Faculty Bibliography

Cardiac action potential is affected by extracellular gradients in potassium, calcium, and magnesium with resultant electrocardiographic changes varying from subtle findings to marked repolarization abnormalities. This report presents marked electrocardiographic changes resulting from a combination of electrolytes depletion in a patient with bulimia and anorexia nervosa.

Hyperkalemia is a life threatening metabolic condition. The common risk factors for hyperkalemia include renal insufficiency, use of angiotensin converting enzyme inhibitors, potassium supplementation and excessive consumption of potassium containing diet. A mild to moderate increase in serum potassium causes an increase in myocardial excitability, but further increase leads to impaired myocardial responsiveness, including that to pacing stimulation. Hyperkalemia has been reported to cause failure of atrial capture due to pacemaker exit block. We report a case where hyperkalemia resulted in failure of both the atrial and the ventricular pacemaker capture.

Atrial tachycardias resulting from recipient-to-donor atrio-atrial conduction after orthotopic heart transplantation are difficult to treat. We present two patients in whom atrial tachycardia originating in the recipient heart were successfully treated by radiofrequency ablation guided by electroanatomical CARTO mapping system. These cases illustrate that such atrial tachycardia are curable by radiofrequency ablation. Electroanatomical CARTO mapping is useful in identifying the site of origin of the tachycardia and the atrio-atrial conduction sites.

Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram. Congenital causes of prolonged QT interval occur in individuals with genetic mutations in genes that control expression of potassium and sodium channels and acquired causes are numerous, predominantly drugs causing prolonged QT interval by blockade of potassium channels. Among the drugs, antiarrhythmic agents most notably quinidine, sotalol, dofetilide and ibutilide have the potential to induce the fatal torsade de pointes. Many non-antiarrhythmic drugs can also cause torsade de pointes. Although it is important to distinguish between the congenital and the acquired forms of long QT syndrome as the later can often be reversed by correction of the underlying disorder or discontinuation of the offending drug, both forms are not mutually exclusive. Clinical considerations and management of torsade de pointes are described.

OBJECTIVE: Ibutilide, a class III antiarrhythmic agent used for pharmacological cardioversion of atrial arrhythmias, has a potential to cause QT-interval prolongation and torsade de pointes. Purpose of this study was to determine whether women are more prone to develop ibutilide-induced torsade de pointes. METHODS: All clinical trials, cases, case series, and related articles in English-language in addition to 51 patients from our institution on the subject were examined. RESULTS: In a database derived from 23 reports in literature and from our institution, 1720 patients received ibutilide for cardioversion of atrial arrhythmias. Only in 87% (n=1492) patients, data were reported whether or not ibutilide caused torsade de pointes. The overall incidence of torsade de pointes was 3.9% (n=58) patients. Data on sex distribution of ibutilide-induced torsade de pointes was available in 73% (n=1096) patients. Torsade de pointes developed in 17 (5.6%) of 304 women and 24 (3%) of 792 men (P=0.05). It occurred during or within 45 min after completion of the infusion of ibutilide. Treatment instituted was with intravenous magnesium sulfate alone in 14% (n=8) patients, magnesium sulfate plus lidocaine in 5% (n=3) patients, magnesium sulfate with electrical cardioversion in 17% (n=10) patients, electrical cardioversion alone in 19% (n=11) patients, and precordial thump in 3% (n=2) patients. In 41% (n=24) of patients who developed torsade de pointes, it resolved without treatment. There were no reported deaths secondary to torsade de pointes associated with ibutilide infusion. CONCLUSION: Incidence of ibutilide-induced torsade de pointes is higher in women than in men. Greater caution must be observed while using ibutilide in women.

Ibutilide is a class III antiarrhythmic drug used for pharmacological cardioversion of recent-onset atrial fibrillation and flutter. The objective of the study was to assess the efficacy of ibutilide in elderly patients (age, >or=65 years). The study population consisted of 32 consecutive elderly patients (17 women, 15 men; mean age, 76 +/- 8 years; age range, 65-94 years) with recent-onset atrial fibrillation (19 patients) or flutter (13 patients). Ibutilide was administered 1-mg intravenously over 10 minutes, and a second 10-minute infusion of 1-mg was given if the arrhythmia did not terminate within 10 minutes after the end of initial infusion. Twenty-six patients received two 1-mg doses of ibutilide. The rate of successful arrhythmia termination was 59% (19 patients): 63% in patients with atrial fibrillation (12 of 19) and 54% in atrial flutter (7 of 12). The mean conversion time was 33 +/- 45 minutes. Three-fourths of the conversions occurred within 45 minutes of treatment. No clinical variables were correlated with success of cardioversion. Patients with a left atrial size of 50 mm or larger had a conversion rate of 50% compared with a conversion rate of 61% in patients with a left atrial size of less than 50 mm (P = NS). Ibutilide-induced lengthening in the QTc interval was of 17 +/- 21 milliseconds. Cardiac complications were torsade de pointes (1 patient), nonsustained ventricular tachycardia (1 patient), and transient bradycardia (1 patient). Torsade de pointes was terminated with direct current cardioversion. Ibutilide appears to be an effective drug for conversion of recent-onset atrial fibrillation and flutter in elderly patients under monitored conditions. Complications are rare and transient.

OBJECTIVE: The purpose of this study was to report a novel electrocardiographic (ECG) phenomenon in acute pulmonary embolism characterized by QT interval prolongation with global T-wave inversion. METHODS: Among a total of 140 study patients with a confirmed diagnosis of acute pulmonary embolism, patients who fulfilled the inclusion criteria for QT interval prolongation with global T-wave inversion were examined. Each of these patients had undergone a detailed clinical evaluation including testing for myocardial injury and echocardiography. RESULTS: QT interval prolongation with global T-wave inversion was found in five patients (age 51-68 years) with acute pulmonary embolism. Four were women. Acute pulmonary embolism was diagnosed by ventilation-perfusion scan in three patients and by spiral computed tomography in other two patients. None of the patients had any right or left ventricular regional wall motion abnormalities on echocardiography. All patients had changes characteristic of hemodynamically significant pulmonary embolism, including right ventricular stunning or hypokinesis and dilatation in five patients with paradoxical septal motion in four. Acute coronary syndrome was ruled out in each patient by clinical evaluation, serial ECGs and cardiac markers, and lack of regional wall motion abnormalities on echocardiography. Prolongation of QT intervals (QTc 456-521 ms) with global T-wave inversion was noted on presentation. The ECG changes gradually resolved in 1 week in all patients with appropriate treatment of acute pulmonary embolism. One patient died. None of the patients developed torsade de pointes. CONCLUSIONS: Acute pulmonary embolism may occasionally result in reversible QT interval prolongation with deep T-wave inversion, and, thus should be considered among the acquired causes of the long QT syndrome.

OBJECTIVE: To evaluate the racial differences in the efficacy and safety of ibutilide in patients with recent-onset (<2 weeks) atrial fibrillation and atrial flutter. METHODS: This study included 58 consecutive patients with recent-onset atrial fibrillation (n = 34) and atrial flutter (n = 24). The mean age was 65.7 +/- 14.6 years (range, 37-86 years), 47% were women (n = 27) and 34% (n = 20) were African Americans. The duration of arrhythmia ranged from 3 hours to 2 weeks. All patients had echocardiography, were on therapeutic anticoagulation, had a fairly well controlled ventricular rate, normal QTc interval on 12-lead electrocardiography, and normal serum electrolytes. Ibutilide was administered as an intravenous infusion with a maximal dose of 2 mg. RESULTS: The overall conversion rate to sinus rhythm was 66% (n = 38), with 62% (n = 21) with atrial fibrillation and 71% (n = 17) of atrial flutter. Most conversions (84%) occurred within 45 minutes of ibutilide infusion. The mean time to arrhythmia conversion was 37.4 +/- 59.8 minutes. Race had a significant impact on efficacy, with increased conversions seen in African Americans (P = 0.004) and increased nonconversion seen in whites (P = 0.02). Successful conversion was not affected by the left atrial size or the presence of valvular heart disease, hypertension, heart failure, coronary heart disease, and diabetes mellitus. QTc intervals were prolonged after drug administration, with a mean change of 24.6 milliseconds for all patients. The QTc prolongation after drug administration was greater in African Americans than in whites (27.4 vs. 23.3 milliseconds). Torsade de pointes occurred in 4 patients (3 African Americans) and was treated with intravenous magnesium sulfate and electrical cardioversion. CONCLUSION: Ibutilide used for pharmacological cardioversion of atrial fibrillation and atrial flutter is more effective in African Americans but carries a higher risk of torsade de pointes.