ABSTRACT
INTRODUCTION It is well known that COVID-19 affects the cardiovascular system by exacerbating heart failure in patients with preexisting conditions and troponin elevation in critically ill patients. The insight into the cardiovascular involvement and sequelae in those with no preexisting conditions is poor. We performed a systematic and comprehensive echocardiographic evaluation of patients hospitalized with COVID-19. The aim of the study was to analyze cardiac performance in subjects with no prior history of structural heart disease in relation to inflammatory markers and clinical outcome. The study is a part of CRACoV project, with prospective design and an assumed 12-month follow-up. Following data are preliminary results of baseline examinations. MATERIAL AND METHODS The study included 106 patients hospitalized with diagnosed COVID-19 infection (age 56.7 ± 12,8 years;39 women). Patients with prior heart failure, known structural heart disease, acute coronary syndrome, acute stroke or acute vascular episode as well as chronic kidney disease, chronic inflammatory or neoplasmatic disease were excluded from the study. In all participants standard clinical assessment and laboratory tests including C-reactive protein (CRP), interleukin 6 (IL-6), cardiac troponin I, N-terminal pro-brain natriuretic peptide (NT-pro-BNP) were performed. Severity of the disease was classified according to World Health Organization criteria. An extended echocardiographic image acquisition protocol was performed in all subjects within 72-hours from admission. All analyses, including left ventricle (LV) longitudinal deformation (GLS), were performed off-line. RESULTS COVID-19 had severe course in 58 subjects, 4 patients in critical condition died during hospitalization. High-flow oxygen therapy was required in 17 subjects. LV systolic function was preserved in all subjects (mean 62.3 ± 5.2%;GLS -19.9 ± ± 6.4;CO 5.51 ± 1.47 l/min). Averaged E/Eè was 6.97 ± 1.80. Right ventricle (RV) was enlarged in 6 patients, in all RV function was preserved (TAPSE 24.6 ± 3.74 mm, RV S' 15.6 ± 3.03 mm). In one patient RV thrombus was detected. Pericardial effusion was present in 8 patients. Elevated NT-pro-BNP (>300 pg/ml) was detected in 34 patients and elevated troponin in 3 subjects. NT-pro-BNP significantly correlated with CRP (r = 0.24;P <0.01);IL-6 (r = 0.28;P <0.01) and negatively with LV GLS (r = -0.27;P = 0.01). In multiple regression the risk of high-flow oxygen therapy was related with male gender (b = -0.30;P = 0.04), CRP (b = 0.50;P <0.005), NT-pro-BNP (b = -0.28;P = 0.04) and RV diameter (b = 0.33;P = 0.02). CONCLUSIONS In subjects with COVID-19 and normal LV systolic function, elevation of NT-pro-BNP is frequent and reflects haemodynamic stress related with acute inflammatory disease. NT-pro-BNP significantly associates with the risk of severe course of COVID-19. RV diameter is independently related with worse prognosis in COVID-19.
ABSTRACT
Introduction: Novel coronavirus disease 2019 (COVID-19) is not only connected with respiratory distress syndrome, but also with gastrointestinal symptoms, hepatic injury and multiorgan and systemic inflammation. Considering the wide range of hepatokines and myokines activities they may influence pathogenesis and infection course. Aims & Methods: Our aim was to assess concentrations of pentraxin 3 (PTX3), fibroblast grow factor 21 (FGF21), irisin and fetuin A among COVID- 19 patients with emphasis on their relationship with COVID-19 severity, concomitant metabolic abnormalities and liver dysfunction. An observational single center cohort study included 70 COVID-19 patients and healthy controls. Hepatokines serum concentrations were measured with enzyme-linked immunosorbent assay in serum collected at the moment of admission to hospital, before any treatment was applied. Results: Serum fetuin A concentrations significantly decreased in COVID- 19 patients compared to healthy volunteers (243.4 [195.0-275.8] vs 333.5 [303.0-371.4] μg/ml;p<0.001). There was no significant difference in serum irisin, FGF21 and PTX3 levels between both groups. Alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT) activities, and ferritin levels were significantly higher in COVID-19 patients (34.0 [20.0-52.5] vs 21.0 [16.0-25.7] U/l;p=0.02, 33.5 [20.0-62.5] vs 14.0 [10.7-24.2] U/l;p=0.003 and 210.0 [114.7-487.0] vs 16.5 [13.0-19.6] μg/l;p<0.001, respectively). Fetuin A levels were down-regulated in COVID-19 patients with higher GGT activity and ferritin concentration (258.8 [219.9-310.9] vs 221.9 [182.1- 256.3] μg/ml;p=0.004 and 257.7 [238.3-311.1] vs 220.5 [178.5-264.1] μg/ ml;p=0.001, respectively). HOMA-IR and C-reactive protein were significantly elevated in COVID-19 patients. The presence of gastrointestinal (GI) symptoms did not influence analyzed hepatokines levels. Pneumonia was found in 32.8% of patients. Fetuin A concentration significantly decreased in patients with pneumonia (217.4 [188.3-248.8] vs 256.3 [218.9-285.7] ng/ml;p<0.001), and those requiring admission to intensive care unit (ICU) (194.0 [124.8-229.8] vs 252.4 [209.4- 276.6] ng/ml;p=0.02). Serum PTX3 concentration significantly increased in ITU patients (4769.0 [2896.9-8394.6] vs 2278.2 [1876.9-3106.3] ng/ml;p<0.001). Conclusion: Surprisingly, pointing to proinflammatory and insulin impairing action of fetuin A, its levels were significantly lower in COVID-19 patients despite of higher HOMA-IR, CRP and ferritin levels. Even, more surprising was significant reduction of fetuin A in patients with pneumonia, those requiring ICU and those with higher ferritin levels and HOMA-IR. It suggests that fetuin A deficiency predispose to more serious COVID-19 course, glucose metabolism abnormalities and its measurement may be additional marker of disease severity. Up-regulated PTX3 may also suggest COVID-19 severity. Impaired liver function revealed by GGT activity was associated with serum fetuin A depletion. Predictive factor which could predispose to a more severe course of COVID-19, including the presence of pneumonia and ICU hospitalization, was GGT activity.