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1.
J Physiol Pharmacol ; 73(1)2022 Feb.
Article in English | MEDLINE | ID: covidwho-1876428

ABSTRACT

Coronavirus disease 2019 (COVID-19) causes cardiovascular damage in the acute period. Knowledge regarding cardiovascular damage after COVID-19 infection and during longer-term follow-up is currently limited. In our study, we aimed to compare cardiac and inflammatory markers and echocardiographic parameters between patients who had recovered from COVID-19 and control group. A total of 224 individuals were included, comprising 126 patients with a history of COVID-19 and 98 healthy controls. The demographic characteristics of the two groups were similar. Complete blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), N-terminal pro-B type natriuretic peptide (NT-ProBNP), D-dimer, haemoglobin A1C, troponin T and creatine kinase myocardial band (CK-MB) levels were compared between both groups. The mean follow-up period of the COVID-19 group was 58.39 ± 39.1 days (range:10 - 180 days post-COVID-19). Red cell distribution width (RDW), ESR, CRP, NT-ProBNP, D-dimer and troponin T values were significantly higher in the COVID-19 group compared to the control group. Left ventricular ejection fraction (LVEF) was significantly lower in the COVID-19 group. Left ventricular diastolic diameter (LVDD) and incidence of pericardial effusion were higher in the COVID-19 group. For multivariate analysis, possible factors identified by univariate analysis were subjected to multivariate logistic regression analysis to determine independent predictors of COVID-19. Among these factors, RDW, CRP and LVEF were independently higher in the COVID-19 group than in the control group. We conclude that although the clinical and prognostic significance of cardiac and other inflammatory markers in the acute phase of COVID-19 is known, we found that these biomarkers and echocardiography parameters can also be used in the follow-up of cardiac injury for a mid-term period post-infection.


Subject(s)
COVID-19 , Heart Diseases , Biomarkers , C-Reactive Protein/metabolism , Echocardiography , Heart Diseases/diagnosis , Heart Diseases/virology , Humans , Stroke Volume , Troponin T , Ventricular Function, Left
2.
Anatolian Journal of Cardiology ; 24(SUPPL 1):112-113, 2020.
Article in English | EMBASE | ID: covidwho-1176035

ABSTRACT

Background and Aim: Coronaviruses are important pathogens of humans and animals that can cause diseases ranging from mildly to seriously and fatally respiratory, enteric, cardiovascular diseases. Recent studies emphasized that some of the patients had COVID 19 associated cardiac injury as an ejection fraction decline and troponin I elevation. In hospitalized patients, cardiac damage leading to cardiac death with a high troponin level were reported to be between 7.2-40%. The aim of this study was to evaluate the relationship between mortality and cardiac laboratory findings in patients who were diagnosed and hospitalized with COVID 19 infection caused by the novel coronavirus SARS-CoV-2. Methods: A total of 105 patients who were hospitalized and diagnosed with COVID 19 infection between 20 March 2020 and 20 June 2020 were included in the study. Patients's medical history, clinical, laboratory, radiological, and treatment data were collected and analyzed. Results: The baseline clinical features of the 2 groups (troponin I high and low group) are summarized in Table 1. There was shown a statistically significant differences between the 2 groups in Table 1 (all p<0.05). A statistically significant correlation was observed between the presence of age, saturation, CK-MB, PT, neutrophil count, lymphocyte count, NLR, hemoglobin, CRP, ferritin, D dimer, calcium, 25-hydroxy vitamin(OH) D3 (r and p values, respectively: 0.478, <0.001;-0.626, <0.001;0.697, <0.001;0.617, <0.001;0.562, <0.001;-0.418, <0.001;0.695, <0.001;-0.368, <0.001;0.587, <0.001;0.531, <0.001;0.683, <0.001;-0.619, <0.001;-0.464, <0.001). We performed univariate and multivariate analyses to determine the independent factors associated with mortality. The troponin I, dyspnea, hypertention, hyperlipidemia, diabetes mellitus, and coronary artery disease were analyzed using the multivariate Cox regression model. In multivariate analyses, a significant association was noted between troponin I, dyspnea and the adjusted risk of mortality (odds ratio=1.002, 95% confidence interval=1.000-1.004;p=0.045;odds ratio=6.639, 95% confidence interval=1.039-42.445;p=0.046, respectively). In a receiver operating characteristic (ROC) curve analysis, troponin I value >7.8 pg/ml was identified as an effective cut-off point in mortality for patients with COVID 19 (area under curve = 0.832, 95% CI=0.654-1.009, p=0.001). A troponin I value of less than 7.8 pg/ml yielded a sensitivity of 78% and a specificityof 86% (Figure1). The Kaplan-Meier curve for mortality according to troponin I group (troponin I >7.8 pg/ml, troponin I ≤7.8 pg/ml) in the entire population of patients (p<0.001 by log-rank test). Conclusions: Troponin value constituted an independent risk indicator for mortality when it was above the cut-off value of >7.8 pg/ml. This highlights the need to monitor more closely patients with troponin levels above this value. Aggressive treatment may be considered for patients at high risk of myocardial injury.

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