BACKGROUND: Angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism may play a role in the pathogenesis of coronavirus-19 disease (COVID-19). OBJECTIVES: Investigate the relationship between ACE I/D polymorphism and the clinical severity of COVID-19. DESIGN: Prospective cohort study. SETTING: Tertiary care hospital. PATIENTS AND METHODS: The study included COVID-19 patients with asymptomatic, mild, and severe disease with clinical data and whole blood samples collected from 1 April 2020 to 1 July 2020. ACE I/D genotypes were determined by polymerase chain reaction and agarose gel electrophoresis. MAIN OUTCOME MEASURE: ACE DD, DI and II genotypes frequencies. SAMPLE SIZE: 90 cases, 30 in each disease severity group. RESULTS: Age and the frequency of general comorbidity increased significantly from the asymptomatic disease group to the severe disease group. Advanced age, diabetes mellitus and presence of ischemic heart disease were independent risk factors for severe COVID-19 [OR and 95 % CI: 1.052 (1.021-1.083), 5.204 (1.006-26.892) and 5.922 (1.109-31.633), respectively]. The ACE II genotype was the dominant genotype (50%) in asymptomatic patients, while the DD genotype was the dominant genotype (63.3 %) in severe disease. The ACE II geno-type was protective against severe COVID-19 [OR and 95% CI: .323 (.112-.929)]. All nine patients (8.9%) who died had severe disease. CONCLUSIONS: The clinical severity of COVID-19 infection may be associated with the ACE I/D polymorphism. LIMITATIONS: Small sample size and single center. CONFLICT OF INTEREST: None.
Introduction Coronavirus disease 2019 (COVID-19) is a newly recognized infectious disease that has spread rapidly. COVID-19 has been associated with a number of cardiovascular complications, including arrhythmias. The mechanism of ventricular arrhythmias in patients with COVID-19 is uncertain. The aim of the present study was to evaluate the ventricular repolarization by using the Tp-e interval, QT dispersion, Tp-e/QT ratio, and Tp-e/QTc ratio as candidate markers of ventricular arrhythmias in patients with newly diagnosed COVID-19. In addition, the relationship between the repolarization parameters and the CRP (C-reactive protein) was investigated. Methods 75 newly diagnosed COVID-19 patients, 75 age and sex matched healthy subjects were included in the study between 20th March 2020 and 10th April 2020. The risk of ventricular arrhythmias was evaluated by calculating the electrocardiographic Tp-e and QT interval, Tp-e dispersion, corrected QT(QTc), QT dispersion (QTd), corrected QTd, Tp-e/QT and Tp-e/QTc ratios. CRP values were also measured in patients with newly diagnosed COVID-19. Results Tp-e interval (80.7 ± 4.6 vs. 70.9 ± 4.8; p < .001), Tp-e / QT ratio (0.21 ± 0.01 vs. 0.19 ± 0.01; p < .001) and Tp-e/QTc ratio (0.19 ± 0.01 vs.0.17 ± 0.01; p < .001) were significantly higher in patients with newly diagnosed COVID-19 than the control group. There was a significant positive correlation between Tp-e interval, Tp-e/QTc ratio and CRP in patients with newly diagnosed COVID-19 (rs = 0.332, p = .005, rs = 0.397, p < .001 consecutively). During their treatment with hydroxychloroquine (HCQ), azithromycin and favipiravir, ventricular tachycardia episodes were observed in in two COVID-19 patients during their hospitalization in the intensive care unit. Conclusion Our study showed for the first time in literature that the Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio, which are evaluated electrocardiographically in patients with newly diagnosed COVID-19, were prolonged compared with normal healthy individuals. A positive correlation was determined between repolarization parameters and CRP. We believe that pre-treatment evaluation of repolarization parameters in newly diagnosed COVID-19 would be beneficial for predicting ventricular arrhythmia risk.
Aim The aim of the current study was to evaluate P-wave dispersion (PWD) as a predictor of atrial fibrillation in patients with newly diagnosed COVID-19. In addition, the relationship between the PWD and inflammation parameters was investigated. Methods A total of 140 newly diagnosed COVID-19 patients and 140 age- and sex-matched healthy individuals were included in the study. The risk of atrial fibrillation was evaluated by calculating the electrocardiographic PWD. C-reactive protein (CRP), white blood cell, neutrophil and neutrophil-to-lymphocyte ratio (NLR) were measured in patients with newly diagnosed COVID-19. Results PWD, white blood cell, NLR and CRP levels were significantly higher in the COVID-19 group than the control group. There was a significant positive correlation between PWD and CRP level (rs = 0.510, P < 0.001) and NLR in COVID-19 group (rs = 0.302, P = 0.001). In their follow-up, 13 (9.3%) patients, 11 of whom were in the ICU, developed new atrial fibrillation. Conclusion Our study showed for the first time in literature that the PWD, evaluated electrocardiographically in patients with newly diagnosed COVID-19, was prolonged compared with normal healthy individuals. A positive correlation was found between PWD, CRP level and NLR. We believe that pretreatment evaluation of PWD in patients with newly diagnosed COVID-19 would be beneficial for predicting atrial fibrillation risk.
Objective The aim of the present study is to evaluate the frequency, etiology, risk factors and clinical outcomes in acute traumatic SCI patients who develop fever and to evaluate the relationship between fever and mortality. Design Retrospective data were collected between January 2007 and August 2016 from patients diagnosed with persistent fever from SCI cases observed in the ICU. Participants Among 5370 intensive care patients, 435 SCI patients were evaluated for the presence of fever. A total of 52 patients meeting the criteria were evaluated. Outcome measures Fever characteristics were evaluated by dividing the patients into two groups: infectious (group-1) and non-infectious (group-2) fever. Demographic and clinical data, ICU and hospital stay, and mortality were evaluated. Results In the patients with noninfectious fever, mortality was significantly higher compared to the group with infectious fever (P < 0.001). Of 52 acute SCI cases, 25 (48.1%) had neurogenic fever that did not respond to treatment in intensive care follow-up, and 22 (88%) of these patients died. Maximal fever was 39.10 ± 0.64 °C in Group-1 and 40.22 ± 1.10 ° C in Group-2 (P = 0.001). There was a significant difference in the duration of ICU stay and hospital stay between the two groups (P = 0.005, P = 0.001, respectively), while there was no difference in the duration of mechanical ventilation between the groups (P = 0.544). Conclusion This study demonstrates that patients diagnosed with neurogenic fever following SCI had higher average body temperature and higher rates of mortality compared to patients diagnosed with infectious fever.
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