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This is a case of a young, 20-year-old, male Navy recruit who was admitted to our healthcare facility with intermittent atypical chest pain and limiting exertional symptoms and was diagnosed with myocardial bridging (MB) as the most likely etiology of his chest after the complete cardiac workup, leading to his career limitations due to potential risks. Our patient presented with atypical chest pain and limiting exertional symptoms. Chest pain was non-radiating.

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Background And Objective: It has been believed that polymorphic ventricular tachycardia (VT) such as torsades de pointes (TdP) seen in patients with long QT syndromes is triggered by creating early afterdepolarization (EAD)-mediated triggered activity (TA). Although the mechanisms creating the TA have been studied intensively, characteristics of the arrhythmogenic (torsadogenic) substrates that link EAD developments to TA formation are still not well understood.

Methods: Computer simulations of excitation propagation in a homogenous two-dimensional ventricular tissue with an anisotropic conduction property were performed to characterize torsadogenic substrates that potentially form TA.

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Premature ventricular contraction (PVC) is characterized by early repolarization of the myocardium originating from Purkinje fibers. PVC may occur in individuals who are otherwise healthy. However, it may be associated with some pathological conditions.

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The impact of obesity on heart rate variability (HRV) and ventricular repolarization, both vital indicators of cardiovascular health, is the focus of this review. Obesity, measured by BMI, waist circumference, and waist-to-hip ratio, significantly increases cardiovascular disease (CVD) risk due to structural and autonomic heart changes. Findings show that obese individuals exhibit prolonged QT and Tpeak-to-Tend (Tpe) intervals, suggesting delayed ventricular recovery and greater arrhythmia risk.

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Kounis Syndrome Following Moxifloxacin and Deflazacort Administration.

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