Electrocardiographic changes in thyrotoxic periodic paralysis.

T periodic paralysis (TPP) is characterized by a combination of muscle weakness, hypokalemia, and thyrotoxicosis, and occurs predominantly in men. In the United States, it is an uncommon complication of hyperthyroidism.1 Only small series of patients have been reported. The thyrotoxic symptoms are often subtle, and despite its distinctive clinical presentation, they are often unrecognized by physicians when the patient is first evaluated.2 TPP episodes are usually benign and resolve in a short period of time. Occasionally, respiratory failure and lifethreatening arrhythmias have been reported.3–5 Studies of electrocardiographic (ECG) manifestations of TTP are scarce. The objective of our report is to analyze ECG manifestations of 6 patients with TPP and to distinguish these characteristics that could help identify this entity when a patient with flaccid paralysis is evaluated. • • • We compared ECG tracings of 6 patients with TPP seen by the endocrinology services of the University of Texas-Houston Medical School and Baylor College of Medicine. All patients had an electrocardiogram recorded simultaneously with serum electrolyte levels during and after the episode. An experienced cardiologist evaluated all electrocardiograms. The QT interval was measured in the frontal plane by averaging 3 consecutive beats in the lead where the T wave was best defined and where the terminal complex crossed the isoelectric line, according to the method of Lepeschikin.6 Intervals after premature beats were not considered and care was taken not to include U waves if present. The QTc was calculated using Bazett’s formula.7 The 6 male patients (mean age 26 4 years) with TPP were admitted to the hospital after the initial evaluation in the emergency room. Results are listed in Table 1. Race was diverse and included 1 black person, which is rare. The mean potassium value at the time of admission was 1.8 0.24 mEq/L. Patient 4 had preexistent cardiovascular disease, with a left ventricular ejection fraction of 20% and persistent atrial fibrillation before and after correction of the hypokalemia. The only subject taking medications was patient 3, who was taking 10 mg of methimazole 3 times/day 3 weeks before the attack. Patient 6 had an ectopic atrial tachycardia before undergoing an episode of ventricular fibrillation that required electrical cardioversion. Patient 1 had the longest PR interval (320 ms) and remained with a first-degree atrioventricular block when normokalemic. Four patients had U waves during the TPP attack; patients 3 and 4 did not have U waves despite having some of the lowest levels of potassium. • • • Hyperthyroidism produces sinus tachycardia in almost 100% of patients, and 10% to 15% will have atrial arrhythmias.8 Conduction of the atrioventricular node is accelerated, resulting in a shortened PR interval9,10 and ST-segment changes are uncommon and should suggest ischemia.8 The QTc is prolonged.11 On the other hand, hypokalemia slows intraventricular conduction, producing characteristic ECG changes, such as ST-segment depression, decreased T-wave amplitude, prominent U waves, prolonged QRS duration, P-wave changes, cardiac arrhythmias, and atrioventricular block.12 Hypokalemic ECG changes appear to predominate in TPP, with the addition of tachycardia, which is uncommon in patients with pure hypokalemia (Figures 1 and 2). Ee and Cheah13 in 1979 described ECG changes characteristic of TPP; these characteristics were consistently seen when serum potassium levels were 2.8 mEq/L and included a U-wave amplitude 1 mm, a U wave amplitude greater than the T wave in the same lead, and ST depression 0.5 mm. The presence of tachycardia did not mask the typical findings of hypokalemia but decreased U-wave amplitude.13 In our study U, T, and P waves were frequently merged, making measurements difficult. QTc was prolonged in all patients and closely followed the degree of hypokalemia, most likely due to the presence of U waves.12 We did not observe ST depression as a common feature. Premature ventricular or atrial contractions were not observed in concordance with Ee and Cheah’s study.13 Our patients’ PR intervals were consistently prolonged, more so than in previous reports in which they were seen with a frequency of 0% to 27%.13,14 Two patients had less typical ECG changes: patient 4 had a dilated cardiomyopathy and patient 3 had been receiving antithyroid treatment. Life-threatening intraventricular conduction abnormalities have been previously reported with TPP including 2 cases of sinus arrest,13 4 cases of Wenckebach atrioventricular blockage,13,15 and 3 cases of right bundle branch block.14 Three of our patients had intraventricular From the Division of Endocrinology, The University of Texas Houston Medical School, Houston; Division of Endocrinology, Baylor College of Medicine/Endocrine Neoplasia and Hormonal Disorders, The University of Texas M.D. Anderson Cancer Center, Houston; and Division of Cardiology, The University of Texas Houston Medical School, Houston, Texas. Dr. Boccalandro’s address is: The University of Texas Houston, MSB Suite 1.246, Houston, Texas 77030. E-mail: fernando.boccalandro@uth.tmc.edu. Manuscript received July 22, 2002; revised manuscript received and accepted November 8, 2002.