scholarly journals QTc prolongation and mortality in SARS-2-CoV-infected patients treated with azithromycin and hydroxychloroquine

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Enrico Baldi ◽  
Roberto Rordorf ◽  
Lucrezia Masiello ◽  
Sabato D’Amore ◽  
Stefano Ghio ◽  
...  
Keyword(s):  
2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
S Kacheva ◽  
K Göller ◽  
N Marx ◽  
K Mischke ◽  
W Karges
Keyword(s):  

2019 ◽  
Vol 9 (2) ◽  
pp. 96-98
Author(s):  
Rupesh George ◽  
◽  
Joseph T Antony ◽  
David Jose ◽  
Anish Preshi ◽  
...  

2021 ◽  
pp. 1-3
Author(s):  
Lesya G. Tomlinson ◽  
Mitchell I. Cohen ◽  
Rebecca E. Levorson ◽  
Megan B. Tzeng

Abstract SARS-CoV-2, which causes the disease COVID-19, generally has a mild disease course in children. However, a severe post-infectious inflammatory process known as multisystem inflammatory syndrome in children has been observed in association with COVID-19. This inflammatory process is a result of an abnormal immune response with similar clinical features to Kawasaki disease. It is well established that multisystem inflammatory syndrome in children is associated with myocardial dysfunction, coronary artery dilation or aneurysms, and occasionally arrhythmias. The most common electrocardiographic abnormalities seen include premature atrial or ventricular ectopy, variable degrees of atrioventricular block, and QTc prolongation, and rarely, haemodynamically significant arrhythmias necessitating extracorporeal membrane oxygenation support. However, presentation with fever, hypotension, and relative bradycardia with a left axis idioventricular rhythm has not been previously reported. We present a case of a young adolescent with multisystem inflammatory syndrome in children with myocarditis and a profoundly inappropriate sinus node response to shock with complete resolution following intravenous immunoglobulin.


Circulation ◽  
2019 ◽  
Vol 140 (5) ◽  
pp. 436-439
Author(s):  
Akihiro Takasaki ◽  
Shiro Nakamori ◽  
Kaoru Dohi

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V.O Baris ◽  
B Dincsoy ◽  
E Gedikli ◽  
A Erdem

Abstract Introduction Sotalol (SOT) is a Class 3 antiarrhythmic drug and commonly used for various arrhythmia treatments. However; it can prolong QT interval and lead to malignant arrhythmias. Empagliflozin is a selective SGLT-2 inhibitor used in the treatment of Type 2 diabetes and has been shown to have positive effects on cardiovascular outcomes. Since the effect of empagliflozin (EMPA) on potassium channel activation is not yet known, there is no recommendation for the concomitant use of these drugs. Purpose In this study, we aimed to evaluate possible protective effects of empagliflozin in sotalol induced QT prolongation. Materials and methods Twenty-four male Wistar Alba rats were randomized into four groups. The first (control) group (n: 6) received only serum physiologic (1ml) via orogastric gavage (OG). The second (EMPA) group (n: 6) received EMPA (10 mg/kg) via OG. The third (SOT) group (n: 6) received SOT (80 mg/kg) via OG. The fourth (EMPA+SOT) group (n: 6) received EMPA (10 mg/kg) and SOT (80 mg/kg) via OG. Under anesthesia; PR, QT intervals and heart rate (HR) were measured and QTc value was also calculated at second hour on lead II using electrocardiogram (ECG). Results In the SOT group; QT intervals, T wave durations and QTc values were found to be statistically longer than the control group, whereas HR was found to be lower than the control group (p<0.01). In the EMPA+SOT group; QT intervals, T wave durations and QTc values were significantly lower and HR was significantly higher compared to the SOT group (p<0.001, p<0.01, p<0.001, p<0.001 respectively) (Table) Conclusion In the present study, we detected that EMPA significantly ameliorates SOT induced QT prolongation. In addition to this, we have also shown that EMPA can be used safely with SOT in clinical practice. With more clinical trials, the routine use of EMPA may be suggested to prevent QTc prolongation in diabetic patients receiving SOT. Finally; our study indicates that EMPA can effect on potassium channels. Funding Acknowledgement Type of funding source: None


Author(s):  
Verena Gotta ◽  
Frank Cools ◽  
Karel van Ammel ◽  
David J. Gallacher ◽  
Sandra A.G. Visser ◽  
...  

2013 ◽  
Vol 38 (2) ◽  
pp. E5-E6 ◽  
Author(s):  
Raymond Lam
Keyword(s):  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Georg Ferber ◽  
Ulrike Lorch ◽  
Jörg Täubel

Concentration-effect (CE) models applied to early clinical QT data from healthy subjects are described in the latest E14 Q&A document as promising analysis to characterise QTc prolongation. The challenges faced if one attempts to replace a TQT study by thorough ECG assessments in Phase I based on CE models are the assurance to obtain sufficient power and the establishment of a substitute for the positive control to show assay sensitivity providing protection against false negatives. To demonstrate that CE models in small studies can reliably predict the absence of an effect on QTc, we investigated the role of some key design features in the power of the analysis. Specifically, the form of the CE model, inclusion of subjects on placebo, and sparse sampling on the performance and power of this analysis were investigated. In this study, the simulations conducted by subsampling subjects from 3 different TQT studies showed that CE model with a treatment effect can be used to exclude small QTc effects. The number of placebo subjects was also shown to increase the power to detect an inactive drug preventing false positives while an effect can be underestimated if time points aroundtmaxare missed.


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