrhagic pericardial effusion with tamponade.7 To our knowledge this is the first case where COVID-19 presents as pericarditis, in the absence of evident respiratory or myocardial involvement.
Acute pericarditis is the most common disease of the pericardium and is responsible for 0.2% of chest pain-related hospitalisations. Conversely 40%–85% of pericarditis cases are of unknown aetiology, probably due to difficulty in obtaining diagnostic pericardial samples. It is commonly seen in viral infections, including coxsackie, enterovirus, herpes simplex, cytomegalovirus, H1N1, respiratory syncytial virus, parvovirus B19, influenza, varicella, HIV, rubella, echovirus, and hepatitis B and C, although the viruses responsible in a given patient may be different genotypes of the same virus or different coexistent viruses.8 9
In this patient respiratory swabs were initially negative, and viraemia first manifested with dry pericarditic symptoms, with a later diagnosis of COVID-19. Defining the underlying causative virus is not always possible. Serological tests are only suggestive of a diagnosis of pericarditis and may yield false negative results. Pericardial inflammation may prompt symptoms, yet may precede the generation of an observable pericardial effusion. TTE is recommended to exclude significant effusion, although the absence of fluid does not rule out active pericarditis. cMRI can describe pericardial thickening or small effusions, which are not appreciated on TTE, assess for myocarditis on T2-weighted imaging, define pericardial inflammation on late gadolinium phase and quantify systolic function.10 Pericardiocentesis is the gold standard for definition of the underlying cause, providing a sufficient depth of fluid at a favourable angle is seen on TTE, although this carries associated risk of serious cardiac injury and a clinical diagnosis may be made if other supportive features are present.
Acute pericarditis is usually self-limiting, although it recurs in up to 30% of cases. Most patients recover in 2–4 weeks with supportive measures, which would conventionally include non-steroidal anti-inflammatory drugs (NSAIDs), colchicines and treating the causative disease. Applying this to a patient with COVID-19 requires balancing this conventional approach with an emerging understanding of pharmacotherapy in COVID-19. Colchicine inhibits microtubule, cell adhesion molecule and inflammasome activity, and is of use in preventing relapse in pericarditis at first presentation.11 It is being trialled as a potential therapeutic anticytokine agent in COVID-19 in Italy, with one report of its use being associated with improvement.12 Conversely the use of NSAIDs in COVID-19 may be harmful, with previously recognised increased risks of stroke and myocardial infarction (MI) with NSAIDs in acute respiratory infections raising concerns. No effective respiratory benefit has been seen with glucocorticoid use in COVID-19, although their use in pericarditis may promote relapse.13 14
Currently, our understanding of the transmission dynamics and the spectrum of clinical illness of COVID-19 is limited. Cardiac involvement with various ECG presentations is possible and clinicians all across the globe need to be aware of this possibility. This case highlights the importance of recognising COVID-19 infection with atypical clinical presentations such as pericarditis and non-specific ECG changes, and coordination with healthcare team regarding prompt isolation to decrease the risk of transmission of the virus and if any need of early hospitalisation. This case report is helpful in treating patients with this unique clinical presentation.
I woke up one day and I had a nagging pain in the center of my chest, which I never had or felt before, sharp like a knife and pressure on top of it as well. It was a constant nagging pain. It was relieving when I was sitting forward and back worsened as I was lying down in the bed. I felt more weak that day and had no energy. Then pain got a bit worse at midday and my wife advised me to visit my doctor -general practitioner as a felt weak. After my doctor saw me, he advised me to go to the hospital and get myself check out to make sure I am not having a heart attack. I and my wife got very nervous. We came urgent to hospital emergency where a nurse examined me first, followed by a doctor and suggested they don’t think that I am having a heart attack. He referred me to heart expert, who suggested that I have to be admitted in the hospital for more tests. They kept me for three days and all my tests like chest and body scans and bloods suggested that I have inflammation around the layers of heart. I was given some medication and discharged home that it will get better in a few days. I went home, the pain was there, it didn’t went completely but improved slightly. It was worse with lying down in the bed. It wasn’t going away despite me doing all what I was told for next few days. I came back to emergency department in 1st march as the pain wasn’t settling at all with the medication. I went through all this process again. I was isolated, swabbed my nose for this new virus-COVID-19. I did not had any sick contact or any other viral contact. I was nervous, and the result came positive. I was kept in separate part of hospital with no direct visitors to me and my family called me on the phone. I thought I am going to die but all the doctors and nurses reassured me. I developed slight cough and flu like illness for 2 days and then I got better next few days and I came home. I was told to follow strict isolation and precautions. No issues since discharge feeling very well. It’s an unpleasant experience to be part of virus and I thought I won’t make it as there was uncertainty about future events. I am greatly thankful to all the team who were involved in my care.
Pericarditis is a potential presentation of COVID-19.
COVID-19 can have an atypical presentation with non-respiratory symptoms.
Recognition of an atypical symptom of COVID-19 allows for early isolation and limits the spread.
Zhu J, Ji P, Pang J, et al. Clinical characteristics of 3062 COVID‐19 patients: a meta‐analysis. J Med Virol 2020;54. doi:doi:10.1002/jmv.25884. [Epub ahead of print: 15 Apr 2020].Google Scholar
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Inciardi RM, Lupi L, Zaccone G, et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020. doi:doi:10.1001/jamacardio.2020.1096. [Epub ahead of print: 27 Mar 2020].pmid:http://www.ncbi.nlm.nih.gov/pubmed/32219357Google Scholar
Shi S, Qin M, Shen B, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol 2020. doi:doi:10.1001/jamacardio.2020.0950. [Epub ahead of print: 25 Mar 2020].pmid:http://www.ncbi.nlm.nih.gov/pubmed/32211816Google Scholar
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Background—The most troublesome complication of acute pericarditis is recurrent episodes of pericardial inflammation, occurring in 15% to 32% of cases. The cause of the recurrence is usually unknown, although in some cases it may be traced to viral infection or may be a consequence of coronary artery bypass grafting. The optimal method for prevention has not been fully established; accepted modalities include nonsteroidal anti-inflammatory drugs, corticosteroids, immunosuppressive agents, and pericardiectomy.
Methods and Results—Based on the proven efficacy of colchicine therapy for familial Mediterranean fever (recurrent polyserositis), several small studies have used colchicine successfully to prevent recurrence of acute pericarditis after failure of conventional treatment. Recently, we reported the results from the largest multicenter international study on 51 patients who were treated with colchicine to prevent further relapses and who were followed up for ≤10 years.
Conclusions—In light of new trial data that have accumulated in the past decade, we review the evidence for the efficacy and safety of colchicine for the prevention of recurrent episodes of pericarditis. Clinical and personal experience shows that colchicine may be an extremely promising adjunct to conventional treatment and may ultimately serve as the initial mode of treatment, especially in idiopathic cases.
Acute inflammation of the pericardium is usually of idiopathic etiology, but it may also be secondary to systemic infection, acute myocardial infarction, cardiac contusion, and autoimmune diseases.1
The most troublesome complication of acute pericarditis is the development of recurrent episodes of pericardial inflammation, occurring in 15% to 32% of cases.2345 Recurrent pericarditis is, in most cases, idiopathic. The pathophysiological process may involve the immune system6,7: high titers of anti-myocardial antibodies have been found in post–open heart surgery patients with acute pericarditis. The optimal method for preventing recurrences has not been established. Therapeutic modalities are nonspecific and include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive agents, and pericardiectomy.18 Relapses may also occur during reduction of drug doses (incessant pericarditis) or at varying intervals after discontinuation of treatment (recurrent pericarditis).9 Because treatment is often difficult and recurrences may occur over a period of many years,10 constant efforts are being directed toward establishing better means for prevention. In light of recent trial data, we will review the evidence supporting the use of colchicine in preventing recurrent episodes of pericarditis.
On the basis of proven efficacy of colchicine in preventing relapses of systemic inflammatory processes in familial Mediterranean fever (recurrent polyserositis),1112 Rodriguez de la Serna and colleagues13 suggested in 1987 that colchicine be used to prevent recurrences of acute pericarditis. They reported on 3 patients who had recurrent pericarditis (2 idiopathic and 1 with systemic lupus erythematosus), despite adequate treatment with corticosteroids. All were treated with colchicine (1 mg/d) with tapering of the corticosteroids within 2 months. There were no relapses throughout the follow-up period of 15 to 35 months.
In a later prospective study, Guindo and colleagues14 reported on 9 patients (5 idiopathic, 2 post–open heart surgery, 1 with Dressler’s syndrome, and 1 with systemic lupus erythematosus) in whom NSAIDs and corticosteroids failed to prevent relapses of pericarditis (mean of 4.3 episodes per patient). All were treated with combined prednisone (20 to 60 mg/d), which was tapered and discontinued within 6 weeks, and colchicine (1 mg/d). Chest pain was effectively relieved, and no recurrences of pericarditis were noted within a 10- to 54-month follow-up period.
Adler and coworkers10 reported on 8 patients with recurrent pericarditis (5 idiopathic, 2 post–open heart surgery, 1 post chest trauma) who had not responded to NSAIDs (6 patients), corticosteroids (7 patients), and pericardiocentesis (3 patients). All responded to colchicine (1 mg/d) and corticosteroids. The corticosteroids were discontinued within 2 to 6 months, and no recurrences were noted during the 18 to 34 months of follow-up. This result contrasts with a total of 26 relapses in these 8 patients before the introduction of colchicine. Four patients in whom colchicine had been withdrawn because of noncompliance or mild gastrointestinal side effects experienced a relapse within 1 to 12 weeks. With reinstitution of colchicine therapy, they remained symptom-free for the 15 to 24 months of follow-up.
Millaire and coworkers15 reported on 19 patients who had recurrent pericarditis and were treated with colchicine (loading dose of 3 mg/d, reduced to 1 mg/d). Fourteen had no recurrences during a follow-up period of 32 to 44 months. In 4 others, relapses were successfully treated with NSAIDs, and these patients remained symptom-free for an additional 11 to 37 months. Only 1 patient had multiple relapses and needed corticosteroids. The authors concluded that colchicine was an effective alternative therapy for recurrent pericarditis and might even replace corticosteroids. In another report by Adler et al,16 colchicine totally prevented relapses in 56% of patients with previous episodes (range, 2 to 15 attacks) in a long-term follow-up (mean, 36 months per patient) study, and when relapses did occur, they were usually mild and easily controlled without steroids. These researchers suggested that colchicine might even serve as the initial mode of therapy for recurrent pericarditis, because most of the patients who experienced relapses after the institution of colchicine or its withdrawal were those who had previously been treated with corticosteroids.16 Indeed, several studies have found that corticosteroids may have severe side effects and lead to new recurrences of pericarditis or prolong disease duration.17181920 Thus, colchicine may also have a role in facilitating their tapering-off process.9 Still, some authors doubt the efficacy of colchicine because a double-blind, controlled study on the subject is difficult to perform.21 It was for this reason that Fowler and Harbin22 examined the natural history of recurrent pericarditis to determine the frequency of spontaneous remissions. Of the 31 patients included in their study, only 8 had a remission period that exceeded 1 year; in 5 of the 8, remission exceeded 2 years.
A partial answer to these doubts may be found in the largest multicenter study on recurrent pericarditis and colchicine published to date.23 Fifty-one affected patients (36 men and 15 women; mean±SD age, 40.8±18.7 years) who were treated with colchicine to prevent further relapses were followed up for ≤10 years (range, 6 to 128 months; mean, 36.0 months). The pericarditis was idiopathic in 33 patients and secondary in 18. Despite treatment with NSAIDs (n=47), corticosteroids (n=29), pericardiocentesis (n=8), or some combination thereof, 187 recurrences (mean, 3.58±3.64; range, 2 to 15) were noted before colchicine therapy was initiated, with a mean interval between crises of 2.0 months (range, 0.5 to 19 months). During 1004 patient-months of colchicine treatment, only 7 of 51 patients (13.7%) presented with new recurrences. Colchicine was discontinued in 39 patients, and 14 of them (35.8%) experienced relapses. These recurrences were generally minor and were effectively controlled in all patients by the reinstitution of colchicine therapy, sometimes with a dose adjustment of the drug (≤2 mg/d). Gastrointestinal side effects were mild (diarrhea and nausea) and resolved in all patients. During the 2333 patient-months of follow-up, 31 patients (60.7%) remained recurrence-free. Comparison of the symptom-free periods before and after colchicine treatment yielded significant statistical differences (3.1±3.3 versus 43.0±35.0 months, P<0.0001). The authors concluded that colchicine was effective and safe for the long-term prevention of recurrent pericarditis.
The exact mechanism whereby colchicine prevents recurrences of pericarditis is still not fully understood. Colchicine has been used for several centuries as an anti-inflammatory agent for acute arthritis and is the most specific known treatment for acute attacks of gout. Colchicine binds to tubulin, blocks mitosis,9 and inhibits a variety of functions of polymorphonuclear leukocytes both in vivo and in vitro.24 Colchicine also interferes with the transcellular movement of collagen.25 The close proximity of lymphoid components and fibroblasts at inflammatory sites and the production of lymphokines, which influence fibroblast chemotaxis, proliferation, and protein synthesis, are now well recognized.26 Thus, colchicine may reduce immunopathic antifibroblastic properties. The peak concentration of colchicine in white blood cells may be ≥16 times the peak concentration in plasma. This preferential concentration of colchicine in lymphocytes is related to its observed therapeutic effect.27
Cumulative anecdotal evidence indicates that colchicine may also be effective in the treatment of the initial episodes of acute pericarditis. Millaire and Durlaux,28 in a study of 19 patients, described the efficacy of colchicine for the first episode of acute pericarditis, especially when it was idiopathic, viral, or post–open heart surgery. Colchicine effectively controlled the acute phase of pericarditis in almost all cases. Only two relapses were noted in a mean follow-up period of 5 months (range, 1 to 12 months), one due to discontinuation of treatment after 8 days and the other due to noncompliance.
Recently, we examined the usefulness of colchicine for the treatment of large pericardial effusions as complications of idiopathic pericarditis.29 Colchicine (1 mg/d) was administered to two patients (26 and 2 years old) with large acute or chronic pericardial effusions who did not respond well to therapy with NSAIDs, corticosteroids, and pericardiocentesis. Response was immediate and dramatic in both cases, with disappearance of the pericardial effusion on echocardiography. Neither patient suffered a relapse during the respective 24 and 6 months of follow-up.
In addition to its apparently greater efficacy compared with corticosteroids,916 colchicine may also have a sparing effect on steroids, which have severe systemic side effects over time and may prolong disease duration.17181920 Furthermore, immunosuppressive drugs and pericardiectomy are generally not appropriate and may even be life threatening,21 whereas colchicine is usually well tolerated, with only minor side effects. During a total of 1004 patient-months of colchicine treatment (mean, 12 months per patient), temporary discontinuation of the drug or a reduction of its dose was needed in only 7 of 51 patients (13.7%).23 This was due to mild gastrointestinal side effects (diarrhea and nausea) in all cases, which are the common drawbacks of colchicine therapy. Drug toxicity with respect to long-term administration of colchicine might be estimated from familial Mediterranean fever or gout patients. Azoospermia and chromosomal abnormalities have been reported with long-term treatment,30 but these findings are debatable.
In conclusion, colchicine seems to be an effective and safe agent for the prevention of recurrent episodes of pericarditis. Colchicine is an extremely promising adjunct to the conventional treatment of recurrent pericarditis and may ultimately serve as the initial mode of treatment, especially in idiopathic cases. Considering that recurrent pericarditis is not life threatening and that long-term treatment is aimed at improving the quality of life, we suggest that corticosteroids should be limited to very severe cases. Milder cases may initially be treated with colchicine as well as with NSAIDs (ibuprofen). The recommended dose of colchicine according to most studies is 1 mg/d for at least 1 year, with a gradual tapering off. The need for a loading dose of 2 to 3 mg/d at the beginning of treatment is unclear. The drug is well tolerated. Gastrointestinal side effects develop in only a small proportion of patients, are usually minor, and do not require discontinuation of treatment in most cases.
Despite the promising data on the efficacy and safety of colchicine for recurrent pericarditis that have accumulated in the past decade, large, controlled, prospective studies are required to provide definitive answers on the subject.
We thank Gloria Ginzach, Marian Propp, and Charlotte Sacks for their editorial and secretarial assistance.
Correspondence to Y. Adler, MD, Department of Cardiology, Rabin Medical Center, Beilinson Campus, Petah Tiqva, 49100, Israel.
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Coronavirus disease-2019 (COVID-19) infection is a multisystem disease not restricted to the lungs. It has a negative impact on the cardiovascular system by causing myocardial damage, vascular inflammation, plaque instability, and myocardial infarction. The presence of myocardial injury is a poor prognostic sign. Electrocardiogram (ECG), a simple bedside diagnostic test with high prognostic value, can be employed to assess early cardiovascular involvement in such patients. Various abnormalities in ECG like ST-T changes, arrhythmia, and conduction defects have been reported in COVID-19. We aimed to find out the ECG abnormalities of COVID-19 patients.
We performed a cross-sectional, hospital-based descriptive study among 315 COVID-19 in-patients who underwent ECG recording on admission. Patients’ clinical profiles were noted from their records, and the ECG abnormalities were studied.
Among the abnormal ECGs 255 (81%), rhythm abnormalities were seen in 9 patients (2.9%), rate abnormalities in 115 patients (36.5%), and prolonged PR interval in 2.9%. Short QRS complex was seen in 8.3%. QT interval was prolonged in 8.3% of the patients. Significant changes in the ST and T segments (42.9%) were observed. In logistic regression analysis, ischemic changes in ECG were associated with systemic hypertension and respiratory failure.
In our study, COVID-19 patients had ischemic changes, rate, rhythm abnormalities, and conduction defects in their ECG. With this ongoing pandemic of COVID-19 and limited health resources, ECG—a simple bedside noninvasive tool is highly beneficial and helps in the early diagnosis and management of cardiac injury.
How to cite this article
Kaliyaperumal D, Bhargavi K, Ramaraju K, Nair KS, Ramalingam S, Alagesan M. Electrocardiographic Changes in COVID-19 Patients: A Hospital-based Descriptive Study. Indian J Crit Care Med 2022;26(1):43–48.Keywords: Coronavirus disease-2019, Electrocardiogram change, Rate abnormalities, ST-T changes
A cluster of pneumonia cases were reported due to “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2) at the end of 2019 in the city of Wuhan, in the Hubei Province of China. Soon coronavirus disease-2019 (COVID-19) was declared as a pandemic owing to its rapid spread across the countries.1 Initially regarded as a respiratory infection, COVID-19 is now known to affect all major systems in the body. Quite a lot is discussed in literature last year about COVID-19 and its effect on lungs and systemic response. However, very little is debated about cardiovascular involvement in COVID. It has been observed that lung involvement is more severe in patients with preexisting cardiac involvement. However, in sharp contrast new-onset cardiac involvement is also noted in a few patients and few patients do present with cardiac symptoms alone without lung involvement.2 The spectrum of presentation is wide-ranging from patients having no cardiac disease at all, asymptomatic but with elevated cardiac markers, having symptoms of overt cardiac disease such as angina, cardiogenic shock, heart failure, cardiac arrhythmias, and sudden cardiac death.
Arrhythmia and acute cardiac injury were reported in 16.7 and 7.2% of the COVID patients.3 In addition to the systemic inflammatory response, the physiological mechanisms identified to cause cardiac involvement in COVID-19 patients are hypoxemia-related myocardial cell injury and endothelial cell damage due to upregulated expression of angiotensin-converting enzyme 2 (ACE 2) in the heart and lungs.4
The electrocardiogram (ECG) changes reflect cardiac involvement with diverse manifestations. Arrhythmia and conduction defects are found to be more prevalent among SARS-CoV-2-infected individuals.5 Myocardial ischemia, myocarditis, shock, hypoxia, and electrolyte abnormalities were the factors identified to cause arrhythmias.6 The presence of cardiac involvement may imply poor prognosis and an adverse outcome.7 Therefore, it is pertinent to assess and monitor the cardiac abnormalities paving way for a prompt action. ECG, a simple bedside diagnostic test with high prognostic value, can be employed to assess cardiovascular involvement in COVID-19 patients. We aimed to find out the ECG abnormalities of patients with SARS-CoV-2 infection.
Materials and Methods
This cross-sectional, hospital-based descriptive study was conducted among 315 COVID-19 patients admitted in our tertiary care center during October to December 2020 after obtaining the human institutional ethics committee clearance and informed consent from the patients participating in the study [IHEC NO: Project No: 20/217]. Patients whose COVID status was confirmed by real-time reverse transcriptase polymerase chain reaction on nasopharyngeal and oropharyngeal swabs were included in the study.
Consecutive patients admitted to our hospital with SARS-CoV-2-positive status underwent ECG testing on admission and were included in the study. Patients’ clinical profiles that include symptoms, duration, and severity of illness, and comorbid status were noted from their clinical records. ECGs were reviewed and interpreted by two physicians (together responsible for the interpretation of >100,000 ECGs per year) who were blinded to the clinical status of the patients. Patients with ventricular pacing, immune suppression, stroke, malignancy and patients on beta blockers and anti-arrhythmic drugs were excluded.
The ECG data include heart rate, rhythm categorized as normal sinus rhythm or atrial fibrillation/flutter, atrial premature contractions, ventricular premature contractions, atrioventricular block, axis deviation, bundle branch block, intraventricular conduction block (QRS duration of >110 ms), Bazett-corrected QT interval (in milliseconds), presence of left or right ventricular hypertrophy, myocardial infarction, and the presence of ST segment or T-wave changes (localized ST elevation, localized T-wave inversion, or other nonspecific repolarization abnormalities).
The data collected from the patients were tabulated using Microsoft Excel. Descriptive statistics were employed for analysis. Data were expressed as mean ± standard deviation for continuous variables and proportions for categorical variables. Logistic regression analysis was employed to study the association between clinical variables and occurrence of various types of ECG abnormalities. The results were expressed in odds ratio with 95% confidence interval after adjusting for important confounders.
A total of 315 patients satisfying the inclusion criteria were included in the study. Out of the total 315 patients studied, 92 (29.2%) were females and 223 (70.8%) were males with an average age of 52.6 ± 16.3 years. Clinical characteristics like symptoms on admission, severity and duration of illness, duration of the hospital stay, disease course, and outcomes are depicted in Table 1.
Demographic and clinical characteristics of the study population
Among the abnormal ECGs 255 (81%), rhythm abnormalities were seen in 9 patients (2.9%); rate abnormalities in 115 patients (36.5%)—bradycardia (12.7%) and tachycardia (23.8%); and prolonged PR interval in 2.9% patients. Short QRS complex was seen in 8.3%. QT interval was prolonged in 8.3% of the patients. There were significant changes in the ST and T segments (Table 2).
Distribution of ECG changes at admission among the study population
In logistic regression model (Table 3), subjects with moderate-to-severe COVID-19 illness were twice likely to have at least one of the above-described abnormalities in ECG independent upon age, gender, and preexisting cardiac diseases [adjusted odds ratio 2.02 (95% confidence interval 1.04–3.95)]. Among all subjects, ischemic changes in ECG (ST segment changes and T-wave inversion) appeared to be associated with systemic hypertension [adjusted odds ratio 1.73 (95% confidence interval 0.96–3.11)] and respiratory failure [adjusted odds ratio 1.58 (95% confidence interval 0.94–2.66)] after adjusting age, gender, and preexisting heart diseases. The above-mentioned associations showed a trend toward statistical significance. No other ECG changes had any significant association with clinical variables studied.
Logistic regression analysis of association between ECG changes and clinical variables
Variable-associated ECG abnormalities
Unadjusted odds ratio (95% confidence interval)
Adjusted odds ratio (95% confidence interval)€
Ischemic changes in ECG (ST segment elevation/depression and/or T inversion)
Of the 315 patients, 19 patients died ultimately due to COVID. The ECG abnormalities studied in these patients are shown in Figure 2. Prolongation of QTc interval (42%) and tachycardia (36.8%) were the commonest changes noted in them. The various ECG abnormalities encountered in the study population and the outcomes in each group are depicted in Figure 3. Adverse final outcomes were noted in 11.5% of the patients who had ST-T changes and QTc prolongation and 8.4% of the patients who had tachycardia.
Stacked column chart depicting the various ECG abnormalities and patient outcomes in each category
Myocardial injury associated with cardiac dysfunction and arrhythmias has been reported in infectious diseases. ECG changes observed in infections include hemorrhagic fever,8,9 leptospirosis,10 scrubtyphus,11 diphtheria,12 trichinellosis,13 and trypanosomiasis.14 Myocardial injury observed in dengue viral infection is evidenced by the presence of ECG abnormalities like atrial and ventricular premature beats, prolonged PR interval, bundle branch block s, and ST and T segment changes.15 Abnormal ECG findings were found to be reported in 28% of the hospitalized patients infected with novel H1N1 influenza virus.16 Similarly, now there is growing evidence that SARS-CoV-2 also has the potential to have a negative impact on the cardiovascular system.
There are multiple proposed mechanisms for cardiac damage in COVID-19. These include cytokine release syndrome,17 direct myocardial damage as in viral myocarditis due to the interaction between virus and ACE 2,18,19 coronary spasm, induction of a hypercoagulable state, plaque instability causing rupture, and acute coronary syndrome.20 Other potential mechanisms may include cardiac toxicity due to antivirals, steroids, and electrolyte abnormalities.
Even the earliest cases in China had evidence of myocardial injury21 and previous studies did estimate the prevalence as between 1 and 7% of the patients and 26% required intensive care.22 Studies by Shi et al. also inferred that cardiac involvement was associated with high mortality.23
In our study, we observed sinus tachycardia (23.8%), sinus bradycardia (12.7%), and atrial arrhythmia (3.5%). This is in accordance with a study by Brit Long where the commonest ECG abnormality in COVID patients was sinus tachycardia followed by atrial fibrillation, ventricular arrhythmias, QTc prolongation, and ST-T segment changes.24 Atrial fibrillation (3.5%), bradyarrhythmia (1.2%), and nonsustained VT (10.4%) were reported in another study conducted among 700 patients with severe acute respiratory syndrome due to SARS-CoV-2 infection.25
In our study, we encountered ischemic changes (ST segment elevation, T-wave inversion) in 32.4% of the COVID-19 patients irrespective of their underlying cardiac health. Italy published a research study of 28 COVID-19 patients who underwent angiogram for ST elevation myocardial infarction in whom 86% had STEMI as the first presentation of COVID showing that acute coronary event had preceded systemic inflammation. Of these, 79% had typical chest pain, while 21% presented with dyspnea without any chest pain.26
In the present study, 16.2% of the COVID-19 patients presented with QT segment changes (prolonged and shortened). QT interval prolongation has been noted in about 13% of the COVID-19 patients. Major contributing factors to this particular abnormality may be the list of several (now unapproved) drugs previously used for COVID-19 treatment like hydroxychloroquine and azithromycin.27,28 QT interval prolongation may cause rhythm disturbances and hemodynamic instability requiring ICU admission and if not attended to may cause sudden cardiac death.
Pulmonary embolism may be a presenting issue of COVID-19 as well as its complication. A recent study of ECG findings in pulmonary embolism in COVID patients showed that abnormalities were mostly nonspecific including sinus tachycardia and minimal ST segment or T-wave changes. Specific and classic findings (classic S1Q3T3 pattern) were seen in less than 10% of the patients.29
All the 19 COVID patients who had succumbed to death had abnormal ECG findings. In a retrospective study to highlight the prognostic significance of ECG in COVID, Yang et al. have compared the ECG changes in survivors and nonsurvivors.30 It was observed that the nonsurvivors had significantly higher rates of prolonged QTc interval, axis deviation, arrhythmias, ST-T changes, and an overall higher abnormal ECG score. In our study population, QTc prolongation and tachycardia were the commonest changes in the deceased.
In a retrospective ECG analysis in the COVID-19 patients, Wang et al. have studied the ECG characteristics in the critically severe and severe group of patients.31 He has observed that 84.5% of the patients had abnormal ECG findings in the critically severe group as against 53% in the severe group. ST-T changes (48.5%) and sinus tachycardia (30%) were the most common abnormalities noted in the critically severe group of patients. In our study population, mortality was observed in 11.5% of the patients who had ST-T changes, 11.5% of the patients who had QTc prolongation, and 8.4% of those who had sinus tachycardia.
Other factors that influence the ECG findings such as age, body mass index (BMI), electrolyte imbalances, inflammatory markers, and specifically cardiac markers were not considered in the analysis. We wish to extend the present study to find out the influence of SARS-CoV-2 virus on electrophysiology of cardiac muscle excluding these factors that affect the ECG parameters. Moreover, correlation of ECG findings with echocardiogram, clinical outcomes, and follow-up will help us understand the pathophysiology of cardiac diseases in COVID-19 disease. This will strengthen the race against COVID infection by enriching our knowledge and unraveling further mysteries around this mysterious infection.
In our study, COVID-19 patients presented with ischemic changes, rhythm abnormalities, and conduction defects. With SARS-CoV-2 having already gained momentum worldwide, it is important to deploy simple, cost-effective bedside examination, and diagnostic tests considering our limited health resources. ECG is of paramount importance in the Emergency COVID Department too as it is central to risk stratification and is predictive of an adverse outcome.
SARS-CoV-2 extends its prongs well beyond the lungs.
There are multiple mechanisms for myocardial damage in COVID-19.
Myocardial injury when present is a poor prognostic sign.
ECG is a simple bedside diagnostic test to screen for cardiac abnormalities.
The commonest ECG abnormalities in our study were sinus tachycardia, ischemic changes, and QTc segment abnormalities.
It is crucial to monitor the patients for cardiac manifestations that will help to identify the complications and initiate prompt treatment.
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Articles from Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine are provided here courtesy of Indian Society of Critical Care Medicine
Five months after being infected with the coronavirus, Nicole Murphy’s pulse rate is going berserk. Normally in the 70s, which is ideal, it has been jumping to 160, 170 and sometimes 210 beats per minute even when she is at rest — putting her at risk of a heart attack, heart failure or stroke.
No one seems to be able to pinpoint why. She’s only 44, never had heart issues, and when a cardiologist near her hometown of Wellsville, Ohio, ran all of the standard tests, “he literally threw up his hands when he saw the results,” she recalled. Her blood pressure was perfect, there were no signs of clogged arteries, and her heart was expanding and contracting well.
Murphy’s boomeranging heart rate is one of a number of mysterious conditions afflicting Americans weeks or months after coronavirus infections that suggest the potential of a looming cardiac crisis.
A pivotal study that looked at health records of more than 153,000 U.S. veterans published this month in Nature Medicine found that their risk of cardiovascular disease of all types increased substantially in the year following infection, even when they had mild cases. The population studied was mostly White and male, but the patterns held even when the researchers analyzed women and people of color separately. When experts factor in the heart damage probably suffered by people who put off medical care, more sedentary lifestyles and eating changes, not to mention the stress of the pandemic, they estimate there may be millions of new onset cardiac cases related to the virus, plus a worsening of disease for many already affected.
“We are expecting a tidal wave of cardiovascular events in the coming years from direct and indirect causes of covid,” said Donald M. Lloyd-Jones, president of the American Heart Association.
In February 2021, the National Institutes of Health launched an initiative to look at the causes and possible treatments for long covid, the constellation of symptoms from brain fog and exercise fatigue to heart-related issues that some people experience well past their initial infections. In addition, the American College of Cardiology has recognized the serious, longer-term effects of the coronavirus by preparing new guidelines, scheduled out in March, for monitoring and returning to exercise after infection. But many experts and patient advocacy groups say more is needed, and are calling on President Biden and other leaders for comprehensive changes in the health care system that would provide more funding for research and treatment, financial support for people who can no longer work and address the social and emotional consequences of illness in the decades to come.
Zaza Soriano, 32, a software engineer from Millersville, Md., who works for a NASA subcontractor, got covid right before Christmas despite being fully vaccinated and boosted, and since then, her blood pressure has remained very high with the bottom number, or diastolic pressure when the heart rests between beats sometimes as high as 110 when it should be lower than 80. She also has brain fog and her joints ache.
“It’s so frustrating we still know so little about why this is happening,” she said.
Ziyad Al-Aly, an assistant professor of medicine at Washington University and a Veterans Affairs physician who co-authored the Nature Medicine study, describes the pandemic as an earthquake. “When the earth stops shaking and the dust settles, we will have to be able to deal with the aftermath on heart and other organ systems,” he said.
“Governments around the world need to pay attention,” Al-Aly emphasized. “We are not sufficiently prepared.”
Heart disease is the planet’s No. 1 killer, responsible for 17.9 million deaths, or a third of the total each year before the pandemic, and there’s already growing evidence of the outsize impact the coronavirus is having on our long-term health.
Multiple studies suggest that Americans’ collective blood pressures has jumped since the crisis began. According to a December study in the journal Circulation, for example, the average blood pressure among a half-million U.S. adults studied from April to December 2020 went up each month for both of the numbers measured by monitors.
The Centers for Disease Control and Prevention as of this month had logged more than 1 million excess deaths or deaths since the start of the pandemic that are beyond what we would have expected in normal times. While most of those were directly caused by the virus, there were also an additional 30,000 deaths due to ischemic heart disease and nearly 62,000 additional deaths due to hypertensive disease.
When the coronavirus first hit the United States in 2020, doctors were surprised by the heart involvement in cases they saw: professional athletes with signs of myocarditis or hardening of the heart walls; patients dying from their illness with hundreds of tiny clots in major organs; children rushed to emergency rooms with an inflammatory reaction involving cardiac complications.
Many of those presentations turned out to be rare or rarely serious. But they led researchers to an important discovery: that SARS-CoV-2 could directly attack the heart and blood vessels, in addition to the lungs.
Myocarditis has mostly been a transient issue, impacting activity or becoming life-threatening in only a small minority of cases; the clotting is more widespread but something that usually can be controlled with blood thinners; and the pediatric inflammatory syndrome has affected only about 6,400 children out of millions of cases, as of January.
The idea that infections increase cardiovascular risk is not new. It has been documented in cases of influenza and other viruses as well. But in coronavirus, that impact seems “enhanced,” said Antonio Abbate, a professor of cardiology at the VCU Pauley Heart Center. And the early and obvious cases, he said, should serve “as a kind of warning” for the type of longer-term cases we may see into the future.
Indeed, as the months since their infections have turned into years, people who initially had mild or even some asymptomatic coronavirus cases are pouring into cardiology practices across the country.
At Memorial Hermann-Texas Medical Center in Houston, Abhijeet Dhoble, an associate professor of cardiovascular medicine, said they are seeing an increase in arrhythmia, an abnormality in the timing of the heartbeat, and cardiomyopathy, a heart muscle disease. The patients, who previously had covid, range in age from their 30s to 70s and many had no previous heart disease.
“We are seeing the same patterns at university clinics and the hospital,” he said.
Two different processes may be at play, according to David Goff, director of the National Heart, Lung and Blood Institute’s division of cardiovascular sciences. The virus may inflict direct damage to the heart muscle cells, some of which could die, resulting in a weaker heart that does not pump as well. Another possibility is that after causing damage to blood vessels through clots and inflammation, the healing process involves scarring that stiffens vessels throughout the body, increasing the work of the heart.
“It could lead over time to failure of the heart to be able to keep up with extra work,” he explained.
Blood vessels and fatigue
David Systrom, a pulmonary and critical care doctor at Brigham and Women’s Hospital in Boston, said he believes blood vessel damage may be responsible for one of the most common and frustrating symptoms of long covid — fatigue.
Systrom and his colleagues recruited 20 people who were having trouble exercising. Ten had long covid. The other half had not been infected with the virus. He inserted catheters into their veins to provide test information before putting them on stationary bikes and took a number of detailed measurements. The study was published in the journal Chest in January.
In the long covid group, he found that they had normal lung function and at peak exercise, their oxygen levels were normal even as they were short of breath. What was abnormal was that some veins and arteries did not appear to be delivering oxygen efficiently to the muscles.
He theorized this could be due to a malfunction in the body’s autonomic nervous system, which controls involuntary actions such as the rate at which the heart beats, or the widening or narrowing of blood vessels.
“When exercising, it acts like a traffic cop that distributes blood flow to muscles away from organ systems like the kidney and gut that don’t need it. But when that is dysfunctional, what results is inadequate oxygen extraction,” he said. That may lead to the feeling of overwhelming exhaustion that covid long haulers are experiencing.
The overall the message from providers is that “covid by itself is a risk factor for heart disease” like obesity, diabetes, or high blood pressure, according to Saurabh Rajpal, a cardiologist at Ohio State University Wexner Medical Center.
“This is a virus that really knocks people down,” agreed Nicole Bhave, a cardiologist with Michigan Medicine and member of the American College of Cardiology’s science committee. “Even young, healthy people don’t often feel very normal for weeks to months, and it’s a real challenge to distinguish what’s just your body slowly healing versus a new pathological problem.”
“People experiencing what appear to be heart issues should have a “a low threshold for seeing their primary care doctor,” she said.
Unexplained high blood pressure has been a common symptom after covid infection.
Lindsay Polega, 28, an attorney from St. Petersburg, Fla., had never had any medical issues before covid. She had been an all-state swimmer in high school and ran, swam or otherwise exercised an hour or more every day since. But after two bouts with covid, the first in early 2020 and the second in spring 2021, she’s been having what doctors call “hypertensive spikes” that result in shooting pains in her chest that make her shaky and weak. During those incidents, which sometimes occur a few times a day, her blood pressure has gone as high as 210/153 — far above the 120/80, that is considered normal.
One incident happened during a light Pilates class and she had to go to the emergency room. Other times, it has happened while walking. “Sometimes I’ll just be on the couch,” she said.
Each specialist she saw referred her to another — endocrinology, immunology, cardiology, neurology. Finally, she found herself at a long-covid clinic where the doctor theorized the issue may be with her adrenal gland. Scientists have documented that the virus can target the adrenal glands, which produce hormones that help regulate blood pressure among other essential functions. Polega was put on a heavy-duty blood pressure drug called eplerenone that’s typically used in patients after a heart attack, and it has helped to reduce but not eliminate the episodes.
The scariest part for Polega is that women taking eplerenone are cautioned against pregnancy due to research in animals showing low birth weights and other potential dangers. Polega and her boyfriend of six years had recently purchased a house together, and were talking about starting a family soon.
“That’s a big thing to have taken away at my age — my future,” she said.
Of all the symptoms of long covid, among the most baffling have been erratic heart rates and skipped heartbeats with no clear cause.
Tiffany Brakefield, a 36-year-old pharmacy tech from Bonita Springs, Fla., who had covid in June 2020, said the spikes are so unpredictable that she found herself having to sit down on the floor at Walmart during a recent shopping excursion.
“I felt like I was going to fall down, and all I could do was wait for it to calm down on its own,” she said. Her doctors had put her on a heart medication, metoprolol, but it has not helped.
Rick Templeton, a 52-year-old community college instructor in Lynchburg, Va., felt chest tightness along with a racing heart rate, but in his case it disappeared five to six months after his infection in September 2020, and doctors never knew why it happened because his test results were normal.
Rajpal, the cardiologist in Ohio, said a large majority of his post-covid cases are similarly vexing.
“The most common type of long haulers we are seeing have shortness of breath, chest discomfort, and fast heart rate. But when we investigate them for heart disease they come back as normal,” he said.
Goff, the NIH scientist, said the presentation looks similar to a condition known as POTS, or postural orthostatic tachycardia syndrome, in which symptoms such as lightheadedness and heart rate changes are related to reduced blood volume, typically worsened by changing positions. A body of emerging evidence suggests that for many people, it could be a post-viral syndrome.
He said the unstable heart rate for many post-covid patients “can be quite serious and debilitating, and can really interfere with ordinary day-to-day activities.” Doctors can use blood pressure medications to try to stabilize heart rates but because they depress blood pressures at the same time, they can be tricky to use.
Murphy, the Ohio long covid patient, said that when her heart rate soars, which happens several times an hour, she said “it feels like a hamster in my chest.”
Her troubles began on Sept. 5, when she and her teenage daughter tested positive for the virus. Her daughter got over her illness in a few days. Murphy was acutely ill for about three weeks, and many of her symptoms never went away.
The 44-year-old single mom says she’s extraordinarily weak and has trouble with her memory sometimes. Before she was infected, she worked 12-hour days as a day care provider, a waitress and a cashier. Now she’s lucky if she can last three to four hours at her job as a DoorDash driver.
She’s tried to stay active by taking walks but sometimes “when I take steps, it’ll be like stars.” When she saw the cardiologist, she passed out during the stress test on the treadmill.
“I constantly live in fear I’m going to have a heart attack or stroke,” she said.
After all her heart tests came back fine except for her EKG, which showed the jumping heart rate, her doctors referred her to the Cleveland Clinic’s long covid group. She hopes they will help her find answers.
Authors: EUROPEAN SOCIETY OF CLINICAL MICROBIOLOGY AND INFECTIOUS DISEASES FEBRUARY 11, 2022
New research to be presented at this year’s European Congress of Clinical Microbiology and Infectious Diseases (ECCMID 2022, Lisbon, April 23-26) suggests that many of the symptoms connected to post-COVID syndrome (PCC, also known as long COVID) could be linked to the effect of the virus on the vagus nerve – one of the most important multi-functional nerves in the body. The study is by Dr. Gemma Lladós and Dr. Lourdes Mateu, University Hospital Germans Trias i Pujol, Badalona, Spain, and colleagues.
The vagus nerve extends from the brain down into the torso and into the heart, lungs, and intestines, as well as several muscles including those involved in swallowing. As such, this nerve is responsible for a wide variety of bodily functions including controlling heart rate, speech, the gag reflex, transferring food from the mouth to the stomach, moving food through the intestines, sweating, and many others.
Long COVID is a potentially disabling syndrome affecting an estimated 10-15% of subjects who survive COVID-19. The authors propose that SARS-CoV-2-mediated vagus nerve dysfunction (VND) could explain some long COVID symptoms, including dysphonia (persistent voice problems), dysphagia (difficulty in swallowing), dizziness, tachycardia (abnormally high heart rate), orthostatic hypotension (low blood pressure) and diarrhea.
The authors performed a pilot, extensive morphological and functional evaluation of the vagus nerve, using imaging and functional tests in a prospective observational cohort of long COVID subjects with symptoms suggestive of VND. In their total cohort of 348 patients, 228 (66%) had at least one symptom suggestive of VND. The current evaluation was performed in the first 22 subjects with VND symptoms (10% of the total) seen in the Long COVID Clinic of University Hospital Germans Trias i Pujol between March and June 2021. The study is ongoing and continues to recruit patients.
Of the 22 subjects analyzed, 20 (91%) were women with a median age of 44 years. The most frequent VND-related symptoms were: diarrhea (73%), tachycardia (59%), dizziness, dysphagia and dysphonia (45% each), and orthostatic hypotension (14%). Almost all (19 subjects, 86%) had at least 3 VND-related symptoms. The median prior duration of symptoms was 14 months. Six of 22 patients (27%) displayed alteration of the vagus nerve in the neck shown by ultrasound – including both thickening of the nerve and increased ‘echogenicity’ which indicates mild inflammatory reactive changes.
A thoracic ultrasound showed flattened ‘diaphragmatic curves’ in 10 out of 22 (46%) subjects (which translates a decrease in diaphragmatic mobility during breathing, or more simply abnormal breathing). A total of 10 of 16 (63%) assessed individuals showed reduced maximum inspiration pressures, showing weakness of breathing muscles.
Eating and digestive function was also affected in some patients, with 13 of 18 assessed (72%) having a positive screen for self-perceived oropharyngeal dysphagia (trouble swallowing). An assessment of gastric and bowel function performed in 19 patients revealed 8 (42%) had their ability to deliver food to the stomach (via the esophagus) impaired, with 2 of these 8 (25%) reporting difficulty in swallowing. Gastroesophageal reflux (acid reflux) was observed in 9 of 19 (47%) individuals; with 4 of these 9 (44%) again having difficulty delivering food to the stomach and 3 of these 9 (33%) with hiatal hernia – which occurs when the upper part of the stomach bulges through the diaphragm into the chest cavity.
A Voice Handicap Index 30 test (a standard way to measure voice function) was abnormal in 8/17 (47%) cases, with 7 of these 8 cases (88%) suffering dysphonia.
The authors say: “In this pilot evaluation, most long COVID subjects with vagus nerve dysfunction symptoms had a range of significant, clinically-relevant, structural and/or functional alterations in their vagus nerve, including nerve thickening, trouble swallowing, and symptoms of impaired breathing. Our findings so far thus point at vagus nerve dysfunction as a central pathophysiological feature of long COVID.”
Meeting: The European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022)