Has COVID-19 changed the spectrum of arrhythmias and the incidence of sudden cardiac death?

Arrhythmic manifestations of COVID-19 include atrial arrhythmias such as atrial fibrillation or atrial flutter, sinus node dysfunction, atrioventricular conduction abnormalities, ventricular tachyarrhythmias, sudden cardiac arrest, and cardiovascular dysautonomias including the so-called long COVID syndrome. Various pathophysiological mechanisms have been implicated, such as direct viral invasion, hypoxemia, local and systemic inflammation, changes in ion channel physiology, immune activation, and autonomic dysregulation. The development of atrial or ventricular arrhythmias in hospitalized COVID-19 patients has been shown to portend a higher risk of in-hospital death. Management of these arrhythmias should be based on published evidence-based guidelines, with special consideration of the acuity of COVID-19 infection, concomitant use of antimicrobial and anti-inflammatory drugs, and the transient nature of some rhythm disorders. In view of new SARS-CoV­2 variants that may evolve, the development and use of newer antiviral and immunomodulator drugs, and the increasing adoption of vaccination, clinicians must remain vigilant for other arrhythmic manifestations that may occur in association with this novel but potentially deadly disease.

[Impact of the COVID-19 pandemic on basic resuscitation and success rate after sudden cardiac arrest]. / A COVID­19-pandémia hatása a hirtelen szívmegállást követo alapszintu újraélesztésre és annak sikerességére.

Since the onset of the coronavirus disease, infection-related mortality has been tracked worldwide and the number of deaths caused by the virus is counted daily. The coronavirus pandemic has not only transformed our daily life, but reorganized the whole healthcare system. In response to the increased demand for hospital admissions, leaders in different countries have implemented a number of emergency actions. The restructuring has had both direct and indirect negative effects on the epidemiology of sudden cardiac death, the willingness of lay rescuer to give cardiopulmonary resuscitation and the use of automated external defibrillators, but these negative effects vary widely across continents and countries. In order to protect lay people and health workers as well as to prevent the spread of the pandemic, the previous recommendations of the European Resuscitation Council on basic and advanced life support have undergone a few modifications. Orv Hetil. 2023; 164(13): 483-487.

Sudden cardiac arrest during the COVID-19 pandemic: A two-year prospective evaluation in a North American community.

BACKGROUND: Early during the coronavirus disease 2019 (COVID-19) pandemic, higher sudden cardiac arrest (SCA) incidence and lower survival rates were reported. However, ongoing effects on SCA during the evolving pandemic have not been evaluated. OBJECTIVE: The purpose of this study was to assess the impact of COVID-19 on SCA during 2 years of the pandemic. METHODS: In a prospective study of Ventura County, California (2020 population 843,843; 44.1% Hispanic), we compared SCA incidence and outcomes during the first 2 years of the COVID-19 pandemic to the prior 4 years. RESULTS: Of 2222 out-of-hospital SCA cases identified, 907 occurred during the pandemic (March 2020 to February 2022) and 1315 occurred prepandemic (March 2016 to February 2020). Overall age-standardized annual SCA incidence increased from 39 per 100,000 (95% confidence [CI] 37-41) prepandemic to 54 per 100,000 (95% CI 50-57; P <.001) during the pandemic. Among Hispanics, incidence increased by 77%, from 38 per 100,000 (95% CI 34-43) to 68 per 100,000 (95% CI 60-76; P <.001). Among non-Hispanics, incidence increased by 26%, from 39 per 100,000 (95% CI 37-42; P <.001) to 50 per 100,000 (95% CI 46-54). SCA incidence rates closely tracked COVID-19 infection rates. During the pandemic, SCA survival was significantly reduced (15% to 10%; P <.001), and Hispanics were less likely than non-Hispanics to receive bystander cardiopulmonary resuscitation (45% vs 55%; P = .005) and to present with shockable rhythm (15% vs 24%; P = .003). CONCLUSION: Overall SCA rates remained consistently higher and survival outcomes consistently lower, with exaggerated effects during COVID infection peaks. This longer evaluation uncovered higher increases in SCA incidence among Hispanics, with worse resuscitation profiles. Potential ethnicity-specific barriers to acute SCA care warrant urgent evaluation and intervention.

Dilated cardiomyopathy in the era of precision medicine: latest concepts and developments.

Dilated cardiomyopathy (DCM) is an umbrella term entailing a wide variety of genetic and non-genetic etiologies, leading to left ventricular systolic dysfunction and dilatation, not explained by abnormal loading conditions or coronary artery disease. The clinical presentation can vary from asymptomatic to heart failure symptoms or sudden cardiac death (SCD) even in previously asymptomatic individuals. In the last 2 decades, there has been striking progress in the understanding of the complex genetic basis of DCM, with the discovery of additional genes and genotype-phenotype correlation studies. Rigorous clinical work-up of DCM patients, meticulous family screening, and the implementation of advanced imaging techniques pave the way for a more efficient and earlier diagnosis as well as more precise indications for implantable cardioverter defibrillator implantation and prevention of SCD. In the era of precision medicine, genotype-directed therapies have started to emerge. In this review, we focus on updates of the genetic background of DCM, characteristic phenotypes caused by recently described pathogenic variants, specific indications for prevention of SCD in those individuals and genotype-directed treatments under development. Finally, the latest developments in distinguishing athletic heart syndrome from subclinical DCM are described.

ACSM-AMSSM Call to Action: Adapting Preparticipation Cardiovascular Screening to the COVID-19 Pandemic.

ABSTRACT: Preparticipation cardiovascular screening, designed to identify cardiovascular pathology responsible for sudden unexpected death, is recommended by all major professional medical organizations overseeing the clinical care of competitive athletes. Data from several large, prospective, cohort studies indicate that cardiac imaging findings consistent with inflammatory heart disease following COVID-19 infection are more common than most forms of heart disease associated with sudden death during exercise. This call-to-action document is intended to provide recommendations about how routine preparticipation cardiovascular screening for young competitive athletes - which has the capacity to detect both COVID-19 cardiovascular complications and pathology unrelated to infection - should be altered to account for recent scientific advances.

Promoting an Emergency Action Plan for Sudden Cardiac Arrest in Youth Sports During a Pandemic.

INTRODUCTION: Pandemic-related restrictions increased the risk of delayed emergency response of bystanders to sudden cardiac arrest among youth athletes. Education and SCA emergency preparedness, implemented by nurse leaders and adapted to environmental changes, can greatly reduce the risks associated with an SCA episode. METHOD: A nurse-led, quality improvement pilot project was implemented in a recreational youth soccer league. The project included the implementation of an emergency action plan (EAP; with or without the pandemic and social-distancing restrictions) for bystanders responding to SCA. RESULTS: Participants showed significant improvement in knowledge and perceptions of SCA and emergency response (p < .001). Willingness to initiate cardiopulmonary resuscitation (CPR) improved (p = .127), and fear to engage in EAP decreased (p = .119) following an educational intervention on SCA. DISCUSSION: Nurse-led SCA education and implementation of youth league EAP successfully demonstrated safety in SCA preparedness and best practice recommendations for youth sports from the Interassociation Task Force.

Urgent Guidance for Navigating and Circumventing the QTc-Prolonging and Torsadogenic Potential of Possible Pharmacotherapies for Coronavirus Disease 19 (COVID-19).

As the coronavirus disease 19 (COVID-19) global pandemic rages across the globe, the race to prevent and treat this deadly disease has led to the "off-label" repurposing of drugs such as hydroxychloroquine and lopinavir/ritonavir, which have the potential for unwanted QT-interval prolongation and a risk of drug-induced sudden cardiac death. With the possibility that a considerable proportion of the world's population soon could receive COVID-19 pharmacotherapies with torsadogenic potential for therapy or postexposure prophylaxis, this document serves to help health care professionals mitigate the risk of drug-induced ventricular arrhythmias while minimizing risk of COVID-19 exposure to personnel and conserving the limited supply of personal protective equipment.

Incidence, Predictors, and Outcomes of In-Hospital Cardiac Arrest in COVID-19 Patients Admitted to Intensive and Non-Intensive Care Units: Insights From the AHA COVID-19 CVD Registry.

Background Limited information is available regarding in-hospital cardiac arrest (IHCA) in patients with COVID-19. Methods and Results We leveraged the American Heart Association COVID-19 Cardiovascular Disease (AHA COVID-19 CVD) Registry to conduct a cohort study of adults hospitalized for COVID-19. IHCA was defined as those with documentation of cardiac arrest requiring medication or electrical shock for resuscitation. Mixed effects models with random intercepts were used to identify independent predictors of IHCA and mortality while accounting for clustering at the hospital level. The study cohort included 8518 patients (6080 not in the intensive care unit [ICU]) with mean age of 61.5 years (SD 17.5). IHCA occurred in 509 (5.9%) patients overall with 375 (73.7%) in the ICU and 134 (26.3%) patients not in the ICU. The majority of patients at the time of ICHA were not in a shockable rhythm (76.5%). Independent predictors of IHCA included older age, Hispanic ethnicity (odds ratio [OR], 1.9; CI, 1.4-2.4; P<0.001), and non-Hispanic Black race (OR, 1.5; CI, 1.1-1.9; P=0.004). Other predictors included oxygen use on admission, quick Sequential Organ Failure Assessment score on admission, and hypertension. Overall, 35 (6.9%) patients with IHCA survived to discharge, with 9.1% for ICU and 0.7% for non-ICU patients. Conclusions Older age, Black race, and Hispanic ethnicity are independent predictors of IHCA in patients with COVID-19. Although the incidence is much lower than in ICU patients, approximately one-quarter of IHCA events in patients with COVID-19 occur in non-ICU settings, with the latter having a substantially lower survival to discharge rate.

A Perspective on Personalized Therapies in Hypertrophic Cardiomyopathy.

ABSTRACT: A dominant mechanism of sudden cardiac death in the young is the progression of maladaptive responses to genes encoding proteins linked to hypertrophic cardiomyopathy. Most are mutant sarcomere proteins that trigger the progression by imposing a biophysical defect on the dynamics and levels of myofilament tension generation. We discuss approaches for personalized treatments that are indicated by recent advanced understanding of the progression.

Implantable Cardioverter-Defibrillator Shocks During COVID-19 Outbreak.

Background COVID-19 was temporally associated with an increase in out-of-hospital cardiac arrests, but the underlying mechanisms are unclear. We sought to determine if patients with implantable defibrillators residing in areas with high COVID-19 activity experienced an increase in defibrillator shocks during the COVID-19 outbreak. Methods and Results Using the Medtronic (Mounds View, MN) Carelink database from 2019 and 2020, we retrospectively determined the incidence of implantable defibrillator shock episodes among patients residing in New York City, New Orleans, LA, and Boston, MA. A total of 14 665 patients with a Medtronic implantable defibrillator (age, 66±13 years; and 72% men) were included in the analysis. Comparing analysis time periods coinciding with the COVID-19 outbreak in 2020 with the same periods in 2019, we observed a larger mean rate of defibrillator shock episodes per 1000 patients in New York City (17.8 versus 11.7, respectively), New Orleans (26.4 versus 13.5, respectively), and Boston (30.9 versus 20.6, respectively) during the COVID-19 surge. Age- and sex-adjusted hurdle model showed that the Poisson distribution rate of defibrillator shocks for patients with ≥1 shock was 3.11 times larger (95% CI, 1.08-8.99; P=0.036) in New York City, 3.74 times larger (95% CI, 0.88-15.89; P=0.074) in New Orleans, and 1.97 times larger (95% CI, 0.69-5.61; P=0.202) in Boston in 2020 versus 2019. However, the binomial odds of any given patient having a shock episode was not different in 2020 versus 2019. Conclusions Defibrillator shock episodes increased during the higher COVID-19 activity in New York City, New Orleans, and Boston. These observations may provide insights into COVID-19-related increase in cardiac arrests.

Modelling sudden cardiac death risks factors in patients with coronavirus disease of 2019: the hydroxychloroquine and azithromycin case.

AIMS: Coronavirus disease of 2019 (COVID-19) has rapidly become a worldwide pandemic. Many clinical trials have been initiated to fight the disease. Among those, hydroxychloroquine and azithromycin had initially been suggested to improve clinical outcomes. Despite any demonstrated beneficial effects, they are still in use in some countries but have been reported to prolong the QT interval and induce life-threatening arrhythmia. Since a significant proportion of the world population may be treated with such COVID-19 therapies, evaluation of the arrhythmogenic risk of any candidate drug is needed. METHODS AND RESULTS: Using the O'Hara-Rudy computer model of human ventricular wedge, we evaluate the arrhythmogenic potential of clinical factors that can further alter repolarization in COVID-19 patients in addition to hydroxychloroquine (HCQ) and azithromycin (AZM) such as tachycardia, hypokalaemia, and subclinical to mild long QT syndrome. Hydroxychloroquine and AZM drugs have little impact on QT duration and do not induce any substrate prone to arrhythmia in COVID-19 patients with normal cardiac repolarization reserve. Nevertheless, in every tested condition in which this reserve is reduced, the model predicts larger electrocardiogram impairments, as with dofetilide. In subclinical conditions, the model suggests that mexiletine limits the deleterious effects of AZM and HCQ. CONCLUSION: By studying the HCQ and AZM co-administration case, we show that the easy-to-use O'Hara-Rudy model can be applied to assess the QT-prolongation potential of off-label drugs, beyond HCQ and AZM, in different conditions representative of COVID-19 patients and to evaluate the potential impact of additional drug used to limit the arrhythmogenic risk.

COVID-19-Myocarditis and Return to Play: Reflections and Recommendations From a Canadian Working Group.

The COVID-19-related pandemic has resulted in profound health, financial, and societal impacts. Organized sporting events, from recreational to the Olympic level, have been cancelled to both mitigate the spread of COVID-19 and protect athletes and highly active individuals from potential acute and long-term infection-associated harms. COVID-19 infection has been associated with increased cardiac morbidity and mortality. Myocarditis and late gadolinium enhancement as a result of COVID-19 infection have been confirmed. Correspondingly, myocarditis has been implicated in sudden cardiac death of athletes. A pragmatic approach is required to guide those who care for athletes and highly active persons with COVID-19 infection. Members of the Community and Athletic Cardiovascular Health Network (CATCHNet) and the writing group for the Canadian Cardiovascular Society/Canadian Heart Rhythm Society Joint Position Statement on the Cardiovascular Screening of Competitive Athletes recommend that highly active persons with suspected or confirmed COVID-19 infection refrain from exercise for 7 days after resolution of viral symptoms before gradual return to exercise. We do not recommend routine troponin testing, resting 12-lead electrocardiography, echocardiography, or cardiac magnetic resonance imaging before return to play. However, medical assessment including history and physical examination with consideration of resting electrocardiography and troponin can be considered in the athlete manifesting new active cardiac symptoms or a marked reduction in fitness. If concerning abnormalities are encountered at the initial medical assessment, then referral to a cardiologist who cares for athletes is recommended.

Coronavirus Disease 2019 and the Athletic Heart: Emerging Perspectives on Pathology, Risks, and Return to Play.

Importance: Cardiac injury with attendant negative prognostic implications is common among patients hospitalized with coronavirus disease 2019 (COVID-19) infection. Whether cardiac injury, including myocarditis, also occurs with asymptomatic or mild-severity COVID-19 infection is uncertain. There is an ongoing concern about COVID-19-associated cardiac pathology among athletes because myocarditis is an important cause of sudden cardiac death during exercise. Observations: Prior to relaxation of stay-at-home orders in the US, the American College of Cardiology's Sports and Exercise Cardiology Section endorsed empirical consensus recommendations advising a conservative return-to-play approach, including cardiac risk stratification, for athletes in competitive sports who have recovered from COVID-19. Emerging observational data coupled with widely publicized reports of athletes in competitive sports with reported COVID-19-associated cardiac pathology suggest that myocardial injury may occur in cases of COVID-19 that are asymptomatic and of mild severity. In the absence of definitive data, there is ongoing uncertainty about the optimal approach to cardiovascular risk stratification of athletes in competitive sports following COVID-19 infection. Conclusions and Relevance: This report was designed to address the most common questions regarding COVID-19 and cardiac pathology in athletes in competitive sports, including the extension of return-to-play considerations to discrete populations of athletes not addressed in prior recommendations. Multicenter registry data documenting cardiovascular outcomes among athletes in competitive sports who have recovered from COVID-19 are currently being collected to determine the prevalence, severity, and clinical relevance of COVID-19-associated cardiac pathology and efficacy of targeted cardiovascular risk stratification. While we await these critical data, early experiences in the clinical oversight of athletes following COVID-19 infection provide an opportunity to address key areas of uncertainty relevant to cardiology and sports medicine practitioners.

Prevention of Ventricular Arrhythmia and Sudden Cardiac Death in COVID-19 Patients.

Since the first case was reported at the end of 2019, COVID-19 has spread throughout the world and has become a pandemic. The high transmission rate of the virus has made it a threat to public health globally. Viral infections may trigger acute coronary syndromes, arrhythmias, and exacerbation of heart failure, due to a combination of effects including significant systemic inflammatory responses and localized vascular inflammation at the arterial plaque level. Indonesian clinical practice guideline stated that (hydroxy)chloroquine alone or in combination with azithromycin may be used to treat for COVID-19. However, chloroquine, hydroxychloroquine, and azithromycin all prolong the QT interval, raising concerns about the risk of arrhythmic death from individual or concurrent use of these medications. To date, there is still no vaccine or specific antiviral treatment for COVID-19. Therefore, prevention of infection in people with cardiovascular risk and mitigation of the adverse effects of treatment is necessary.

Cardiorespiratory considerations for return-to-play in elite athletes after COVID-19 infection: a practical guide for sport and exercise medicine physicians.

SARS-CoV-2 is the causative virus responsible for the COVID-19 pandemic. This pandemic has necessitated that all professional and elite sport is either suspended, postponed or cancelled altogether to minimise the risk of viral spread. As infection rates drop and quarantine restrictions are lifted, the question how athletes can safely resume competitive sport is being asked. Given the rapidly evolving knowledge base about the virus and changing governmental and public health recommendations, a precise answer to this question is fraught with complexity and nuance. Without robust data to inform policy, return-to-play (RTP) decisions are especially difficult for elite athletes on the suspicion that the COVID-19 virus could result in significant cardiorespiratory compromise in a minority of afflicted athletes. There are now consistent reports of athletes reporting persistent and residual symptoms many weeks to months after initial COVID-19 infection. These symptoms include cough, tachycardia and extreme fatigue. To support safe RTP, we provide sport and exercise medicine physicians with practical recommendations on how to exclude cardiorespiratory complications of COVID-19 in elite athletes who place high demand on their cardiorespiratory system. As new evidence emerges, guidance for a safe RTP should be updated.