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Title: Antibiotics May Expose Subclinical Long QT Syndrome (IMAGES excluded from abstract) Authors: Jessen Jacob, MD, MPH and Scott Sakaguchi, MD Background: • Typical feature of Torsades de Pointes is usually an ectopic ventricular beat followed by a compensatory pause that is terminated by a sinus beat with prolonged QT interval and U wave; another ventricular ectopic beat often falls on the exaggerated U wave of the sinus beat which precipitates TdP (short-long RR intervals) • The two important K+ currents involved in ventricular repolarization are the rapid delayed rectifier current (Ikr) and slow delayed rectifier current (Iks). Most drugs block Ikr causing QTc prolongation. Prolonged repolarization allows for early after depolarization and triggered activity • HERG controls the repolarizing current Ikr; mutations in HERG reduce IKr and thus prolong action potentials in individual cells; drugs that prolong the QT interval and cause torsade de pointes also block IKr (KCNH2 gene) • 5 to 10 percent of persons in whom torsade de pointes develops on exposure to QT-interval–prolonging drugs have mutations associated with the long-QT syndrome; they may have a subclinical form of the congenital syndrome. • Family members with near-normal QT intervals may carry the same mutations in genes associated with long-QT–syndrome disease as their relatives. Hospital Course: • A 24 year-old man with no significant past medical history presented with worsening chest discomfort and dyspnea of approximately 4 months duration. The symptoms began ~ 4 months ago with cough, yellow sputum production, intermittent fevers and night sweats. The patient endorsed 2 pillow orthopnea and paroxysmal nocturnal dyspnea. • The patient was empirically started on IV Levofloxacin for concern of a pneumonia. The following morning the patient was found to be unresponsive • CPR initiated (~2 minutes), given 1 shock at 200J, IV Magnesium and IV Amiodarone with ROSC. At ~ 5PM, the pt was once again found to be unresponsive and pulseless at which time CPR was initiated. The patient was in polymorphic VT with 1 shock applied at 150J Imaging: - excluded from abstract (Cardiac MRI and Electrocardiograms) Conclusion: • Fluoroquinolone and macrolide antibiotics prolong the QT interval through concentration-dependent blockade of the rapidly activating delayed rectifier potassium channel (hERG/IKr channel). • Antibiotics are weak IKr blockers, and antibiotic-induced TdP or QTc prolongation in young patients with no high-risk factors (4–6% of the cases) is potentially unmasking a subclinical disease.