James R. Foster

Atrial excitability and conduction in patients with interatrial conduction defects

Prolongation of P-wave duration is an accepted indicator of an interatrial conduction disturbance and may predispose patients to atrial arrhythmias. This study was performed to monitor electrophysiologic characteristics of the atria in patients with a prolonged P-wave duration. Atrial excitability and conduction times were compared in 7 patients with a P-wave duration of less than 115 ms (Group I), and 13 patients with a duration of greater than of equal to 115 ms (Group II). In contrast of the Group I patients, most of the 13 patients in Group II had atrial arrhythmias, including sinus nodal dysfunction (3 patients) and a history of atrial fibrillation or ectopic atrial tachycardia (6 patients). Electrophysiologic differences between the 2 groups included a higher late diastolic threshold in Group II (0.8 +/- 0.2 mA versus 1.3 +/- 0.2 mA; p less than 0.005), and a greater increase in intraatrial conduction time (5 +/- 10 ms versus 30 +/- 20 ms; p less than 0.005) and interatrial conduction time (5 +/- 15 ms versus 30 +/- 15 ms; p less than 0.05) of early premature responses. There were no differences between the 2 groups in refractory periods, shape of the strength interval curve, or conduction times of premature responses occurring late in diastole. These abnormalities in conduction time and excitability found in patients with a prolonged P-wave duration may predispose to the initiation of certain atrial tachyarrhythmias.

Exercise-induced distal atrioventricular block

Three patients with 1:1 atrioventricular (AV) conduction at rest developed fixed 2:1 or 3:1 AV block during treadmill exercise testing. Electrophysiologic study documented block distal to the AV node in all three patients, and suggested that the exercise-induced block occurred because of increased atrial rate and abnormal refractoriness of the His-Purkinje conduction system. The findings in these three patients suggest that high grade AV block appearing during exercise reflects conduction disease of the His-Purkinje system rather than of the AV node, even in the absence of bundle branch block. Patients with this diagnosis should be considered for permanent cardiac pacing.

Thresholds, refractory periods, and conduction times of the normal and diseased human atrium

In order to better understand the electrophysiology of the diseased human atrium, we measured high right atrial refractory periods, threshold, and conduction times of 61 patients undergoing routine electrophysiologic study. Refractory periods and conduction times of patients with apparently normal atria were compared to those of patients with a history of persistent sinus bradycardia, atrial fibrillation, or other forms of primary atrial tachyarrhythmia. Refractory periods and thresholds were derived from strength-interval curves. Conduction times were measured for all premature beats induced. Threshold, refractory periods, and conduction times of premature beats induced late in the cardiac cycle did not distinguish patients with normal atria from patients with bradycardia or tachycardia. In contrast, increases in conduction time of early cycle premature beats separated patients with these abnormalities from patients with normal atria. The increases in interatrial and intraatrial conduction time of early cycle premature beats were the strongest correlates of primary atrial tachyarrhythmia (r = 0.52, p = 0.0065 and r = 0.274, p = 0.041, respectively) and induction of repetitive atrial firing (r = 0.65, p = 0.002, and r = 0.59, p = 0.0001, respectively). This increase in conduction time of early cycle premature beats may predispose these patients to primary atrial tachyarrhythmias.

Reproducibility and treatment of exercise-induced ventricular tachycardia☆

Fourteen patients with exercise-induced ventricular tachycardia (VT) underwent serial treadmill testing, and those with reproducible arrhythmia were treated with a beta-adrenergic blocking agent. In 11 patients (79%), VT of similar rate, morphologic characteristics and duration was reproduced on 2 consecutive treadmill tests performed 1 to 14 days apart. Beta blockade prevented recurrent VT during acute testing in 10 of 11 patients and during chronic therapy in 9. Eight patients had a consistent relation between a critical sinus rate and the onset of VT. In these patients, successful therapy correlated with preventing achievement of the critical sinus rate during maximal exercise. Thus, serial exercise testing is an appropriate means of assessing efficacy of therapy in patients with exercise-induced VT, provided that reproducibility is established on 2 control tests before beginning treatment. Therapy with beta-blocking agents is effective, especially when guided by the presence of a critical sinus rate-VT relation.

Interventricular septal motion during preexcitation and normal conduction in Wolff-Parkinson-White syndrome: Echocardiographic and electrophysiologic correlation☆

Interventricular septal motion was studied by echocardiogram in 20 consecutive patients with documented Wolff-Parkinson-White (WPW) syndrome before and during electrophysiologic evaluation using His bundle recordings and pacing techniques. Characteristic abnormal interventricular septal motion was seen in 8 of 11 patients with type B WPW syndrome (groups I and II). All eight patients had electrocardiographic patterns consistent with an anomalous pathway located in the anterior right ventricular wall (group I). In five of these eight patients normalization of the QRS complex for one or more beats was accomplished and produced normalization of the septal motion in four; whereas in the fifth patient, who had an underlying atrial septal defect, the abnormal septal motion remained abnormal. All nine patients with type A WPW syndrome (groups III to V) had normal septal motion both during total preexcitation and during normalization of the QRS complex. The normalization of the abnormal interventricular septal motion with normalization of the QRS complex in type B WPW syndrome strongly suggests that the abnormal motion is related to an abnormal sequence of ventricular depolarization during preexcitation. Furthermore, persistent abnormal septal motion after normalization of the QRS complex suggests that other factors such as right ventricular volume overload may be responsible. Likewise, when abnormal septal motion occurs in the presence of type A WPW syndrome, an explanation other than preexcitation must be sought.

Efficacy of verapamil in exercise-induced ventricular tachycardia☆

The antiarrhythmic efficacy of verapamil was determined by serial treadmill testing in 16 patients with reproducible exercise-induced ventricular tachycardia (VT). Twelve of the 16 patients responded to verapamil, 0.2 mg/kg intravenously; in 8 of these 12 responders, an oral verapamil regimen of 160 to 320 mg given every 8 hours also prevented exercise-induced VT. Plasma verapamil concentration was significantly higher in the responders than in the nonresponders to intravenous verapamil, but levels were similar in responders and nonresponders to oral therapy. The 8 responders to the oral drug were followed up while receiving verapamil therapy for 6 to 22 months (mean 15), and exercise-induced VT did not recur in any patient. Five of the 8 responders also had concomitant spontaneous VT unrelated to exercise which verapamil suppressed initially as well: 4 remained free of spontaneous VT, while 1 patient had recurrence of spontaneous VT. Thus, in patients with exercise-induced VT, verapamil is a promising alternative therapy to beta-adrenergic blocking agents. The effectiveness of verapamil is consistent with a mechanism of arrhythmogenesis involving calcium channels.

Intravenous Amiodarone during Prolonged Resuscitation from Cardiac Arrest

Excerpt Because only 13% of patients with in-hospital cardiac arrest survive to discharge from the hospital (1, 2), with none surviving when resuscitation exceeds 30 minutes (1), there is an urgent...

Stratification of sudden death risk in patients receiving long-term amiodarone treatment for sustained ventricular tachycardia or ventricular fibrillation

One hundred twenty-two patients treated chronically with amiodarone for sustained ventricular tachycardia or ventricular fibrillation after failing conventional antiarrhythmic therapy were analyzed to determine which factors were predictive of sudden cardiac death during follow-up. The mean left ventricular ejection fraction in the study group was 0.32, and 87% of the patients had coronary artery disease with a prior myocardial infarction. During a median follow-up of 19.5 months, 30 patients died suddenly. The only variable that was predictive of sudden death was left ventricular ejection fraction. Twenty-nine of the 84 patients with ejection fractions < 0.40 died suddenly, compared with 1 of 35 patients with ejection fractions > or = 0.40. The actuarial probability of sudden death at 5 years was 49% when the ejection fraction was < 0.40, and 5% when the ejection fraction was > or = 0.40 (p = 0.0004). These results indicate that patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation whose ejection fractions are > or = 0.40 are at low risk for sudden death. Patients with ejection fractions < 0.40 remain at high risk for sudden death, and should be considered for additional or alternative therapy.

Myxedema coma during long-term amiodarone therapy

Amiodarone is a potent new antiarrhythmic drug that has multiple effects on thyroid function, including inhibition of extrathyroidal triiodothyronine production and rarely, iodine-induced hypothyroidism. This report describes a man with recurrent ventricular tachycardia in whom hypothyroidism developed during amiodarone therapy and who died of probable myxedema coma. Parenteral and oral thyroxine therapy promptly reduced serum thyroid-stimulating hormone concentrations without increasing the patients very low serum triiodothyronine concentration. This response to thyroxine suggests that thyroxine itself may have biologic activity and participate directly in regulation of thyrotropin secretion. Because amiodarone-induced hypothyroidism may be life-threatening, thyroid function should be monitored before and during amiodarone therapy, and the drug discontinued or appropriate therapy instituted if hypothyroidism develops.

The Electrophysiological Substrate of Atrial Fibrillation

The electrophysiological substrate that predisposes the human atrium to sustain alrial fibrillation is incompletely understood. However, abnormalities of atrial size, refractory period and conduction are important precursors to this arrhythmia. The propensity of various disease states, cardio active drugs and the autonomic nervous system to potentiate atrial fibrillation may be explained by changes in these electrophysiological properties.