Abstract
Funding AcknowledgementsType of funding sources: None.Introduction.Changes in the myocardium in patients with arterial hypertension (AH) can cause fatal arrhythmias. The effects of inflammation and drugs on the heart in COVID-19 pneumonia can also increase the risk of sudden arrhythmic death.The aim of the paper is to study interrelationship of ECG markers of malignant arrhythmias and clinical and laboratory findings in patients with AH and COVID-19 pneumonia.Methods.48 patients with AH hospitalized for COVID-19 pneumonia (32 women aged 34 to 83, 16 men aged 48-80) were included in the study in October-November 2020. Exclusion criteria: congestive heart failure, previous myocardial infarction, reduced ejection fraction, valvular disease, life-threatening COVID-19 and other serious diseases. Main clinical characteristics and recommended laboratory findings were taken into account. Corrected QT and Tpeak-Tend were analyzed.Results.The QTc fluctuations were from 353 ms to 494 ms. The QTc values were higher than normal in 28%. The QTc duration correlated with C-reactive protein level (Kendall R = 0.59) and NYHA class (Gamma = 0.48). The Tpeak-Tend value correlated with coronary heart disease (Gamma 0.65), C-reactive protein (Kendall R = 0.57) and taking dexamethasone (Gamma 0.44) and fluoroquinolones (Gamma 0.58). Multivariate analysis has showed that high level of C-reactive protein (Wald = 7.4) and the presence of heart failure (Wald = 5.2) were independent predictors of QTc increase. Coronary heart disease (Wald = 4,8) and taking respiratory fluoroquinolones (Wald= 3.7) were independent predictors of Tpeak-Tend increase. Age, SatO2, taking betablockers and other analyzed indicators were not significantly related to QTc and Tpeak-Tend.Conclusion.Systemic inflammatory response, heart diseases and taking respiratory fluoroquinolones can adversely affect the myocardial repolarization indicators associated with the risk of sudden death in patients with AH hospitalized for COVID-19 pneumonia.
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