Alan Woelfel

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.

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.

Unexpected ventricular tachyarrhythmias soon after cardiac surgery

Abstract Cardiac arrest due to ventricular tachyarrhythmia occurring after cardiac surgery is a rare but catastrophic event. When arrhythmia is clearly precipitated by perioperative myocardial infarction, hemodynamic instability or electrolyte derangement, the therapeutic approach is dictated by these circumstances. However, often an etiology is not readily apparent, and little has been published to guide the management of such patients. 1,2 This report provides additional clinical information on the occurrence of postoperative sustained ventricular tachyarrhythmias and describes an approach to differentiating patients with arrhythmias due to transient conditions from those with a persistent substrate and long-term arrhythmic susceptibility.

Use dependence of amiodarone during the sinus tachycardia of exercise in coronary artery disease

The QRS duration at rest and during exercise was studied in 19 patients with coronary artery disease before and after oral amiodarone therapy to determine if this drug produces detectable rate-dependent conduction slowing during physiologic increases in heart rate. QRS duration did not change significantly during exercise in the absence of the drug. However, after amiodarone, QRS duration at rest increased from 99 to 114 ms (p less than 0.001), and increased further from 114 to 127 ms (p less than 0.001) during the 45 beats/min mean increase in heart rate produced by exercise. The magnitude of this effect was related to the resting QRS duration. After amiodarone therapy, the QRS increased during exercise by only 6% in 8 patients with QRS less than 110 ms, while in 12 patients with QRS greater than or equal to 110 ms, the QRS increased by 15% (p less than 0.05). Rate-dependent conduction slowing occurs during the sinus tachycardia of exercise in patients treated with amiodarone, presumbably due to use-dependent sodium channel blockade. This result is most pronounced in patients with abnormal ventricular conduction at rest.

Induction of ventricular tachycardia in patients with left ventricular aneurysms and no history of arrhythmia

We recently reported 5 patients who developed sustained entricular tachycardia (VT) for the first time after a left ventricular (LV) aneurysmectomy performed for nonarrhythmic indications.1 It was unclear whether the aneurysmectomy directly precipitated the arrhythmia in those patients, or simply failed to remove a preexisting VT substrate. If the latter were true, recognition of the substrate before surgery and ablation by endocardial resection at the time of aneurysmectomy2,3 could have prevented the postoperative arrhythmia. Therefore, the current study was undertaken to determine how often aneurysms provide a substrate for VT detectable by programmed stimulation and whether any clinical or angiographic variables predict arrhythmia inducibility.

Management of atrial fibrillation and flutter: A reappraisal of digitalis therapy

PreviewDigitalis has long been used as an antiarrhythmic drug in treatment of paroxysmal supraventricular tachycardia, atrial fibrillation and flutter, and arrhythmias associated with congestive heart failure. However, newer evidence indicates that this cardiac glycoside has limited potency as an antiarrhythmic drug. In this review, the authors describe the effect of digitalis on cardiovascular function in management of atrial fibrillation and flutter. They conclude that while widespread use of digitalis as initial treatment for these supraventricular arrhythmias is justified by its low cost, ease of administration, and relatively few noncardiac side effects, newer drugs may ultimately prove more useful.