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1.
Curr Sports Med Rep ; 21(5): 159-162, 2022 May 01.
Article in English | MEDLINE | ID: covidwho-1833454

ABSTRACT

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.


Subject(s)
COVID-19 , Cardiovascular Diseases , Cardiovascular System , Athletes , Cardiovascular Diseases/prevention & control , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Electrocardiography/adverse effects , Humans , Mass Screening/methods , Pandemics , Physical Examination , Prospective Studies
3.
J Pediatr Health Care ; 36(2): 110-114, 2022.
Article in English | MEDLINE | ID: covidwho-1619702

ABSTRACT

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.


Subject(s)
Cardiopulmonary Resuscitation , Emergency Medical Services , Sports , Youth Sports , Adolescent , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/prevention & control , Defibrillators , Humans , Pandemics/prevention & control , Pilot Projects
5.
Mayo Clin Proc ; 95(6): 1213-1221, 2020 06.
Article in English | MEDLINE | ID: covidwho-1450185

ABSTRACT

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.


Subject(s)
Death, Sudden, Cardiac , Hydroxychloroquine , Long QT Syndrome , Lopinavir , Risk Adjustment/methods , Ritonavir , Torsades de Pointes , Anti-Infective Agents/administration & dosage , Anti-Infective Agents/adverse effects , Betacoronavirus/drug effects , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Drug Combinations , Drug Monitoring/methods , Drug Repositioning/ethics , Drug Repositioning/methods , Electrocardiography/methods , Humans , Hydroxychloroquine/administration & dosage , Hydroxychloroquine/adverse effects , Long QT Syndrome/chemically induced , Long QT Syndrome/mortality , Long QT Syndrome/therapy , Lopinavir/administration & dosage , Lopinavir/adverse effects , Pandemics , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Ritonavir/administration & dosage , Ritonavir/adverse effects , SARS-CoV-2 , Torsades de Pointes/chemically induced , Torsades de Pointes/mortality , Torsades de Pointes/therapy
6.
J Am Heart Assoc ; 10(16): e021204, 2021 08 17.
Article in English | MEDLINE | ID: covidwho-1352600

ABSTRACT

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.


Subject(s)
African Americans , COVID-19 , Heart Arrest/ethnology , Inpatients , Intensive Care Units , Patient Admission , Age Factors , Aged , Aged, 80 and over , Death, Sudden, Cardiac/ethnology , Death, Sudden, Cardiac/prevention & control , Female , Heart Arrest/diagnosis , Heart Arrest/mortality , Heart Arrest/therapy , Hospital Mortality/ethnology , Humans , Incidence , Male , Middle Aged , Prognosis , Race Factors , Registries , Risk Assessment , Risk Factors , Time Factors , United States/epidemiology
7.
J Cardiovasc Pharmacol ; 77(3): 317-322, 2021 03 01.
Article in English | MEDLINE | ID: covidwho-1262260

ABSTRACT

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.


Subject(s)
Cardiomyopathy, Hypertrophic/therapy , Death, Sudden, Cardiac/prevention & control , Precision Medicine , COVID-19/complications , Cardiomyopathy, Hypertrophic/complications , Cardiomyopathy, Hypertrophic/genetics , Cardiomyopathy, Hypertrophic/physiopathology , Clinical Decision-Making , Death, Sudden, Cardiac/etiology , Genetic Predisposition to Disease , Humans , Mutation , Phenotype , Prognosis , Risk Assessment , Risk Factors , Transcriptome
8.
J Am Heart Assoc ; 10(11): e019708, 2021 06.
Article in English | MEDLINE | ID: covidwho-1247457

ABSTRACT

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.


Subject(s)
COVID-19 , Death, Sudden, Cardiac , Defibrillators, Implantable , Electric Countershock , Out-of-Hospital Cardiac Arrest , Aged , Boston/epidemiology , COVID-19/complications , COVID-19/epidemiology , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/prevention & control , Electric Countershock/instrumentation , Electric Countershock/statistics & numerical data , Female , Humans , Incidence , Male , New Orleans/epidemiology , New York City/epidemiology , Out-of-Hospital Cardiac Arrest/epidemiology , Out-of-Hospital Cardiac Arrest/etiology , Poisson Distribution , SARS-CoV-2
9.
Europace ; 23(7): 1124-1133, 2021 07 18.
Article in English | MEDLINE | ID: covidwho-1233851

ABSTRACT

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.


Subject(s)
COVID-19 , Long QT Syndrome , Azithromycin/adverse effects , COVID-19/drug therapy , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Humans , Hydroxychloroquine/adverse effects , Long QT Syndrome/chemically induced , Long QT Syndrome/diagnosis , SARS-CoV-2
12.
Can J Cardiol ; 37(8): 1165-1174, 2021 08.
Article in English | MEDLINE | ID: covidwho-942925

ABSTRACT

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.


Subject(s)
COVID-19 , Death, Sudden, Cardiac/prevention & control , Myocarditis , Physical Fitness , Return to Sport , Sports Medicine , Athletes , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/therapy , Canada , Cardiorespiratory Fitness , Communicable Disease Control/methods , Death, Sudden, Cardiac/etiology , Echocardiography/methods , Humans , Myocarditis/complications , Myocarditis/physiopathology , Myocarditis/therapy , Myocarditis/virology , Physical Examination/methods , Return to Sport/physiology , Return to Sport/standards , SARS-CoV-2 , Sports Medicine/standards , Sports Medicine/trends
13.
JAMA Cardiol ; 6(2): 219-227, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-887987

ABSTRACT

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.


Subject(s)
COVID-19/complications , Death, Sudden, Cardiac/prevention & control , Mass Screening/methods , Pandemics , Return to Sport , SARS-CoV-2 , Sports Medicine/standards , Athletes , COVID-19/epidemiology , Cardiology , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/etiology , Humans
14.
Acta Med Indones ; 52(3): 290-296, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-833791

ABSTRACT

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.


Subject(s)
Anti-Arrhythmia Agents/therapeutic use , Betacoronavirus , Coronavirus Infections/complications , Death, Sudden, Cardiac/prevention & control , Pneumonia, Viral/complications , Tachycardia, Ventricular/prevention & control , COVID-19 , Coronavirus Infections/epidemiology , Death, Sudden, Cardiac/etiology , Electrocardiography , Humans , Pandemics , Pneumonia, Viral/epidemiology , Prognosis , SARS-CoV-2 , Tachycardia, Ventricular/etiology
16.
Br J Sports Med ; 54(19): 1157-1161, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-744836

ABSTRACT

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.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Myocarditis/diagnosis , Pneumonia, Viral/complications , Practice Guidelines as Topic , Respiration Disorders/diagnosis , Return to Sport/standards , Athletes , Biomarkers/blood , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Death, Sudden, Cardiac/prevention & control , Electrocardiography , Humans , Myocarditis/blood , Myocarditis/etiology , Myocardium/pathology , Necrosis/etiology , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , Respiration Disorders/etiology , SARS-CoV-2 , Sports Medicine/standards , Symptom Assessment , Troponin/blood
17.
J Cardiopulm Rehabil Prev ; 40(5): 285-286, 2020 09.
Article in English | MEDLINE | ID: covidwho-721004

ABSTRACT

PURPOSE: The coronavirus disease-2019 (COVID-19) pandemic has been spreading rapidly worldwide since late January 2020. The strict lockdown strategy prompted by the Italian government, to hamper severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) spreading, has reduced the possibility of performing either outdoor or gym physical activity (PA). This study investigated and quantified the reduction of PA in patients with automatic implantable cardioverter-defibrillators (ICDs) for primary prevention of sudden death. METHODS: Daily PA of 24 patients was estimated by processing recorded data from ICD-embedded accelerometric sensors used by the rate-responsive pacing systems. RESULTS: During the forced 40-d in-home confinement, a mean 25% reduction of PA was observed as compared with the 40-d confinement-free period (1.2 ± 0.3 vs 1.6 ± 0.5 hr/d, respectively, P = .0001). CONCLUSIONS: This objective quantification of the impact of the COVID-19 pandemic on PA determined by an ICD device showed an abrupt and statistically significant reduction of PA in primary prevention ICD patients, during the in-home confinement quarantine. To counteract the deleterious effects of physical inactivity during the COVID-19 outbreak, patients should be encouraged to perform indoor exercise-based personalized rehabilitative programs.


Subject(s)
Cardiac Rehabilitation , Coronavirus Infections , Death, Sudden, Cardiac/prevention & control , Defibrillators, Implantable , Exercise/physiology , Pandemics , Pneumonia, Viral , Telerehabilitation/organization & administration , Aged , Betacoronavirus , COVID-19 , Cardiac Rehabilitation/methods , Cardiac Rehabilitation/trends , Communicable Disease Control/methods , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Electric Countershock/instrumentation , Female , Humans , Italy/epidemiology , Male , Needs Assessment , Pandemics/prevention & control , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Quarantine/methods , SARS-CoV-2
18.
Acta Cardiol ; 76(8): 805-824, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-655373

ABSTRACT

Brugada syndrome (BrS) is an inherited cardiac arrhythmia syndrome that causes a heightened risk for ventricular tachyarrhythmias and sudden cardiac death. BrS is characterised by a coved ST-segment elevation in right precordial leads. The prevalence is estimated to range between 1 in 5,000 to 1 in 2,000 in different populations, with the highest being in Southeast Asia and in males. More than 18 genes associated with BrS have been discovered and recent evidence has suggested a complex polygenic mode of inheritance with multiple common and rare genetic variants acting in concert to produce the BrS phenotype. Diagnosis of BrS in patients currently relies on presentation with a type-1 Brugada pattern on ECG either spontaneously or following a drug provocation test using a sodium channel blocker. Risk assessment in patients diagnosed with BrS is controversial, especially with regard to the predictive value of programmed electrical stimulation and novel ECG parameters, such as QRS fragmentation. The first line of BrS therapy remains an implantable cardioverter defibrillator (ICD), although radiofrequency catheter ablation has been shown to be an effective option in patients with contraindications for an ICD. True BrS can be unmasked on ECG in susceptible individuals by monitoring factors such as fever, and this has been recently evident in several patients infected with the 2019 novel coronavirus (COVID-19). Aggressive antipyretic therapy and regular ECG monitoring until fever resolves are current recommendations to help reduce the arrhythmic risk in these COVID-19 patients. In this review, we summarise the current knowledge on the epidemiology, pathophysiology, genetics, clinical diagnosis, risk stratification and treatment of patients with BrS, with special emphasis on COVID-19 comorbidity.


Subject(s)
Brugada Syndrome , Brugada Syndrome/diagnosis , Brugada Syndrome/epidemiology , Brugada Syndrome/genetics , COVID-19 , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Electrocardiography , Humans
19.
Int J Cardiol ; 316: 280-284, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-306251

ABSTRACT

BACKGROUND: Hydroxychloroquine and azithromycin combination therapy is often prescribed for coronavirus disease 2019 (COVID-19). Electrocardiographic (ECG) monitoring is warranted because both medications cause corrected QT-interval (QTc) prolongation. Whether QTc duration significantly varies during the day, potentially requiring multiple ECGs, remains to be established. METHODS: We performed 12­lead ECGs and 12­lead 24-h Holter ECG monitoring in all patients aged <80 years admitted to our medical unit for COVID-19, in oral therapy with hydroxychloroquine (200 mg, twice daily) and azithromycin (500 mg, once daily) for at least 3 days. A group of healthy individuals matched for age and sex served as control. RESULTS: Out of 126 patients, 22 (median age 64, 82% men) met the inclusion criteria. ECG after therapy showed longer QTc-interval than before therapy (450 vs 426 ms, p = .02). Four patients had a QTc ≥ 480 ms: they showed higher values of aspartate aminotransferase (52 vs 30 U/L, p = .03) and alanine aminotransferase (108 vs 33 U/L, p < .01) compared with those with QTc < 480 ms. At 24-h Holter ECG monitoring, 1 COVID-19 patient and no control had ≥1 run of non-sustained ventricular tachycardia (p = .4). No patients showed "R on T" premature ventricular beats. Analysis of 24-h QTc dynamics revealed that COVID-19 patients had higher QTc values than controls, with no significant hourly variability. CONCLUSION: Therapy with hydroxychloroquine and azithromycin prolongs QTc interval in patients with COVID-19, particularly in those with high levels of transaminases. Because QTc duration remains stable during the 24 h, multiple daily ECG are not recommendable.


Subject(s)
Azithromycin , Coronavirus Infections/drug therapy , Electrocardiography/methods , Hydroxychloroquine , Long QT Syndrome , Pandemics , Pneumonia, Viral/drug therapy , Antiviral Agents/administration & dosage , Antiviral Agents/adverse effects , Azithromycin/administration & dosage , Azithromycin/adverse effects , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/physiopathology , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/prevention & control , Drug Monitoring/methods , Female , Hospitalization/statistics & numerical data , Humans , Hydroxychloroquine/administration & dosage , Hydroxychloroquine/adverse effects , Long QT Syndrome/chemically induced , Long QT Syndrome/complications , Long QT Syndrome/diagnosis , Male , Middle Aged , Outcome and Process Assessment, Health Care , Pneumonia, Viral/diagnosis , Pneumonia, Viral/physiopathology , SARS-CoV-2
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