Chin-Feng Tsai, MD; Der-Jinn Wu, MD, PhD; Ming-Cheng Lin, MD, PhD; Kwo-Chang Ueng, MD, PhD; Chung-Sheng Lin, MD, PhD
Grant Support: In part by the National Science Council (NSC-99-2314-B-040-017), Taiwan, Republic of China.
Potential Conflicts of Interest: None disclosed.
Tsai C, Wu D, Lin M, Ueng K, Lin C. A Brugada-Pattern Electrocardiogram and Thyrotoxic Periodic Paralysis. Ann Intern Med. 2010;153:848-849. doi: 10.7326/0003-4819-153-12-201012210-00015
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Published: Ann Intern Med. 2010;153(12):848-849.
Background: The Brugada syndrome is an inherited arrhythmogenic disease characterized by distinct coved-type ST-segment elevation in the right precordial leads with susceptibility to life-threatening ventricular arrhythmias. Several medications and disease states may induce a Brugada-pattern electrocardiogram (ECG) in some patients, but whether these patients are at risk for ventricular arrhythmias is uncertain (1).
Objective: To describe a patient with thyrotoxic periodic paralysis who had a Brugada-pattern ECG without evidence of genetically determined Brugada syndrome.
Case Report: An otherwise healthy 51-year-old man presented to our emergency department in January 2005 with sudden onset of bilateral leg weakness hours after having a large meal with liquor. On physical examination, we found marked reduction in proximal muscle strength and decreased deep tendon reflexes. Laboratory tests showed a low potassium level of 1.9 mmol/L, a glucose level of 7.9 mmol/L (144 mg/dL), a low thyroid-stimulating hormone level less than 0.004 mIU/L (normal range, 0.35 to 4.94 mIU/L), and an elevated free thyroxine level of 28.4 pmol/L (2.21 ng/dL) (normal range, 19.5 to 23.2 pmol/L [0.7 to 1.8 ng/dL]). The ECG showed J-point and ST-segment elevation of 1 mm in V1 to V2 (Figure, top). The patient's muscle weakness recovered shortly after intravenous administration of 40 mEq of potassium chloride. We prescribed oral methimazole and propranolol to control his hyperthyroidism. In October 2008, he had a recurrent episode of flaccid paralysis after a heavy, late-night meal. Laboratory tests showed a low potassium level of 2.3 mmol/L, an elevated glucose level of 13.7 mmol/L (248 mg/dL), a low thyroid-stimulating hormone level of 0.1944 mIU/L, and a normal free thyroxine level of 16.9 pmol/L (1.31 ng/dL). He was afebrile. His ECG showed a PR interval of 240 ms; QRS width of 120 ms; and high-takeoff, coved ST-segment elevation greater than 2 mm followed by a negative T wave in V1 to V2 (Figure, middle). The ECG pattern normalized on resolution of hypokalemia and hyperglycemia (Figure, bottom). Echocardiography was unremarkable. He had no family or personal history of syncope or aborted sudden death. A subsequent propafenone challenge test with ECG recording at upper intercostal spaces did not elicit a Brugada-pattern ECG. The patient declined genetic analysis for mutations implicated in the Brugada syndrome. He was managed conservatively and was doing well at 6-year follow-up.
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