The Potential Mechanisms of Arrhythmia in Coronavirus disease-2019.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) leads to coronavirus disease-2019 (COVID-19) which can cause severe cardiovascular complications including myocardial injury, arrhythmias, acute coronary syndrome and others. Among these complications, arrhythmias are considered serious and life-threatening. Although arrhythmias have been associated with factors such as direct virus invasion leading to myocardial injury, myocarditis, immune response disorder, cytokine storms, myocardial ischemia/hypoxia, electrolyte abnormalities, intravascular volume imbalances, drug interactions, side effects of COVID-19 vaccines and autonomic nervous system dysfunction, the exact mechanisms of arrhythmic complications in patients with COVID-19 are complex and not well understood. In the present review, the literature was extensively searched to investigate the potential mechanisms of arrhythmias in patients with COVID-19. The aim of the current review is to provide clinicians with a comprehensive foundation for the prevention and treatment of arrhythmias associated with long COVID-19.

Cardiac arrhythmia and immune response in COVID-19 patients

The coronavirus disease 2019 (COVID-19) pandemic has presented substantial challenges for providing health care due to the numerous complications on the respiratory and cardiovascular systems of people. Cardiac arrhythmia is one of the cardiac complications, and it was observed in COVID-19 patients. Moreover, arrhythmia and cardiac arrest are common in COVID-19 patients in the intensive care unit. The occurrence of cardiac arrhythmia in COVID-19 patients is associated with hypoxia, cytokine storm, myocardial ischemia and inflammatory disease such as congestive heart failure. It is necessary to know the occurrence and mechanisms of tachyarrhythmia and bradyarrhythmia in patients with COVID-19 infection for their proper management. This review provides an overview of the association between COVID-19 and arrhythmias by detailing possible pathophysiological mechanisms (AU)

Afección pericárdica y miocárdica tras infección por SARS-CoV-2: estudio descriptivo transversal en trabajadores sanitarios / Pericardial and myocardial involvement after SARS-CoV-2 infection: a cross-sectional descriptive study in healthcare workers

Introducción y objetivos Las secuelas cardiacas tras la infección por SARS-CoV-2 todavía están poco documentadas. Se realizó un estudio transversal en trabajadores sanitarios para estudiar la prevalencia de afección pericárdica y miocárdica tras la infección por SARS-CoV-2. Métodos Se estudió a 139 trabajadores sanitarios con infección previa confirmada por SARS-CoV-2. Los participantes se sometieron a evaluación clínica, electrocardiograma, laboratorio, incluido el perfil de células inmunitarias, y resonancia magnética cardiaca (RMC). El diagnóstico clínico de pericarditis se realizó ante la presencia de los criterios clásicos y el diagnóstico clínico de miocarditis ante la presencia de al menos 2 criterios de RMC. Resultados La mediana de edad fue de 52 (41–57) años, el 71,9% eran mujeres, y el 16,5% había sido hospitalizado previamente por neumonía por COVID-19. En la evaluación (10,4 [9,3–11,0] semanas después de los síntomas de infección), todos los participantes presentaban estabilidad hemodinámica. El 41,7% presentaba dolor torácico, disnea o palpitaciones; el 49,6%, alteraciones electrocardiográficas; el 7,9%, elevación de NT-proBNP; el 0,7%, elevación de troponina; y el 60,4%, alteraciones en la RMC (AU)

Introduction and objectives The cardiac sequelae of SARS-CoV-2 infection are still poorly documented. We conducted a cross-sectional study in healthcare workers to report evidence of pericardial and myocardial involvement after SARS-CoV-2 infection. Methods We studied 139 healthcare workers with confirmed past SARS-CoV-2 infection. Participants underwent clinical assessment, electrocardiography, and laboratory tests, including immune cell profiling and cardiac magnetic resonance (CMR). Clinically suspected pericarditis was diagnosed when classic criteria were present and clinically suspected myocarditis was based on the combination of at least 2 CMR criteria. Results Median age was 52 (41-57) years, 71.9% were women, and 16.5% were previously hospitalized for COVID-19 pneumonia. On examination (10.4 [9.3-11.0] weeks after infection-like symptoms), participants showed hemodynamic stability. Chest pain, dyspnea or palpitations were present in 41.7% participants, electrocardiographic abnormalities in 49.6%, NT-proBNP elevation in 7.9%, troponin in 0.7%, and CMR abnormalities in 60.4%. A total of 30.9% participants met criteria for either pericarditis and/or myocarditis: isolated pericarditis was diagnosed in 5.8%, myopericarditis in 7.9%, and isolated myocarditis in 17.3%. Most participants (73.2%) showed altered immune cell counts in blood, particularly decreased eosinophil (27.3%; P<.001) and increased cytotoxic T cell numbers (17.3%; P <.001). Clinically suspected pericarditis was associated (P <.005) with particularly elevated cytotoxic T cells and decreased eosinophil counts, while participants diagnosed with clinically suspected myopericarditis or myocarditis had lower (P <.05) neutrophil counts, natural killer-cells, and plasma cells. Conclusions Pericardial and myocardial involvement with clinical stability are frequent after SARS-CoV-2 infection and are associated with specific immune cell profiles (AU)

Arrhythmogenic Risk and Mechanisms of QT-Prolonging Drugs to Treat COVID-19.

While looking for a solution to treat COVID-19, the massive off-label use of several drugs in COVID-19 has generated concerns in the early phase of the pandemic because of possible arrhythmogenic effects in relation to QTc interval prolongation. Indeed, some of these drugs have been historically associated with QT prolongation and Torsade de Point, a potentially lethal ventricular arrhythmia, and their first-time use on a very large scale has raised several concerns in the scientific community. This work aims to summarize the underlying arrhythmogenic mechanisms related to the use of potentially QT-prolonging drugs used during the pandemic to treat COVID-19.

COVID-19 and arrhythmia: An overview.

Arrhythmias in COVID-19 patients are associated with hypoxia, myocardial ischemia, cytokines, inflammation, electrolyte abnormalities, pro-arrhythmic or QT-prolonging medications, and underlying heart conditions such as severe congestive heart failure, inherited arrhythmia syndromes, or congenital heart conditions. In the pediatric population, multisystem inflammatory syndrome can lead to cardiac injury and arrhythmias. In addition, arrhythmias and cardiac arrests are most prevalent in the critically ill intensive care unit COVID-19 patient population. This review presents an overview of the association between COVID-19 and arrhythmias by detailing possible pathophysiological mechanisms, existing knowledge of pro-arrhythmic factors, and results from studies in adult and pediatric COVID-19 populations, and the clinical implications.

Cardiac Dysfunction and Arrhythmias 3 Months After Hospitalization for COVID-19.

Background The extent of cardiac dysfunction post-COVID-19 varies, and there is a lack of data on arrhythmic burden. Methods and Results This was a combined multicenter prospective cohort study and cross-sectional case-control study. Cardiac function assessed by echocardiography in patients with COVID-19 3 to 4 months after hospital discharge was compared with matched controls. The 24-hour ECGs were recorded in patients with COVID-19. A total of 204 patients with COVID-19 consented to participate (mean age, 58.5 years; 44% women), and 204 controls were included (mean age, 58.4 years; 44% women). Patients with COVID-19 had worse right ventricle free wall longitudinal strain (adjusted estimated mean difference, 1.5 percentage points; 95% CI, -2.6 to -0.5; P=0.005) and lower tricuspid annular plane systolic excursion (-0.10 cm; 95% CI, -0.14 to -0.05; P<0.001) and cardiac index (-0.26 L/min per m2; 95% CI, -0.40 to -0.12; P<0.001), but slightly better left ventricle global strain (-0.8 percentage points; 95% CI, 0.2-1.3; P=0.008) compared with controls. Reduced diastolic function was twice as common compared with controls (60 [30%] versus 29 [15%], respectively; odds ratio, 2.4; P=0.001). Having dyspnea or fatigue were not associated with cardiac function. Right ventricle free wall longitudinal strain was worse after intensive care treatment. Arrhythmias were found in 27% of the patients, mainly premature ventricular contractions and nonsustained ventricular tachycardia (18% and 5%, respectively). Conclusions At 3 months after hospital discharge with COVID-19, right ventricular function was mildly impaired, and diastolic dysfunction was twice as common compared with controls. There was little evidence for an association between cardiac function and intensive care treatment, dyspnea, or fatigue. Ventricular arrhythmias were common, but the clinical importance is unknown. Registration URL: http://clinicaltrials.gov. Unique Identifier: NCT04535154.

Prognostic Value of Electrocardiographic QRS Diminution in Patients Hospitalized With COVID-19 or Influenza.

During the clinical care of hospitalized patients with COVID-19, diminished QRS amplitude on the surface electrocardiogram (ECG) was observed to precede clinical decompensation, culminating in death. This prompted investigation into the prognostic utility and specificity of low QRS complex amplitude (LoQRS) in COVID-19. We retrospectively analyzed consecutive adults admitted to a telemetry service with SARS-CoV-2 (n = 140) or influenza (n = 281) infection with a final disposition-death or discharge. LoQRS was defined as a composite of QRS amplitude <5 mm or <10 mm in the limb or precordial leads, respectively, or a ≥50% decrease in QRS amplitude on follow-up ECG during hospitalization. LoQRS was more prevalent in patients with COVID-19 than influenza (24.3% vs 11.7%, p = 0.001), and in patients who died than survived with either COVID-19 (48.1% vs 10.2%, p <0.001) or influenza (38.9% vs 9.9%, p <0.001). LoQRS was independently associated with mortality in patients with COVID-19 when adjusted for baseline clinical variables (odds ratio [OR] 11.5, 95% confidence interval [CI] 3.9 to 33.8, p <0.001), presenting and peak troponin, D-dimer, C-reactive protein, albumin, intubation, and vasopressor requirement (OR 13.8, 95% CI 1.3 to 145.5, p = 0.029). The median time to death in COVID-19 from the first ECG with LoQRS was 52 hours (interquartile range 18 to 130). Dynamic QRS amplitude diminution is a strong independent predictor of death over not only the course of COVID-19 infection, but also influenza infection. In conclusion, this finding may serve as a pragmatic prognostication tool reflecting evolving clinical changes during hospitalization, over a potentially actionable time interval for clinical reassessment.

Long-term effects of coronavirus disease 2019 on the cardiovascular system, CV COVID registry: A structured summary of a study protocol.

BACKGROUND: Patients presenting with the coronavirus-2019 disease (COVID-19) may have a high risk of cardiovascular adverse events, including death from cardiovascular causes. The long-term cardiovascular outcomes of these patients are entirely unknown. We aim to perform a registry of patients who have undergone a diagnostic nasopharyngeal swab for SARS-CoV-2 and to determine their long-term cardiovascular outcomes. STUDY AND DESIGN: This is a multicenter, observational, retrospective registry to be conducted at 17 centers in Spain and Italy (ClinicalTrials.gov number: NCT04359927). Consecutive patients older than 18 years, who underwent a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for SARS-CoV2 in the participating institutions, will be included since March 2020, to August 2020. Patients will be classified into two groups, according to the results of the RT-PCR: COVID-19 positive or negative. The primary outcome will be cardiovascular mortality at 1 year. The secondary outcomes will be acute myocardial infarction, stroke, heart failure hospitalization, pulmonary embolism, and serious cardiac arrhythmias, at 1 year. Outcomes will be compared between the two groups. Events will be adjudicated by an independent clinical event committee. CONCLUSION: The results of this registry will contribute to a better understanding of the long-term cardiovascular implications of the COVID19.

Arrhythmias and electrocardiographic findings in Coronavirus disease 2019: A systematic review and meta-analysis.

BACKGROUND: Coronavirus disease 2019 (COVID-19) primarily causes lung infection, but recent studies have shown that cardiac involvement is associated with a worse prognosis. OBJECTIVES: We conducted a systematic review and meta-analysis to examine the prevalence of cardiac arrhythmias detected by the electrocardiogram and their relationships with adverse outcomes in patients with COVID-19. METHODS: PubMed and Google were searched for studies that reported on cardiac arrhythmias and/or examined the relationship between arrhythmias and adverse outcomes. RESULTS: Thirty studies with 12,713 participants were included in the systematic review, and 28 studies (n = 12,499) in the meta-analysis. The mean age was 61.3 ± 16.8 years; 39.3% were female. In 25 studies with 7578 patients, the overall prevalence of cardiac arrhythmias was 10.3% (95% confidence interval [CI]: 8.4%-12.3%). The most common arrhythmias documented during hospitalization were supraventricular arrhythmias (6.2%, 95% CI: 4.4%-8.1%) followed by ventricular arrhythmias (2.5%, 95% CI: 1.8%-3.1%). The incidence of cardiac arrhythmias was higher among critically ill patients (relative risk [RR]: 12.1, 95% CI: 8.5-17.3) and among non-survivors (RR: 3.8, 95%, CI: 1.7-8.7). Eight studies reported changes in the QT interval. The prevalence of QTc > 500 ms was 12.3% (95% CI: 6.9%-17.8%). ST-segment deviation was reported in eight studies, with a pooled estimate of 8.7% (95% CI: 7.3% to 10.0%). CONCLUSION: Our meta-analysis showed that QTc prolongation, ST-segment deviation, and various other cardiac arrhythmias were observed in patients hospitalized with COVID-19. The presence of cardiac arrhythmias was associated with a worse prognosis.

Arrhythmia Risk Profile and Ventricular Repolarization Indices in COVID-19 Patients: A Systematic Review and Meta-Analysis.

INTRODUCTION: Coronavirus disease 2019 (COVID-19) has been associated with cardiac arrhythmias. Several electrocardiographic markers have been used to predict the risk of arrhythmia in patients with COVID-19. We aim to investigate the electrocardiographic (ECG) ventricular repolarization indices in patients with COVID-19. METHODOLOGY: We performed a comprehensive systematic literature search from PubMed, EuropePMC, SCOPUS, Cochrane Central Database, and Google Scholar Preprint Servers. The primary endpoints of this search were: Tp-e (T-peak-to-T-end) interval, QTd (QT dispersion), and Tp-e/QTc ratio in patients with newly diagnosed COVID-19 from inception up until August 2020. RESULTS: There were a total of 241 patients from 2 studies. Meta-analysis showed that Tp-e/QTc ratio was higher in COVID-19 group (mean difference 0.02 [0.01, 0.02], p < 0.001; I2: 18%,). Tp-e interval was more prolonged in COVID-19 group (mean difference 7.76 [3.11, 12.41], p < 0.001; I2: 80%) compared to control group. QT dispersion (QTd) also was increased in COVID-19 group (mean difference 1.22 [0.61, 1.83], p < 0.001 ; I2:30%). CONCLUSIONS: Several electrocardiographic markers including Tp-e/QTc, Tp-e interval, and QTd are significantly increased in patients with COVID-19.

Arrhythmias in patients with coronavirus disease 2019 (COVID-19) in Wuhan, China: Incidences and implications.

BACKGROUND: Coronavirus disease 2019 (COVID-19) continues to impact populations around the globe. Information regarding the incidences and implications of arrhythmias in COVID-19 is limited. METHODS: A total of 463 patients with COVID-19 and who had at least one electrocardiogram recording from February 1 to March 19, 2020, in Wuhan Union Hospital were enrolled in the study. RESULTS: Arrhythmias occurred in 85 of 463 (18.4%) patients: atrial arrhythmias in 10.2%, junctional arrhythmias in 0.2%, ventricular arrhythmias in 3.5%, and conduction block in 7.3%. Compared with patients without arrhythmias, those with arrhythmias had higher mortality, both during the time from symptom onset (p < 0.001) and from admission to follow-up (p < 0.001). The frequencies of severe COVID-19 (44.7% vs. 21.2%; p < 0.001) and death (25.9% vs. 10.1%; p < 0.001) were higher in patients with arrhythmias than in those without arrhythmias. Atrial arrhythmias and ventricular arrhythmias could predict severity and mortality, their odds ratios (OR) were 4.45 (95% confidence interval [CI] 2.35 to 8.40), 5.80 (95% CI 1.89 to 17.76) respectively for severity, and were 3.51 (95% CI 1.74 to 7.08), 3.41 (95% CI 1.13 to 10.24) respectively for mortality. High levels of interleukin-6 (IL-6) and IL-10 were associated with the occurrence of arrhythmias (all p < 0.05). CONCLUSION: Arrhythmias were significantly associated with COVID-19 severity and mortality. Atrial arrhythmia was the most frequent arrhythmia type. IL-6 and IL-10 levels can predict the risk of arrhythmias in COVID-19 patients.

Potential Mechanisms of Cardiac Injury and Common Pathways of Inflammation in Patients With COVID-19.

Due to the lack of prospective, randomized, controlled clinical studies on inflammation and cardiovascular involvement, the exact mechanism of cardiac injury among patients with Coronavirus Disease 2019 (COVID-19) still remains uncertain. It was demonstrated that there is a high and significantly positive linear correlation between troponin T and plasma high-sensitivity C-reactive protein levels, biomarkers of cardiac injury and systemic inflammation, respectively. Cardiac injury and inflammation is a relatively common association among patients hospitalized with COVID-19, and it is related to higher risk of in-hospital mortality. In our literature search, we identified several potential mechanisms of myocardial tissue damage, namely, coronavirus-associated acute myocarditis, angiotensin-converting enzyme 2 receptor binding affinity to the virus Spike protein, increased cytokine secretion, and hypoxia-induced cardiac myocyte apoptosis. Elucidation of the disease pathogenesis and prospective histopathological studies are crucial for future proper treatment in case of renewed outbreaks. Of interest is that with hundred of thousands of bodies available for autopsy studies, no prospective investigation has been reported so far. Strong efforts and continued research of the cardiovascular complications and identification of risk factors for poor prognosis in COVID-19 are steadily needed. The high morbidity and mortality of COVID-19, its monumental economic burden and social impact, the despair of a new pandemic outbreak, and the thread of potential utilization of novel severe acute respiratory syndrome coronavirus 2 as biologic weapons make it a preponderant necessity to better comprehend the therapeutic management of this lethal disease. Emerging as an acute infectious disease, COVID-19 may become a chronic epidemic because of genetic recombination. Therefore, we should be ready for the reemergence of COVID-19 or other coronaviruses.

Coronavirus disease-19 and cardiovascular disease: A risk factor or a risk marker?

Severe acute respiratory syndrome coronavirus-2 causes the clinical syndrome of coronavirus disease of 2019 (COVID-19) which has become a global pandemic resulting in significant morbidity and mortality. While the virus primarily affects the respiratory system, it also causes a wide variety of complex cardiac manifestations such as acute myopericarditis, acute coronary syndrome, congested heart failure, cardiogenic shock and cardiac arrhythmias. There are numerous proposed mechanisms of cardiac injury, including direct cellular injury, pro-inflammatory cytokine storm, myocardial oxygen-demand mismatch, and systemic inflammation causing multi-organ failure. Additionally, medications commonly used to treat COVID-19 patients have various cardiovascular side effects. We aim to provide a succinct review about the pathophysiology and cardiac manifestations of COVID-19, as well as treatment considerations and the various adaptations made to the current healthcare structure as a result of the pandemic.

Disease Severity Affects Ventricular Repolarization Parameters in Patients With COVID-19. / A Gravidade da Doença Afeta os Parâmetros de Repolarização Ventricular em Pacientes com COVID-19.

BACKGROUND: There is no study evaluating the Tpeak-Tend (Tpe) interval, Tpe/QT ratio, and Tpe/QTc ratio to assess cardiac arrhythmias in patients with COVID-19. OBJECTIVE: We aimed to examine whether there is a change in QT, QTc, Tpe interval, Tpe/QT ratio, and Tpe/QTc ratio in patients with COVID-19. METHODS: The study included 90 patients with COVID-19 infection and 30 age-and-sex-matched healthy controls. QT, QTc, Tpe interval, Tpe/QT ratio, and Tpe/QTc ratio were measured. The participants included in the study were divided into the following 4 groups: healthy controls (group I), patients with COVID-19 without pneumonia (group II), patients with COVID-19 and mild pneumonia (group III), and patients with COVID-19 and severe pneumonia (group IV). Statistical significance was set at p < 0.05. RESULTS: It was found that baseline heart rate, presence of hypertension and diabetes, white blood cell count, blood urea nitrogen, creatinine, potassium, aspartate aminotransferase, alanine aminotransferase, NT-proBNP, high sensitive C reactive protein, D-dimer, hs-cTnI, Tpe, Tpe/QT, and Tpe/QTc increased from group I to group IV, and they were significantly higher in all patients in group IV (p < 0.05). Systolic-diastolic blood pressure, hemoglobin, and calcium levels were found to be lowest in group IV and significantly lower than in other groups (< 0.05). QT and QTc intervals were similar between groups. It was determined that increased heart rate, calcium, D-dimer, NT-proBNP and hs-CRP levels were significantly related to Tpe, Tpe/QT, and Tpe/QTc. CONCLUSIONS: In patients with COVID-19 and severe pneumonia, Tpe, Tpe/QT ratio, and Tpe/QTc ratio, which are among ventricular repolarization parameters, were found to be increased, without prolonged QT and QTc intervals. In this study, we cannot definitively conclude that the ECG changes observed are directly related to COVID-19 infection or inflammation, but rather associated with severe COVID-19 scenarios, which might involve other causes of inflammation and comorbidities. (Arq Bras Cardiol. 2020; 115(5):907-913).

FUNDAMENTO: Não há estudos avaliando o intervalo Tpico-Tfim (Tpe), a relação Tpe/QT e a relação Tpe/QTc para avaliar arritmias cardíacas em pacientes com COVID-19. OBJETIVO: Visamos investigar se há alterações nos intervalos QT, QTc e Tpe e nas relações Tpe/QT e Tpe/QTc em pacientes com COVID-19. MÉTODOS: O estudo incluiu 90 pacientes com infecção por COVID-19 e 30 controles saudáveis pareados por sexo e idade. Foram aferidos os intervalos QT, QTc e Tpe e as relações Tpe/QT e Tpe/QTc. Os participantes incluídos no estudo foram divididos nos seguintes 4 grupos: controles saudáveis (grupo I), pacientes com COVID-19 sem pneumonia (grupo II), pacientes com COVID-19 e pneumonia leve (grupo III) e pacientes com COVID-19 e pneumonia grave (grupo IV). Significância estatística foi definida por valor p < 0,05. RESULTADOS: Verificou-se que a frequência cardíaca basal, a presença de hipertensão e diabetes, a contagem de leucócitos, o nitrogênio ureico no sangue, a creatinina, o potássio, o aspartato aminotransferase, a alanina aminotransferase, o NT-proBNP, a proteína C reativa de alta sensibilidade, o dímero-D, a TncI-as, o intervalo Tpe, a relação Tpe/QT e a relação Tpe/QTc aumentaram do grupo I para o grupo IV e foram significativamente mais altos em todos os pacientes do grupo IV (p < 0,05). A pressão arterial sistólica, a hemoglobina e os níveis de cálcio eram menores no grupo IV e significativamente menores em comparação com os demais grupos (< 0,05). Os intervalos QT e QTc eram semelhantes entre grupos. Determinou-se que os níveis elevados de frequência cardíaca, cálcio, dímero-D, NT-proBNP e PCR-as eram significativamente relacionados a Tpe, Tpe/QT e Tpe/QTc. CONCLUSÕES: Em pacientes com COVID-19 e pneumonia grave, o intervalo Tpe, a relação Tpe/QT e a relação Tpe/QTc, que estão entre os parâmetros de repolarização ventricular, foram aumentados, sem prolongação dos intervalos QT e QTc. A partir deste estudo, não podemos definitivamente concluir que as alterações eletrocardiográficas observadas estão diretamente relacionadas à infecção por COVID-19 ou à inflamação, mas sim associadas a cenários graves de COVID-19, que podem envolver outras causas de inflamação e comorbidades.

A Gravidade da Doença Afeta os Parâmetros de Repolarização Ventricular em Pacientes com COVID-19 / Disease Severity Affects Ventricular Repolarization Parameters in Patients With COVID-19

Resumo Fundamento: Não há estudos avaliando o intervalo Tpico-Tfim (Tpe), a relação Tpe/QT e a relação Tpe/QTc para avaliar arritmias cardíacas em pacientes com COVID-19. Objetivo: Visamos investigar se há alterações nos intervalos QT, QTc e Tpe e nas relações Tpe/QT e Tpe/QTc em pacientes com COVID-19. Métodos: O estudo incluiu 90 pacientes com infecção por COVID-19 e 30 controles saudáveis pareados por sexo e idade. Foram aferidos os intervalos QT, QTc e Tpe e as relações Tpe/QT e Tpe/QTc. Os participantes incluídos no estudo foram divididos nos seguintes 4 grupos: controles saudáveis (grupo I), pacientes com COVID-19 sem pneumonia (grupo II), pacientes com COVID-19 e pneumonia leve (grupo III) e pacientes com COVID-19 e pneumonia grave (grupo IV). Significância estatística foi definida por valor p < 0,05. Resultados: Verificou-se que a frequência cardíaca basal, a presença de hipertensão e diabetes, a contagem de leucócitos, o nitrogênio ureico no sangue, a creatinina, o potássio, o aspartato aminotransferase, a alanina aminotransferase, o NT-proBNP, a proteína C reativa de alta sensibilidade, o dímero-D, a TncI-as, o intervalo Tpe, a relação Tpe/QT e a relação Tpe/QTc aumentaram do grupo I para o grupo IV e foram significativamente mais altos em todos os pacientes do grupo IV (p < 0,05). A pressão arterial sistólica, a hemoglobina e os níveis de cálcio eram menores no grupo IV e significativamente menores em comparação com os demais grupos (< 0,05). Os intervalos QT e QTc eram semelhantes entre grupos. Determinou-se que os níveis elevados de frequência cardíaca, cálcio, dímero-D, NT-proBNP e PCR-as eram significativamente relacionados a Tpe, Tpe/QT e Tpe/QTc. Conclusões: Em pacientes com COVID-19 e pneumonia grave, o intervalo Tpe, a relação Tpe/QT e a relação Tpe/QTc, que estão entre os parâmetros de repolarização ventricular, foram aumentados, sem prolongação dos intervalos QT e QTc. A partir deste estudo, não podemos definitivamente concluir que as alterações eletrocardiográficas observadas estão diretamente relacionadas à infecção por COVID-19 ou à inflamação, mas sim associadas a cenários graves de COVID-19, que podem envolver outras causas de inflamação e comorbidades.

Abstract Background: There is no study evaluating the Tpeak-Tend (Tpe) interval, Tpe/QT ratio, and Tpe/QTc ratio to assess cardiac arrhythmias in patients with COVID-19. Objective: We aimed to examine whether there is a change in QT, QTc, Tpe interval, Tpe/QT ratio, and Tpe/QTc ratio in patients with COVID-19. Methods: The study included 90 patients with COVID-19 infection and 30 age-and-sex-matched healthy controls. QT, QTc, Tpe interval, Tpe/QT ratio, and Tpe/QTc ratio were measured. The participants included in the study were divided into the following 4 groups: healthy controls (group I), patients with COVID-19 without pneumonia (group II), patients with COVID-19 and mild pneumonia (group III), and patients with COVID-19 and severe pneumonia (group IV). Statistical significance was set at p < 0.05. Results: It was found that baseline heart rate, presence of hypertension and diabetes, white blood cell count, blood urea nitrogen, creatinine, potassium, aspartate aminotransferase, alanine aminotransferase, NT-proBNP, high sensitive C reactive protein, D-dimer, hs-cTnI, Tpe, Tpe/QT, and Tpe/QTc increased from group I to group IV, and they were significantly higher in all patients in group IV (p < 0.05). Systolic-diastolic blood pressure, hemoglobin, and calcium levels were found to be lowest in group IV and significantly lower than in other groups (< 0.05). QT and QTc intervals were similar between groups. It was determined that increased heart rate, calcium, D-dimer, NT-proBNP and hs-CRP levels were significantly related to Tpe, Tpe/QT, and Tpe/QTc. Conclusions: In patients with COVID-19 and severe pneumonia, Tpe, Tpe/QT ratio, and Tpe/QTc ratio, which are among ventricular repolarization parameters, were found to be increased, without prolonged QT and QTc intervals. In this study, we cannot definitively conclude that the ECG changes observed are directly related to COVID-19 infection or inflammation, but rather associated with severe COVID-19 scenarios, which might involve other causes of inflammation and comorbidities. (Arq Bras Cardiol. 2020; 115(5):907-913)

Alteraciones EKG en Tiempos de COVID-19, KGC 2020

Alteraciones EKG en Tiempos de COVID-19, KGC 2020

Electrocardiographic features of 431 consecutive, critically ill COVID-19 patients: an insight into the mechanisms of cardiac involvement.

AIMS: Our aim was to describe the electrocardiographic features of critical COVID-19 patients. METHODS AND RESULTS: We carried out a multicentric, cross-sectional, retrospective analysis of 431 consecutive COVID-19 patients hospitalized between 10 March and 14 April 2020 who died or were treated with invasive mechanical ventilation. This project is registered on ClinicalTrials.gov (identifier: NCT04367129). Standard ECG was recorded at hospital admission. ECG was abnormal in 93% of the patients. Atrial fibrillation/flutter was detected in 22% of the patients. ECG signs suggesting acute right ventricular pressure overload (RVPO) were detected in 30% of the patients. In particular, 43 (10%) patients had the S1Q3T3 pattern, 38 (9%) had incomplete right bundle branch block (RBBB), and 49 (11%) had complete RBBB. ECG signs of acute RVPO were not statistically different between patients with (n = 104) or without (n=327) invasive mechanical ventilation during ECG recording (36% vs. 28%, P = 0.10). Non-specific repolarization abnormalities and low QRS voltage in peripheral leads were present in 176 (41%) and 23 (5%), respectively. In four patients showing ST-segment elevation, acute myocardial infarction was confirmed with coronary angiography. No ST-T abnormalities suggestive of acute myocarditis were detected. In the subgroup of 110 patients where high-sensitivity troponin I was available, ECG features were not statistically different when stratified for above or below the 5 times upper reference limit value. CONCLUSIONS: The ECG is abnormal in almost all critically ill COVID-19 patients and shows a large spectrum of abnormalities, with signs of acute RVPO in 30% of the patients. Rapid and simple identification of these cases with ECG at hospital admission can facilitate classification of the patients and provide pathophysiological insights.

Arrhythmic safety of hydroxychloroquine in COVID-19 patients from different clinical settings.

AIMS: The aim of the study was to describe ECG modifications and arrhythmic events in COVID-19 patients undergoing hydroxychloroquine (HCQ) therapy in different clinical settings. METHODS AND RESULTS: COVID-19 patients at seven institutions receiving HCQ therapy from whom a baseline and at least one ECG at 48+ h were available were enrolled in the study. QT/QTc prolongation, QT-associated and QT-independent arrhythmic events, arrhythmic mortality, and overall mortality during HCQ therapy were assessed. A total of 649 COVID-19 patients (61.9 ± 18.7 years, 46.1% males) were enrolled. HCQ therapy was administrated as a home therapy regimen in 126 (19.4%) patients, and as an in-hospital-treatment to 495 (76.3%) hospitalized and 28 (4.3%) intensive care unit (ICU) patients. At 36-72 and at 96+ h after the first HCQ dose, 358 and 404 ECGs were obtained, respectively. A significant QT/QTc interval prolongation was observed (P < 0.001), but the magnitude of the increase was modest [+13 (9-16) ms]. Baseline QT/QTc length and presence of fever (P = 0.001) at admission represented the most important determinants of QT/QTc prolongation. No arrhythmic-related deaths were reported. The overall major ventricular arrhythmia rate was low (1.1%), with all events found not to be related to QT or HCQ therapy at a centralized event evaluation. No differences in QT/QTc prolongation and QT-related arrhythmias were observed across different clinical settings, with non-QT-related arrhythmias being more common in the intensive care setting. CONCLUSION: HCQ administration is safe for a short-term treatment for patients with COVID-19 infection regardless of the clinical setting of delivery, causing only modest QTc prolongation and no directly attributable arrhythmic deaths.

[Dengue caused life-threatening arrhythmia]. / Denguefeber orsakade arytmi.

Dengue is a mosquito-borne viral disease found in tropical and sub-tropical climates worldwide. Due to globalization and climate change dengue is an increasing global concern. Symptoms typically appear 3-14 days after inoculation by the Aedes mosquito and most commonly manifests as a self-limiting febrile illness. However, in severe dengue, plasma leakage may be profound and result in hemorrhage, disseminated intravascular coagulation and circulatory collapse. The dengue virus may also cause organ dysfunction. Cases of myocarditis, myocardial dysfunction and arrhythmias including atrioventricular block have been reported. The atrioventricular block often resolves spontaneously but pharmacological and pacing support may be required. We report a case of dengue in a patient who was admitted to a Swedish hospital after visiting India. In this case total atrioventricular block without ventricular escape rhythm resolved spontaneously and no pacemaker was necessary.

COVID-19 infection and cardiac arrhythmias.

As the coronavirus 2019 (COVID-19) pandemic marches unrelentingly, more patients with cardiac arrhythmias are emerging due to the effects of the virus on the respiratory and cardiovascular (CV) systems and the systemic inflammation that it incurs, and also as a result of the proarrhythmic effects of COVID-19 pharmacotherapies and other drug interactions and the associated autonomic imbalance that enhance arrhythmogenicity. The most worrisome of all arrhythmogenic mechanisms is the QT prolonging effect of various anti-COVID pharmacotherapies that can lead to polymorphic ventricular tachycardia in the form of torsade des pointes and sudden cardiac death. It is therefore imperative to monitor the QT interval during treatment; however, conventional approaches to such monitoring increase the transmission risk for the staff and strain the health system. Hence, there is dire need for contactless monitoring and telemetry for inpatients, especially those admitted to the intensive care unit, as well as for outpatients needing continued management. In this context, recent technological advances have ushered in a new era in implementing digital health monitoring tools that circumvent these obstacles. All these issues are herein discussed and a large body of recent relevant data are reviewed.