Bradycardia-Associated Torsade de Pointes and the Long-QT Syndromes: A Case Report and Review of the Literature

Military Medicine, May 2005 by Ashworth, Simeon W, Levsky, Marc E, Marley, Chad T, Kang, Christopher S

We report a case of bradycardia-associated torsade de pointes in which the underlying long-QT syndrome appeared to be attributable to primary cardiac conducting system disease. Our patient presented complaining of presyncope and syncope. Serial electrocardiograms obtained over a period of 10 years demonstrated slowly progressive conduction system abnormalities, and evaluation revealed no other cause. The patient's dysrhythmia was refractory to magnesium but abated with cardiac pacing at a moderate rate. A review of the relevant literature on congenital and acquired long-QT syndrome is included.

Case Report

The patient was the 74-year-old wife of a retired noncommissioned officer, who presented to the emergency department of a military treatment facility by privately owned vehicle, complaining of two episodes of dizziness and one episode of syncope. The patient's episodes of dizziness both occurred during periods of minimal exertion, while the patient was walking in her home. The first episode of dizziness occurred the day before presentation and the second occurred earlier on the day of presentation. The patient described the episodes as "lightheadedness" and a presyncopal sensation, which resolved within a few seconds of sitting down. The episode of syncope occurred the evening before presentation, while the patient was exercising on a cross-country ski simulator in her home. The episode was witnessed by her husband, who stated that it caused her to fall off the machine. It was preceded by a very brief presyncopal sensation, similar to the other two episodes she described. According to her husband, her unconsciousness lasted "a few minutes." Because the episode was brief and she recovered her baseline function quickly, appeared uninjured, and felt well thereafter, the patient did not seek medical attention at that time. Her husband stated that the patient had no convulsive activity, tongue biting, or incontinence with the syncopal episode. The patient denied chest pain, shortness of breath, or palpitations with any of the episodes. She had a history of hypertension and cigarette smoking but denied any history of heart disease, diabetes mellitus, stroke, or other major medical problems. She had no known drug allergies, and her only medications were aspirin, ramipril, and estrogen/progesterone hormone replacement. She stated that she exercised for 30 to 60 minutes several times per week with her home equipment and had never experienced symptoms with exercise before the day of presentation. During the initial evaluation, the patient said that she felt completely well and she denied symptoms of any kind.

The patient's initial vital signs were blood pressure of 166/77 mm Hg, pulse of 51 beats per minute (regular), respiratory rate of 20 breaths per minute, and temperature of 97.6°F. Room air oxygen saturation was 100%. On physical examination, the patient was alert and completely oriented. No jugular venous distension was noted. Auscultation of the lungs was remarkable for minimal bibasilar crackles. Cardiac auscultation revealed bradycardia with a rate in the low 50s and regular rhythm; no murmurs or gallops were noted. The abdomen was soft and nontender, without a palpable mass or organomegaly. The extremities were with normal peripheral pulses throughout, with no cyanosis or edema. The neurological examination indicated no deficits.

The initial electrocardiogram (ECG) (Fig. 1) showed a sinus rhythm with a ventricular rate of 44 beats per minute, first-degree atrioventricular block, right bundle branch block, and corrected QT interval (QTc) of 596 milliseconds. Compared with an ECG dated approximately 1 year previously, the morphological features and rate were essentially the same, although the QTc on the old tracing was 470 milliseconds. An ECG from ~4.5 years previously (Fig. 2) demonstrated a sinus rhythm with a rate of 53 beats per minute, PR interval of 204 milliseconds, nonspecific intraventricular conduction delay, prominent U waves, and QTc of 417 milliseconds. An ECG from 10 years previously (Fig. 3) showed the same nonspecific intraventricular conduction delay morphological features and U waves but was otherwise normal. Initial laboratory values are given in Table I. The initial chest X-ray was remarkable for slightly increased bibasilar interstitial markings but no cardiomegaly or other abnormalities.

While in the emergency department, the patient was noted to have several runs of nonsustained ventricular tachycardia, which reproduced the patient's lightheadedness and presyncopal sensation but did not cause chest pain or palpitations. At first, the runs lasted for 4 or 5 beats and appeared monomorphic. The runs occurred once every 1 to 2 minutes. The patient had a palpable radial pulse during these intervals and was completely awake and conversant during the episodes, although she complained of dizziness. The patient was given 100 mg of lidocaine intravenously, and a lidocaine drip was started; the runs of ventricular tachycardia continued. The patient then had a long run of ventricular tachycardia, the rhythm strip for which is shown in Figure 4. During this episode, the undulating QRS amplitude classic for torsade de pointes (TdP) was identified. Lidocaine treatment was discontinued, and the patient was given magnesium sulfate (2 g) intravenously. Despite this, the runs of ventricular tachycardia persisted.