ABSTRACT
Background: the COVID19 pandemic has resulted in worldwide morbidity at unprecedented scale. Troponin elevation is a frequent laboratory finding in hospitalized patients with the disease, and may reflect direct vascular injury or nonspecific supply demand imbalance. In this work, we assessed the correlation between different ranges of Troponin elevation, Electrocardiographic (ECG) abnormalities and mortality. Methods. We retrospectively studied 204 consecutive patients hospitalized at NYU Langone Health with COVID19. Serial ECG tracings were evaluated in conjunction with laboratory data including Troponin. Mortality was analyzed in respect to the degree of Troponin elevation and the presence of ECG changes including ST elevation, ST depression or T wave inversion. Results. Mortality increased in parallel with increase in Troponin elevation groups and reached 60% when Troponin was >1 ng/ml. In patients with mild Troponin rise (0.05 to 1.00 ng/ml) the presence of ECG abnormality resulted in significantly greater mortality. Conclusion. ECG repolarization abnormalities may represent a marker of clinical severity in patients with mild elevation in Troponin values. This finding can be used to enhance risk stratification in patients hospitalized with COVID19.
Subject(s)
COVID-19 , Depressive Disorder , Cerebrovascular TraumaABSTRACT
The term chimeric virus was not popular in the last decades. Recently, according to current sequencing efforts in discovering COVID-19 Secrets, the generated information assumed the presence of 6 Coronavirus main strains, but coronavirus diverges into hundreds of sub-strains. the bottleneck is the mutation rate. With two mutation/month, humanity will meet a new sub-strain every month. Tracking new sequenced viruses is urgently needed because of the pathogenic effect of the new sub-strains. here we introduce COVATOR, A user-friendly and python-based software that identifies viral chimerism. COVATOR aligns input genome and protein that has no known source, against genomes and protein with known source, then gives the user a graphical summary.
Subject(s)
COVID-19ABSTRACT
Background: The emergence of the COVID-19 pandemic has resulted in over two million affected and over 150 thousand deaths to date. There is no known effective therapy for the disease. Initial reports suggesting the potential benefit of Hydroxychloroquine/Azithromycin (HY/AZ) have resulted in massive adoption of this combination worldwide. However, while the true efficacy of this regimen is unknown, initial reports have raised concerns regarding the potential risk of QT prolongation and induction of torsade de pointes (TdP). Methods: This is a multicenter retrospective study of 251 patients with COVID-19 treated with HY/AZ. We reviewed ECG tracings from baseline and until 3 days after completion of therapy to determine the progression of QTc and incidence of arrhythmia and mortality. Results: QTc prolonged in parallel with increasing drug exposure and incompletely shortened after its completion. Extreme new QTc prolongation to > 500 ms, a known marker of high risk for TdP had developed in 15.9% of patients. One patient developed TdP requiring emergent cardioversion. Seven patients required premature termination of therapy. The baseline QTc of patients exhibiting QTc prolongation of > 60 ms was normal. Conclusion: The combination of HY/AZ significantly prolongs the QTc in patients with COVID-19. This prolongation may be responsible for life threating arrhythmia in the form of TdP. This risk mandates careful consideration of HY/AZ therapy in lights of its unproven efficacy. Strict QTc monitoring should be performed if the regimen is given.
Subject(s)
COVID-19 , Arrhythmias, Cardiac , Torsades de Pointes , Long QT SyndromeABSTRACT
We report the change in the QT interval in 84 adult patients with SARS-CoV-2 infection treated with Hydroxychloroquine/Azithromycin combination. QTc prolonged maximally from baseline between days 3 and 4. in 30% of patients QTc increased by greater than 40ms. In 11% of patients QTc increased to >500 ms, representing high risk group for arrhythmia. The development of acute renal failure but not baseline QTc was a strong predictor of extreme QTc prolongation.