Background and aim: Uric acid elevation has been shown to be an important risk factor for cardiovascular and cerebrobascular disease. QT dispersion (QTd) is a parameter that shows the heterogeneity of ventricular repolarization and can be calculated noninvasively from surface electrocardiography. Increased QTd has been associated with severe arrhythmia and risk of sudden death in many patients and disease groups. In this context, we aimed to investigate the effect of uric acid levels on QTd and the effects of decrease in uric acid levels on QTd. Methods: A total of 225 patients with normal renal function were included in the study; 133 of these patients were hyperuricemic (>7 mg/dL), and the remaining 72 patients were normouricemic (Group 1). The hyperuricemic patients were randomly divided into 2 groups, one group (n = 67) was given placebo (Group 2) for 4 months, and the remaining 66 patients were given allopurinol 300 mg/day (Group 3). Results: Hyperuricemic patients had higher hsCRP and QTd and lower eGFR values compared to the normouricemic control group. After 4 months of treatment, 66 patients treated with allopurinol showed a significant decrease in serum uric acid, systolic and diastolic blood pressure, and hsCRP levels, and a significant increase in eGFR. Although the QTd values in the treatment group did not decrease to the same levels as in the normouricemic control group, a statistically significant decrease was found compared to their baseline values. In hyperuricemic control and normouricemic control patients, there were no differences in the levels of uric acid, hsCRP, eGFR, systolic and diastolic blood pressure, and QTd values compared to baseline values. Conclusions: There was a significant association between elevated serum uric acid and QTd, as well as with inflammatory biomarkers. Also, patients who had received hypouricemic therapy during the follow-up period presented a significant decrease in inflammatory markers as well as QTd. This indicates the beneficial effects of decreasing uric acid levels in decreasing the risk for future major adverse events related to ventricular arrhythmias.

Background and aim: The aim of this study was to evaluate the relationship between ECG findings and blood parameters indicative of inflammation and myocardial injury in COVID-19 patients. Methods: The study included 159 females and 194 males. Demographics, ECG findings (axis, rhythm, branch block, ST- and T-wave changes, premature ventricular contractions, early repolarization, S1Q3T3, fragmented QRS [fQRS], rate, PR, QRS, QT interval, QTc, P-wave dispersion) and albumin, D-dimer, ferritin, pro-BNP, procalcitonin, protein, troponin T, neutrophil-to-lymphocyte ratio (NLR), C-reactive protein/albumin ratio (CAR) were recorded. Results: In the study, 45% of the cases were female and 55% were male. The mean age of the included patients was 45.7 ± 24.4 years. The most frequent comorbidities were chronic obstructive pulmonary disease (COPD) and hypertension (HT) in both groups. The incidence of fQRS on the 1st day was significantly higher in patients with negative COVID- 19 test (23% for positive RT-PCR versus 35.6% for negative RT-PCR, p = 0.016). QTc values on the 3rd and 5th day were significantly higher in patients with negative RT-PCR (p = 0.045 and p = 0.042, respectively). Albumin and procalcitonin were significantly higher in patients with positive COVID-19 test results (p = 0.018 and p <0.001, respectively). Patients with fragmented QRS presented significantly lower serum albumin (40.62 ± 4.73 g/L vs. 42.92 ± 3.72 g/L, p = 0.01), and protein levels (p = 0.02), as well as lower lymphocyte count, and significantly higher levels of C-reactive protein (47.01 ± 65.01 mg/L vs. 24.55 ± 44.17 mg/L, p = 0.001), D-dimer (p = 0.009), neutrophil count, pro-BNP (p = 0.004), troponin T (p <0.001), NRL and CAR (1.28 ± 1.83 versus 0.6 ± 1.11, p <0.001). Conclusion: Patients with COVID-19 infection presented significantly higher levels of C-reactive protein, D-dimer, neutrophil, pro-BNP, procalcitonin, troponin T, NLR, and CAR, and significantly lower levels of albumin, lymphocyte count, and serum proteins, indicating the level of inflammation and its relationship with myocardial injury. Further follow-up studies are required, on larger patient sets, for the development of risk prediction tools in COVID-19 patients.

Introduction: Severe back pain caused by a thrombosed and ruptured aortic abdominal aneurysm can imitate a lumbar disc herniation. Case presentation: We present the case of a 72-year-old dia-betic patient with chronic atrial fibrillation, who had been experiencing highintensity low back pain and claudication in the last year prior to his presentation. After experiencing a minor trauma, a lumbar MRI examination was performed, which revealed a retroperitoneal tumoral mass compressing and eroding the L2–L4 vertebral bodies. Computed tomography angiography showed an infrarenal aortic aneurysm (3.374 Å~ 3.765 cm) which appeared to have ruptured and thrombosed. The question arising was when did the rupture occur, how massive was the damage, and how suitable for reconstruction was the aortic wall below the origin of the renal arteries. An open repair was scheduled and performed. The intraoperative finding was ruptured aneurysm of the thrombosed infra-abdominal aorta. The thrombosis extended along the common iliac and external iliac branches. We performed an aortobifemoral bypass using a 16 Å~ 8 mm Dacron graft, clamping the aorta above the origin of the renal arteries. Conclusion: The unintentional diagnosis, due to a minor fall, was overall a fortunate event for this patient. Aortic aneurysms may present with lumbar pain that can be mistakenly interpreted as a spinal issue.