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A6885 - Polymorphic Ventricular Tachycardia in the Setting of Acute Subdural Hematoma and a Normal QT Interval
Author Block: M. Dogra1, M. Abdelghany2, K. Wagle2, H. Dharia3, Z. Bhatti4, R. Carhart2; 1Internal Medicine, SUNY upstate, Syracuse, NY, United States, 2Cardiology, SUNY upstate, syracuse, NY, United States, 3Internal Medicine, SUNY upstate, syracuse, NY, United States, 4Suny upstate, Syracuse, NY, United States.
Introduction Polymorphic ventricular tachycardia (PVT) is a life threatening rhythm that may result from acute cardiac or neurological events. The etiology of ventricular arrhythmias in patients with acute neurological events is not completely understood. Case Description A 76-year-old female with a history of hypertension, diabetes and asthma presented to the hospital complaining of headache, lightheadedness and confusion that started shortly after she had a mechanical fall earlier the same day. Her initial vital signs showed a heart rate of 65/min, blood pressure of 160/90 mmhg, respiratory rate of 16/min. At the emergency department she became unresponsive. ECG showed PVT that was treated successfully with emergent defibrillation followed by amiodarone drip. On recovery ECG showed normal sinus rhythm with normal QT interval. Laboratory workup showed no electrolyte disturbances. Echocardiography showed an ejection fraction of 55-60% with no regional wall motion abnormalities. Cardiac enzymes and troponin were negative. CT scan of the head revealed an acute subdural hematoma with midline shift. Repeat CT head at 6 and 12 hours showed a stable subdural hematoma, so no surgical intervention was warranted. She had no further episodes of ventricular tachycardia. Amiodarone was discontinued and metoprolol was initiated to antagonize the acute sympathetic surge. Given the new onset of PVT in the light of acute subdural hematoma, and complete resolution of arrhythmia following beta-blocker therapy and normal echocardiography, she did not undergo cardiac catheterization. She eventually had a successful recovery and was discharged home. Six months later, she continued to be asymptomatic with no recurrence of arrhythmia. Discussion PVT can be caused by acute ischemia, coronary vasospasm, electrolyte abnormalities, and acquired or congenital long QT syndrome. PVT is very rarely described following acute brain injuries, such as ischemic stroke, intracranial hemorrhage and subarachnoid hemorrhage. Patients with acute brain injuries have a high sympathetic surge which probably causes PVT. Also, intracranial bleeding can cause prolongation of the QT interval that may trigger PVT and torsade de pointes. Observations have reported female sex as an independent risk factor for severe QTc prolongation related to acute brain injuries. Medical therapy includes treatment of the underlying cause and antiarrhythmic drugs. Beta-blockers are of special benefit for short and long term therapy to suppress the high sympathetic tone. Prognosis is generally poor in patients with intracranial hemorrhage complicated with PVT and torsade de pointes. Early identification and appropriate management is crucial to avoid fatal complications.