COVID-19 Collection
Autonomic dysfunction and post–COVID-19 syndrome: A still elusive link
Infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the long-lasting pandemic coronavirus disease 2019 (COVID-19), with dramatic clinical, social, and economic implications. Importantly, evolving experience consistently shows that, in addition to issues related to the acute phase, patients who recover from COVID-19 may present a wide variety of bothersome symptoms, which may be debilitating and significantly impair their quality of life. This condition, when it persists beyond 12 weeks after recovery, is defined as “post–COVID-19” or “long COVID-19” syndrome.Pacing through a pandemic—Coping with the “tip of the iceberg”
The coronavirus disease 2019 (COVID-19) pandemic has presented a once in a generation challenge to our health care systems worldwide. In its early phases, confusion existed about modes of transmission, levels of infection control, and risk to health care personnel. This combined with lack of resources for adequate personal protective equipment (PPE) generated high levels of anxiety for medical teams and rationing of PPE in the early phase. Advise and local guidelines were changing on an almost daily basis, with major challenges in procedural risk assessment in the absence of immediate polymerase chain reaction testing: COVID-19 positivity was assumed until proven otherwise.COVID-19 does not only disturb our social rhythm
With 10 vaccines currently approved and another 81 potentially to be approved in the coming months, the focus on the coronavirus disease 2019 (COVID-19) pandemic has changed from confinement to elimination. However, it is a known viral law that when the going gets tough, the tough get going, with natural selection bringing forth the most favorable mutations. Among these, the most worrying were found in South Africa, Brazil, and the United Kingdom, of which the latter initially has been designated as a “variant of concern.” Early research shows that mutations in these variants might (partly) escape the immune response.Excess out-of-hospital sudden deaths during the COVID-19 pandemic: A direct or indirect effect of SARS-CoV-2 infections?
Since its emergence from Wuhan, China, in December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19), has claimed the lives of >1.7 million individuals worldwide and >317,000 individuals in the United States alone (as of December 21, 2020, 1 PM CST).1,2 Although the acute respiratory and thrombotic complications of COVID-19 seem to explain much of the observed morbidity and mortality, cardiac involvement, including myocardial infarction, myocarditis, and life-threatening ventricular arrhythmias,3–5 seems to be relatively common.COllaboration is a Valuable International/Interdisciplinary Directive for Electrophysiology Progress: NOvel & Tangible Important Lessons Learned COVID-EP: NOT ILL Digital health lessons learned from the COVID experience can improve arrhythmic outcomes
In a crisis, be aware of the danger—but recognize the opportunity.John Fitzgerald KennedyCOVID-19 treatments, QT interval, and arrhythmic risk: The need for an international registry on arrhythmias
In December 2019, the Chinese public health authorities reported several cases of acute respiratory syndrome in the city of Wuhan caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).1,2 In our hyperconnected world, the initial outbreak underwent unprecedented dissemination and has now become this century’s worst pandemic, with more than 8 million people infected and almost 450,000 deaths to date.3Electrophysiology and COVID-19: An era of new potential
During the COVID-19 pandemic and with worldwide medical colleagues, the electrophysiology (EP) community has encountered challenges that are unique in our collective consciousness. Just a few short weeks ago, we focused on accessory pathway potentials, or local abnormal ventricular activation, or pulmonary vein potentials, and/or those from the His bundle. Now, our expanded focus on “potentials” includes arenas outside the EP laboratory as we expand our partnership with procedure centers, hospitals, regions, nations, and the world.EP News: Basic and Translational
Liu et al (Circulation April 15, 2020;doi:10.1161/CIRCULATIONAHA.120.047549, PMID 32293910) provided an overview of coronavirus disease 2019 (COVID-19) that is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The high infectivity of the SARS-CoV-2 virus is contributed by new mutations in the receptor-binding domain and acquisition of a furin cleavage site in the S spike protein. The virus uses the angiotensin-converting enzyme 2 (ACE2) receptor for cell entry, which is mediated by the host cell serine protease TMPRSS2.EP News: Case Reports
Coronavirus disease 2019 (COVID-19) is highly infectious and causes significant strains on health care systems. Routine testing within the hospital is weighed for needed value to minimize exposure to staff. The combination of hydroxychloroquine and azithromycin, both known to prolong the QT interval, was shown to lower the viral load, and early in the COVID-19 pandemic, the drugs were used to try to lower the morbidity and mortality of the infection. Gabriels et al (doi: https://doi.org/10.1016/j.hrcr.2020.03.017 ) shared a case of a 72-year-old woman with paroxysmal atrial fibrillation, treated with flecainide and metoprolol, who presented with dyspnea, cough, fevers, and chills.EP News: Basic and Translational
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has been shown to be associated with a high inflammatory burden that can induce vascular inflammation, myocarditis, and cardiac arrhythmias. The current study by Hoffmann et al (Cell 2020;doi:10.1016/j.cell.2020.02.052; PMID 32142651) investigates the mechanisms of SARS-CoV-2 entry into mammalian cells. The spike (S) protein of coronaviruses facilitates viral entry into target cells by binding of the surface unit (S1) of the S protein to a cellular receptor, angiotensin-converting enzyme 2 (ACE2), as the entry receptor.EP News: Allied Professionals
In a departure from the usual format of review of 1 article followed by a discussion of 1 topic, given the unusual times, the discussion of 1 topic will predominate. There are already hundreds of articles with topics such as the cardiovascular manifestations of coronavirus disease (COVID-19), the increased risk to patients with preexisting cardiovascular disease, arrhythmias associated with infection, and proarrhythmic effects of proposed treatments to be found with a simple Google or PubMed search.EP News: Clinical
Lakkireddy et al (Heart Rhythm April 1, 2020; https://doi.org/10.1016/j.hrthm.2020.03.028 , PMID 32228309) summarized the available evidence and provided recommendations for electrophysiologists related to coronavirus 2019 (COVID-19) in a consensus document from the Heart Rhythm Society, American College of Cardiology, and American Heart Association. They noted that electrophysiologists, like all cardiologists and other health care workers, have been affected personally and professionally by this global catastrophe.EP News: Case Reports
The phenotype of Brugada syndrome is associated with a decrease in the sodium current and can manifest with sudden death in previously healthy individuals. Many triggers have been described, including fever, alcohol intake, and medications that cause sodium channel blockade. Coronavirus disease 2019 (COVID-19) most commonly presents with fever and a cough. Chang et al (doi: https://doi.org/10.1016/j.hrcr.2020.03.012 ) shared a case of a 49-year-old Bangladeshi man without a significant medical history who presented after an episode of syncope and fever.
