QTc interval prolongation, inflammation, and mortality in patients with COVID-19.

PURPOSE: Systemic inflammation has been associated with corrected QT (QTc) interval prolongation. The role of inflammation on QTc prolongation in COVID-19 patients was investigated. METHODS: Patients with a laboratory-confirmed SARS-CoV-2 infection admitted to IRCCS San Raffaele Scientific Institute (Milan, Italy) between March 14, 2020, and March 30, 2020 were included. QTc-I was defined as the QTc interval by Bazett formula in the first ECG performed during the hospitalization, before any new drug treatment; QTc-II was the QTc in the ECG performed after the initiation of hydroxychloroquine drug treatment. RESULTS: QTc-I was long in 45 patients (45%) and normal in 55 patients (55%). Patients with long QTc-I were older and more frequently males. C-Reactive protein (CRP) and white blood cell (WBC) count at hospitalization were higher in patients with long QTc-I and long QTc-II. QTc-I was significantly correlated with CRP levels at hospitalization. After a median follow-up of 83 days, 14 patients (14%) died. There were no deaths attributed to ventricular arrhythmias. Patients with long QTc-I and long QTc-II had a shorter survival, compared with normal QTc-I and QTc-II patients, respectively. In Cox multivariate analysis, independent predictors of mortality were age (HR = 1.1, CI 95% 1.04-1.18, p = 0.002) and CRP at ECG II (HR 1.1, CI 95% 1.0-1.1, p = 0.02). CONCLUSIONS: QTc at hospitalization is a simple risk marker of mortality risk in COVID-19 patients and reflects the myocardial inflammatory status.

Subclinical myocardial dysfunction in patients recovered from COVID-19.

BACKGROUND: Myocardial injury (MI) can be detected during the acute phase of Coronavirus disease 19 (COVID-19) and is associated with a dismal prognosis. Recent imaging studies described the persistence of cardiac abnormalities after the recovery. The aim of the study was to investigate the spectrum of cardiac abnormalities at mid-term follow-up in patients recovered from COVID-19 using clinical assessment, laboratory tests, and imaging evaluation with comprehensive echocardiography. METHODS: This is an observational, cross-sectional study assessing an unselected cohort of consecutive patients recovered from COVID-19. MI was defined by elevated plasma levels of high sensitive troponin T (hsTnT). At the follow-up, a complete examination including echocardiography was performed. RESULTS: The 123 patients included were divided into two groups according to the presence of MI during hospitalization: group A (without MI) and group B (with MI). After a median of 85 days, group B patients were more frequently symptomatic for dyspnea and had significantly higher values of hsTnT and N-Terminal prohormone of Brain Natriuretic Peptide (NT-proBNP), compared to Group A. No differences between the two groups in left nor right ventricle dimension and ejection fraction were found. However, in group B a significant reduction of mean left ventricle global longitudinal strain was observed (-15.7±.7 vs -18.1± .3 in group A, p < 0.001), together with higher frequency of impaired diastolic function and higher values of pulmonary pressure. CONCLUSIONS: In patients recovered from COVID-19, echocardiography with speckle-tracking analysis may be an useful imaging tool to identify subclinical myocardial dysfunction and potentially guide management strategies.