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The identification of left atrial and left ventricular myocardial deformation using speckle tracking echocardiography in patients with PS allows subclinical LV dysfunction and subclinical electrophysiologic changes to be detected earlier.

Background and Objectives: This study aimed to evaluate the relationship between mortality and cardiac laboratory findings in patients who were hospitalized after a positive PCR for COVID-19 infection. Materials and Methods: This study included patients who were admitted to or referred to the hospital between 20 March and 20 June 2020, diagnosed with COVID-19 via a positive RT-PCR from nasal and pharyngeal swab samples. The troponin I level was measured from each patient. Medical records of patients were retrospectively reviewed and analyzed. Results: A hundred and five patients who were diagnosed with COVID-19 and hospitalized, or who died in the hospital due to COVID-19, were included in this study. There was a statistically significant difference between the troponin I high and low level groups in terms of age (years), BMI, shortness of breath (SB), oxygen saturation (%), hypertension, length of stay in the ICU; and for mortality, C-reactive protein, the neutrophil-to-lymphocyte ratio, hemoglobin, lactate dehydrogenase, ferritin, D-dimer, creatine kinase-MB, prothrombin time, calcium, and 25-hydroxy vitamin 25(OH)D3 (all p < 0.05). In the logistic analyses, a significant association was noted between troponin I and the adjusted risk of mortality. A ROC curve analysis identified troponin I values > 7.8 pg/mL as an effective cut-off point in mortality for patients with COVID-19. A troponin I value of higher than 7.8 pg/mL yielded a sensitivity of 78% and a specificity of 86%. Conclusions: The hospital mortality rate was higher among patients diagnosed with COVID-19 accompanied by troponin levels higher than 7.8 pg/mL. Therefore, in patients diagnosed with COVID-19, elevated troponin I levels >7.8 pg/mL can be considered an independent risk factor for mortality.

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(1) To investigate the role of azurocidin, an antimicrobial protein, in patients with ST segment elevation myocardial infarction (STEMI). (2) This single-center prospective observational study included patients with STEMI and healthy age- and sex-matched control subjects. Baseline demographic, clinical and biochemical data were compared between the two groups. Azurocidin levels at baseline were determined using an enzyme-linked immunosorbent assay. Multivariate linear regression analysis with enter method was used to test the association between azurocidin and independent variables, such as the thrombolysis in myocardial infarction (TIMI) score, synergy between percutaneous coronary intervention with TAXUS and cardiac surgery score, global registry of acute coronary events score, Killip class, C-reactive protein (CRP), and creatinine kinase-myocardial band (CK-MB). (3) A total of 76 patients with STEMI and 30 healthy control subjects were enrolled in the study. Mean ± SD azurocidin levels were significantly higher in patients compared with healthy controls (18.07 ± 13.99 versus 10.09 ± 5.29 ng/mL, respectively). In a receiver-operating characteristic curve analysis, an azurocidin cut-off level of >11.46 ng/mL had 74% sensitivity and 58% specificity in predicting myocardial infarction. Azurocidin levels had a positive correlation with TIMI score (r = 0.651). In multivariate linear regression analysis, the TIMI score was an independent predictor of the azurocidin level. (4) Azurocidin is an infection marker that may be important in patients with STEMI.