Background: For cardiologists, management of acute chest pain continues to be a challenge. Physicians struggle to avoid unnecessary admissions and at the same time not to miss highrisk patients needing urgent intervention. Therefore, diagnostic strategies focus on identifying patients in whom an acute coronary syndrome can be safely ruled out based on findings from history, physical examination, and early cardiac marker measurement. The HEART score, a clinical prediction rule, was developed to provide the clinician with a simple and reliable predictor of cardiac risk. Aim: This study aimed to investigate the role of neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) as independent laboratory biomarkers when associated with the HEART risk score. Method: A cross-sectional study of 120 patients who attended the emergency department with acute chest pain. NLR and PLR were both measured. In addition, the HEART score was the valid instrument used in evaluating and risk stratifying patients into low-, intermediate-, and high-risk group. Results: There was a positive correlation between the HEART score and the mean PLR and NLR (p = 0.000*). PLR and NLR were found to be significantly higher in the high-risk HEART score group (p = 0.05 and 0.0001*, respectively). A PLR of 115.5 and above had a sensitivity of 73% and specificity of 78%, while an NLR of 3.95 and above had a sensitivity of 75% and specificity of 86% to detect high-risk HEART score patients. Conclusion: PLR and NLR proved to be a useful tool to identify highrisk patients when validated against the HEART score.

Background The dramatic increase in the use of cardiovascular implantable electronic devices (CIED) was associated with an increased rate of CIED infection, which has a high management cost. Aim of the Study To test the safety and efficacy of a single‐session protocol, aiming to reuse the infected pocket side and the same device and leads in patients with CIED pocket infection. Patients and Methods We included patients with isolated pocket infection between January 2015 and November 2019. The Patient was prepared by taking a swab for culture and sensitivity before the procedure. The pocket was debrided and the capsule was removed, the pocket was rinsed with povidone‐iodine and hydrogen peroxide mixture, then packed with gauze sponge soaked with povidone‐iodine. The device was debrided using ultrasonic irrigation and sterilized using gas plasma. The device was reimplanted and the wound was closed in layers. Results During the period of the study, we had 12 patients with isolated pocket infection. Nine presented with erosion, two with impending erosion, and one with a chronic sinus. Patient's age was 61.5 ± 7.64 years. The infection was diagnosed 14.2 ± 8.22 weeks post device implantation. They were admitted for 7.6 ± 1.54 days postprocedure. The follow‐up duration was 26.5 ± 15 (1.7–52) months. Only one patient (8%) had a recurrence of the infection after 50 days of the procedure. Conclusion Our protocol was successful in treating 92% of device‐related pocket infection without the need to replace the device or the pocket side.

Background: Most diabetic patients have silent ischemia and cardiac dysfunction that is usually observed in the late phase of the disease when it becomes clinically obvious. We hypothesized that left ventricular dyssynchrony (LVdys) (or dispersion) is an early marker of myocardial involvement in asymptomatic early type 2 diabetes mellitus (T2DM) patients. Therefore, we aimed to detect early markers of myocardial dysfunction in early T2DM using LVdys and left ventricular mechanical reserve (LVMR). Methods: We examined 91 consecutive subjects with early T2DM with speckle tracking imaging to evaluate LVdys and with dobutamine stress to evaluate LVMR (defined as left ventricular mechanical reserve global longitudinal strain [LVMR GLS ] ≥2%). Our patients were divided into two groups according to LVdys: group 1 with LVdys (n = 49), and group 2 without LVdys (n = 42). Results: We found that 49 (54%) subjects in our cohort had resting LVdys (standard deviation of tissue synchronization of the 12 left ventricular segments [Ts-SD-12] ≥34.2 ms). GLS and strain rate were comparable at rest between patients with and without LVdys. On the other hand, LVMR was blunted in those with LVdys (p < 0.001). We found that HbA1c, high-sensitivity C-reactive protein, and left atrial volume index were inversely correlated with LVMR. Multivariate analysis showed that LVdys was the strongest predictor (p < 0.001) of blunted LVMR. Using receiver operating characteristic curve analysis, we found that a Ts-SD-12 ≥36.5 ms was the best cutoff value to predict blunted LVMR (area under the curve = 0.89, p < 0.001). Conclusion: The LVdys (Ts-SD-12) cutoff ≥36.5 ms was the optimal value for prediction of impaired LVMR and might be an early marker of subclinical cardiac dysfunction and risk stratification of subjects with asymptomatic early T2DM with preserved left ventricular ejection fraction.

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