Subject(s)
COVID-19 Vaccines/adverse effects , Defibrillators, Implantable , Electric Countershock/instrumentation , Long QT Syndrome/surgery , Tachycardia, Ventricular/chemically induced , Vaccination/adverse effects , Ventricular Premature Complexes/chemically induced , Action Potentials , BNT162 Vaccine , COVID-19 Vaccines/administration & dosage , Electrocardiography , Female , Heart Rate , Humans , Long QT Syndrome/diagnosis , Long QT Syndrome/physiopathology , Middle Aged , Risk Factors , Tachycardia, Ventricular/diagnosis , Tachycardia, Ventricular/physiopathology , Time Factors , Ventricular Premature Complexes/diagnosis , Ventricular Premature Complexes/physiopathologyABSTRACT
BACKGROUND: J-waves represent a common finding in routine ECGs (5-6%) and are closely linked to ventricular tachycardias. While arrhythmias and non-specific ECG alterations are a frequent finding in COVID-19, an analysis of J-wave incidence in acute COVID-19 is lacking. METHODS: A total of 386 patients consecutively, hospitalized due to acute COVID-19 pneumonia were included in this retrospective analysis. Admission ECGs were analyzed, screened for J-waves and correlated to clinical characteristics and 28-day mortality. RESULTS: J-waves were present in 12.2% of patients. Factors associated with the presence of J-waves were old age, female sex, a history of stroke and/or heart failure, high CRP levels as well as a high BMI. Mortality rates were significantly higher in patients with J-waves in the admission ECG compared to the non-J-wave cohort (J-wave: 14.9% vs. non-J-wave 3.8%, p = 0.001). After adjusting for confounders using a multivariable cox regression model, the incidence of J-waves was an independent predictor of mortality at 28-days (OR 2.76 95% CI: 1.15-6.63; p = 0.023). J-waves disappeared or declined in 36.4% of COVID-19 survivors with available ECGs for 6-8 months follow-up. CONCLUSION: J-waves are frequently and often transiently found in the admission ECG of patients hospitalized with acute COVID-19. Furthermore, they seem to be an independent predictor of 28-day mortality.
Subject(s)
Arrhythmias, Cardiac/physiopathology , COVID-19/physiopathology , Tachycardia, Ventricular/physiopathology , Aged , Arrhythmias, Cardiac/mortality , COVID-19/mortality , Electrocardiography , Female , Humans , Male , Middle Aged , Prognosis , Retrospective Studies , Tachycardia, Ventricular/mortalitySubject(s)
Ablation Techniques/methods , COVID-19/complications , Cardiomyopathies/complications , Coronary Sinus/diagnostic imaging , Ethanol/therapeutic use , Tachycardia, Ventricular/therapy , Ventricular Septum/diagnostic imaging , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Phlebography , SARS-CoV-2 , Tachycardia, Ventricular/complications , Tachycardia, Ventricular/physiopathologyABSTRACT
The COVID-19 pandemic has had a huge influence in almost all areas of life, affecting societies, economics, and health care systems worldwide. The paediatric cardiology community is no exception. As the challenging battle with COVID-19 continues, professionals from the Association for the European Paediatric and Congenital Cardiology receive many questions regarding COVID-19 in a Paediatric and Congenital Cardiology setting. The aim of this paper is to present the AEPC position on frequently asked questions based on the most recent scientific data, as well as to frame a discussion on how to take care of our patients during this unprecedented crisis. As the times are changing quickly and information regarding COVID-19 is very dynamic, continuous collection of evidence will help guide constructive decision-making.
Subject(s)
Anti-Arrhythmia Agents/therapeutic use , Anticoagulants/therapeutic use , Antiviral Agents/therapeutic use , Arrhythmias, Cardiac/drug therapy , COVID-19 Drug Treatment , Heart Defects, Congenital/therapy , Immunologic Factors/therapeutic use , Adenosine Monophosphate/analogs & derivatives , Adenosine Monophosphate/therapeutic use , Alanine/analogs & derivatives , Alanine/therapeutic use , Arrhythmias, Cardiac/epidemiology , Arrhythmias, Cardiac/physiopathology , Brugada Syndrome/drug therapy , Brugada Syndrome/epidemiology , Brugada Syndrome/physiopathology , COVID-19/epidemiology , COVID-19/physiopathology , Cardiac Surgical Procedures , Cardiology , Heart Defects, Congenital/epidemiology , Heart Defects, Congenital/physiopathology , Heart Transplantation , Humans , Infectious Disease Transmission, Vertical , Long QT Syndrome/drug therapy , Long QT Syndrome/epidemiology , Long QT Syndrome/physiopathology , Myocarditis/epidemiology , Myocarditis/physiopathology , Myocardium , Pediatrics , Risk Assessment , SARS-CoV-2 , Societies, Medical , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/epidemiology , Systemic Inflammatory Response Syndrome/physiopathology , Tachycardia, Ventricular/drug therapy , Tachycardia, Ventricular/epidemiology , Tachycardia, Ventricular/physiopathologyABSTRACT
Symptoms of COVID-19, as reported during the SARS-CoV-2 pandemic in 2019-2020, are primarily respiratory and gastrointestinal, with sparse reports on neurological manifestations. We describe the case of a 17-year old female with Cornelia de Lange syndrome and well controlled epilepsy, who sustained significant cortical injury during a COVID-19 associated multi-inflammatory syndrome.
Subject(s)
Brain Diseases/physiopathology , COVID-19/physiopathology , De Lange Syndrome/complications , Epilepsy/physiopathology , Seizures/physiopathology , Systemic Inflammatory Response Syndrome/physiopathology , Acute Kidney Injury/etiology , Adolescent , Airway Extubation , Anticonvulsants/therapeutic use , Blood Coagulation Disorders/etiology , Bone Marrow Failure Disorders , Brain Diseases/diagnostic imaging , Brain Diseases/etiology , Brain Diseases/pathology , Brain Edema/diagnostic imaging , Brain Edema/etiology , C-Reactive Protein/immunology , COVID-19/complications , COVID-19/immunology , COVID-19/therapy , Disease Progression , Electroencephalography , Epilepsy/complications , Epilepsy/drug therapy , Female , Ferritins/metabolism , Humans , Influenza B virus , Influenza, Human/complications , Levetiracetam/therapeutic use , Magnetic Resonance Imaging , Midazolam/therapeutic use , Necrosis , Phenobarbital/therapeutic use , Pseudomonas Infections/complications , Respiration, Artificial , Rhabdomyolysis/complications , Rhabdomyolysis/etiology , SARS-CoV-2 , Seizures/drug therapy , Seizures/etiology , Sepsis/etiology , Sepsis/physiopathology , Sepsis/therapy , Systemic Inflammatory Response Syndrome/complications , Systemic Inflammatory Response Syndrome/immunology , Systemic Inflammatory Response Syndrome/therapy , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/physiopathology , Tachycardia, Ventricular/therapyABSTRACT
The mandatory use of facemasks is a public health measure implemented by various countries in response to the novel coronavirus disease 19 (COVID-19) pandemic. However, there have been case reports of sudden cardiac death (SCD) with the wearing of facemasks during exercise. In this paper, we hypothesize that exercise with facemasks may increase the risk of ventricular tachycardia/ventricular fibrillation (VT/VF) leading to SCD via the development of acute and/or intermittent hypoxia and hypercapnia. We discuss the potential underlying mechanisms including increases in adrenergic stimulation and oxidative stress leading to electrophysiological abnormalities that promote arrhythmias via non-reentrant and reentrant mechanisms. Given the interplay of multiple variables contributing to the increased arrhythmic risk, we advise avoidance of a facemask during high intensity exercise, or if wearing of a mask is mandatory, exercise intensity should remain low to avoid precipitation of lethal arrhythmias. However, we cannot exclude the possibility of an arrhythmic substrate even with low intensity exercise especially in those with established chronic cardiovascular disease in whom baseline electrophysiological abnormalities may be found.
Subject(s)
COVID-19/complications , COVID-19/mortality , Death, Sudden, Cardiac , Electrophysiological Phenomena , Exercise , Masks , Arrhythmias, Cardiac/physiopathology , COVID-19/physiopathology , Electrocardiography , Humans , Hypercapnia , Hypoxia , Models, Theoretical , Oxidative Stress , Reactive Oxygen Species/metabolism , Risk , Tachycardia, Ventricular/physiopathology , Ventricular Fibrillation/physiopathologyABSTRACT
Recent reports have suggested an increased risk of QT prolongation and subsequent life-threatening ventricular arrhythmias, particularly torsade de pointes, in patients with coronavirus disease-2019 (COVID-19) treated with hydroxychloroquine and azithromycin. In this article, we report the case of a 75-year-old female with a baseline prolonged QT interval in whom the COVID-19 illness resulted in further remarkable QT prolongation (>700 ms), precipitating recurrent self-terminating episodes of torsade de pointes that necessitated temporary cardiac pacing. Despite the correction of hypoxemia and the absence of reversible factors, such as adverse medication effects, electrolyte derangements, and usage of hydroxychloroquine/azithromycin, the QT interval remained persistently prolonged compared with the baseline with subsequent degeneration into ventricular tachycardia and death. Thus, we highlight that COVID-19 illness itself can potentially lead to further prolongation of QT interval and unmask fatal ventricular arrhythmias in patients who have a prolonged QT and low repolarization reserve at baseline.
Subject(s)
Betacoronavirus , Coronavirus Infections/physiopathology , Long QT Syndrome/physiopathology , Pneumonia, Viral/physiopathology , Tachycardia, Ventricular/physiopathology , Aged , Azithromycin/therapeutic use , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/diet therapy , Coronavirus Infections/drug therapy , Coronavirus Infections/metabolism , Fatal Outcome , Female , Humans , Hydroxychloroquine/therapeutic use , Long QT Syndrome/drug therapy , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/diet therapy , SARS-CoV-2 , Tachycardia, Ventricular/etiology , COVID-19 Drug TreatmentSubject(s)
Betacoronavirus , Coronavirus Infections/complications , Pandemics , Pneumonia, Viral/complications , Ventricular Dysfunction, Left/diagnosis , Azithromycin/administration & dosage , Azithromycin/adverse effects , Azithromycin/therapeutic use , Betacoronavirus/isolation & purification , Biomarkers , COVID-19 , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Diagnosis, Differential , Drug Therapy, Combination , Humans , Hydroxychloroquine/administration & dosage , Hydroxychloroquine/adverse effects , Hydroxychloroquine/therapeutic use , Hypoxia/etiology , Hypoxia/physiopathology , Long QT Syndrome/chemically induced , Myocardial Infarction/diagnosis , Myocarditis/etiology , Myocarditis/physiopathology , Pericarditis/etiology , Pericarditis/physiopathology , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/etiology , Systemic Inflammatory Response Syndrome/physiopathology , Tachycardia, Ventricular/etiology , Tachycardia, Ventricular/physiopathology , Thrombophilia/blood , Thrombophilia/etiology , Ventricular Dysfunction, Left/etiology , Ventricular Dysfunction, Left/physiopathology , Ventricular Fibrillation/etiology , Ventricular Fibrillation/physiopathologyABSTRACT
OBJECTIVE: We aimed to detect the malignant arrhythmic potential of COVID-19 with surface electrocardiographic (ECG) markers. MATERIAL AND METHOD: Of the ECG parameters PR, QT, QTc, QTd, TPe, and Tpe/QTc were measured in 51 COVID-19 patients and 40 in control subjects. RESULTS: Compared to control group mean QTc (410.8 ± 24.3 msec vs. 394.6 ± 20.3 msec, p < .001) and Tpe/QTc (0.19 ± 0.02 vs. 0.18 ± 0.04, p = .036) and median QTd (47.52 vs. 46.5) values were significantly higher in COVID-19 patients. Troponin levels were significantly correlated with heart rate (r = 0.387, p = .006) but not with ECG parameters. CONCLUSION: Several ventricular arrhythmia surface ECG predictors including QTc, QTd, and Tpe/QTc are increased in COVID-19 patients. Since medications used in COVID-19 patients have the potential to affect these parameters, giving importance to these ECG markers may have a significant contribution in decreasing disease-related arrhythmias.