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
Objective: The COVID-19 lockdown caused unprecedented decline in environmental noise pollution. We aimed to evaluate the impact of aircraft noise exposure decrease during lockdown on blood pressure (BP) and selected hypertensionmediated organ damages. Design and method: As previously reported (J Hypertens. 2019;37) in 2015 (1st observation) we examined group of inhabitants exposed to high (>60 dB) aircraft noise living near Cracow Airport (n=101), and compared them to unexposed group (<55 dB) (n=100). In June 2020, 4 months after COVID-19 pandemic restrictions introduction, we reassessed (2nd observation) 74 and 75 participants from previously exposed and unexposed groups, respectively, using the same study protocol. We collected medical history, office and ambulatory BP, echocardiographic and arterial stiffness data. Results: In exposed to aircraft noise group the prevalence of arterial hypertension increased from 1st to 2nd observation (P<0.05). During lockdown in the noise exposed group office and 24 hour diastolic BP (DBP, P<0.022) decreased signifi-cantly, which was accompanied by a significant drop in annoyance (P=0.006). In this group in 2nd observation DBP was significantly lower than estimated DBP (i.e. calculated as a sum of DBP at 1st observation and parameter estimates of crosssectional association of DBP and age multiplied by 5.5 year-time period between observations) (P=0.047). The obtained decline in DBP from 1st to 2nd observation was grater in noise exposed than unexposed participants, even after adjustment for covariates. The carotid-femoral pulse wave velocity (PWV), initially higher in noise exposed group, decreased from 1st to 2nd observation in both groups, however this was more pronounced in the exposed than unexposed group (P=0.003). In 1st observation PWV in noise exposed participants did not show any relationship with age (Parameter Estimate (PE)=0.01 m/s/year;P= 0.71), while in 2nd observation, during aircraft noise decline caused by COVID-19 lockdown, the expected positive relation of PWV with age was reinstituted (PE=0.15 m/s/year;P<0.001). Conclusions: As our previous study indicated, aircraft noise exposure may increase BP and accelerate arterial stiffening. The decrease in BP and PWV due to noise intensity diminution, observed during COVID-19 lockdown, in fact provides evidence for this observation.