Dysrhythmias associated with COVID-19: Review and management considerations

Alblaihed, Leen; Brady, William J.; Al-Salamah, Tareq; Mattu, Amal

doi:10.1016/j.ajem.2022.12.004

Cited by 4 publications

(5 citation statements)

References 68 publications

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“…However, there were few data supporting the effectiveness of these drugs so far, and the cardiovascular side effects and toxicity are also considerable (Parvu et al 2022 ; Chimenti et al 2022 ). HCQ and chloroquine can inhibit the funny current channels ( I f ), delay rectifier potassium currents ( I Kr ) and L-type calcium ion currents ( I CaL ), and prolong the QT interval (Gautret et al 2020 ; Giudicessi et al 2020 ; Alblaihed et al 2023 ). In COVID-19 patients with abnormal cardiac structure or function (such as left ventricular hypertrophy or reduced ejection fraction), QT prolongation may increase the risk of torsade de pointes ventricular tachycardia.…”

Section: Cardiovascular Side Effects Of Covid-19 Treatmentmentioning

confidence: 99%

Pathogenic mechanisms of cardiovascular damage in COVID-19

Shao,

Yin

2024

Mol Med

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Background COVID-19 is a new infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Since the outbreak in December 2019, it has caused an unprecedented world pandemic, leading to a global human health crisis. Although SARS CoV-2 mainly affects the lungs, causing interstitial pneumonia and severe acute respiratory distress syndrome, a number of patients often have extensive clinical manifestations, such as gastrointestinal symptoms, cardiovascular damage and renal dysfunction. Purpose This review article discusses the pathogenic mechanisms of cardiovascular damage in COVID-19 patients and provides some useful suggestions for future clinical diagnosis, treatment and prevention. Methods An English-language literature search was conducted in PubMed and Web of Science databases up to 12th April, 2024 for the terms “COVID-19”, “SARS CoV-2”, “cardiovascular damage”, “myocardial injury”, “myocarditis”, “hypertension”, “arrhythmia”, “heart failure” and “coronary heart disease”, especially update articles in 2023 and 2024. Salient medical literatures regarding the cardiovascular damage of COVID-19 were selected, extracted and synthesized. Results The most common cardiovascular damage was myocarditis and pericarditis, hypertension, arrhythmia, myocardial injury and heart failure, coronary heart disease, stress cardiomyopathy, ischemic stroke, blood coagulation abnormalities, and dyslipidemia. Two important pathogenic mechanisms of the cardiovascular damage may be direct viral cytotoxicity as well as indirect hyperimmune responses of the body to SARS CoV-2 infection. Conclusions Cardiovascular damage in COVID-19 patients is common and portends a worse prognosis. Although the underlying pathophysiological mechanisms of cardiovascular damage related to COVID-19 are not completely clear, two important pathogenic mechanisms of cardiovascular damage may be the direct damage of the SARSCoV-2 infection and the indirect hyperimmune responses.

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Section: Cardiovascular Side Effects Of Covid-19 Treatmentmentioning

confidence: 99%

Pathogenic mechanisms of cardiovascular damage in COVID-19

Shao,

Yin

2024

Mol Med

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“…Another study in the USA reported a 9.6% rate of arrhythmias [44], in which atrial fibrillation was the most commonly reported tachyarrhythmia at 20.8%, along with paroxysmal supraventricular tachycardia at 5.7%, atrial flutter at 5.4%, and sustained atrial tachycardia at 3.5%. Bradycardias, AV blocks, ventricular dysrhythmias, and torsades de pointes have all been reported in patients with COVID-19 [45, 46]. In addition, a multicenter retrospective analysis reported that patients with atrial fibrillation had an increased risk of mortality (risk ratio 2.249, 95% CI 1.766–2.864, p < 0.001) and major adverse cardiovascular events (risk ratio 1.753, 95% CI 1.473–2.085, p < 0.001) as compared with those with sinus rhythm [47].…”

Section: Cardiac Arrhythmiamentioning

confidence: 99%

“…Arrhythmogenicity in patients with COVID-19 can be caused by direct damage to the myocardium and conduction system as well as by the disease’s effect on the various organ systems, resulting in hypoxia, plaque rupture, electrolyte and fluid imbalance, catecholamine surge, inflammatory changes, and cytokine storm [46]. Targeting these pathophysiologic factors of arrhythmia with COVID-19, the main strategies of management of arrhythmia are active treatment of primary disease, control of inflammation and hypoxia, improvement of cardiac function, maintaining electrolyte balance in body fluids, paying close attention to ECG signs of prolonged QT interval during drug therapies with certain antiviral and antibiotics, and avoiding the use of cardiotoxic drugs.…”

Section: Cardiac Arrhythmiamentioning

confidence: 99%

Pathological Interplay and Clinical Complications between COVID-19 and Cardiovascular Diseases: An Overview in 2023

Zhou,

Zhang,

Liao

et al. 2023

Cardiology

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The coronavirus disease 2019 (COVID-19) involves all organs of the body, of which the interaction with cardiovascular diseases is the most important. Numerous studies have reported that COVID-19 patients complicated with cardiovascular comorbidities (hypertension, coronary heart disease, chronic heart failure, cerebrovascular disease) are more likely to develop into critical illness and have higher mortality. Conversely, COVID-19 may also cause myocardial injury in patients through various pathological mechanisms such as direct virus attack on cardiomyocytes, overactivation of immune response, microthrombus formation, which may lead to fatal acute ST-segment elevation myocardial infarction, arrhythmia, acute worsening of chronic heart failure, etc. In addition, the symptoms of the so-called long-COVID may remain in some patients who survived the acute viral infection. Positional tachycardia has been widely reported, and cardiovascular autonomic disorders are thought to play a pathogenic role.

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“…У пациентов с COVID-19 наблюдаются брадикардия, AV-блокада, ЖТА (в том числе torsade de pointes), но наиболее часто -фибрилляция предсердий. Воспаление миокарда может возникать при воздействии провоспалительных цитокинов, макрофагов, а также из-за клеточно-опосредованной цитотоксичности CD8 и Т-лимфоцитов, приводящей к повреждению кардиомиоцитов и в конечном итоге к развитию аритмий [40]. Следует учитывать, что около 13% пациентов с COVID-19 имеют удлиненный интервал QT.…”

Section: патогенез жизнеопасных нарушений ритма при миокардитеunclassified

“…С одной стороны, этому способствуют свойства некоторых лекарственных препаратов, используемых для лечения коронавирусной инфекции (антибиотики, аминохинолиновые, противовирусные и антиаритмические средства). С другой стороны, само заболевание сопровождается удлинением интервала QT вследствие системного воспаления, почечной дисфункции, поражения сердца и дисбаланса электролитов [40].…”

Section: патогенез жизнеопасных нарушений ритма при миокардитеunclassified

Sudden cardiac death in myocarditis

Тарадин

Игнатенко

Куглер

2023

Almanac of Clinical Medicine

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According to statistics, myocarditis is one of the leading causes of sudden cardiac death (SCD) in children and young adults. The etiology of myocarditis includes infectious and non-infectious, including autoimmune diseases, as well as toxicities and hypersensitivity to various drugs or bites of insects, spiders, snakes, etc. The risk of myocarditis among patients with COVID-19 is 15.7-fold higher than that in the general population. The most common cause of death in myocarditis is heart arrhythmia, such as ventricular tachyarrhythmia, ventricular fibrillation, or severe bradycardia. Genetic predisposition, ion and metabolic disorders, mechanisms of autoimmune response, and direct cardiotoxic action in viral diseases play a role in the pathophysiology of inflammatory myocardial damage. While the majority of patients with myocarditis, who died suddenly, was asymptomatic or had few symptoms, a timely and accurate diagnosis of myocarditis seems to be an important challenge for prevention or minimization of SCD risk. Nonetheless, at present there is no convincing evidence of an association between laboratory and instrumental parameters and the SCD risk in such patients. Endomyocardial biopsy remains the "golden standard" in the diagnosis of myocarditis. Biomarkers (troponins or creatine phosphokinase) are not highly specific. The most common electrocardiographic findings in myocarditis are sinus tachycardia and nonspecific changes in the ST-T segment. The presence of Q wave, bundle branch block, Brugada syndrome, shortened or prolonged QT interval, and early ventricular repolarization are associated with an increased risk of SCD in myocarditis. Given the absence of specific echocardiographic signs of myocarditis, special attention is paid to the assessment of the size of the cardiac chambers, wall thicknesses, global and regional systolic and diastolic function of both the left and right ventricles, visualization of pericardial effusion and intracardiac thrombi. A combined cardiac magnetic resonance imaging using T2-weighted imaging and early and late gadolinium enhancement provides high diagnostic accuracy and seems to be a useful tool in the stratification of patients with suspected acute myocarditis. With the established etiology of myocarditis, specific therapy is necessary to eliminate the pathogen. It is necessary to take into account the likely arrhythmogenic effects of the drugs used in treatment. Non-steroidal anti-inflammatory drugs are generally not indicated in patients with myocarditis because they cause renal impairment and sodium retention, which can exacerbate left ventricular dysfunction and increase the risk of SCD. In the case of severe conduction disturbances and ventricular tachyarrhythmias, implantation of a pacemaker or cardioverter-defibrillator is necessary.

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Dysrhythmias associated with COVID-19: Review and management considerations

Cited by 4 publications

References 68 publications

Pathogenic mechanisms of cardiovascular damage in COVID-19

Pathogenic mechanisms of cardiovascular damage in COVID-19

Pathological Interplay and Clinical Complications between COVID-19 and Cardiovascular Diseases: An Overview in 2023

Sudden cardiac death in myocarditis

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