Volume 115 Number 6 changes. A VVI pacemaker was implanted, which resulted in symptomatic improvement. Case No. 3. C.C., a 50-year-old woman with a history of hypertension, presented with frequent episodes of palpi- tations, dizziness, fatigue, and shortness of breath, usually related to exertion. The resting ECG was normal (PR = 0.16 second). Ambulatory ECG monitoring revealed episodes of type II second-degree AV block during sinus tachycardia (with periods of 2:l conduction) that were inconsistently related to symptoms. During treadmill exercise testing, she developed 2:l AV block at a sinus rate of 148 associated with dyspnea, palpitations, fatigue, and dizziness. There were no ischemic changes. Electrophysiologic study revealed normal AH and HV intervals (HV = 45 msec); however, 3:2 type II block in the His bundle developed during atria1 pacing at a rate of 120. A DDD pacemaker was implanted with clinical improvement. Subsequent ECGs have demonstrated pacemaker dependence with underlying sinus rhythm but no supraventricular capture. When the pacemaker is turned off, advanced AV block without capture or ventric- ular escape has been noted for up to 6 seconds. Fewer than 20 cases of exercise-induced second-degree or higher grade AV block occurring in patients with 1:l AV conduction at rest have been reported.1-8 Electrophysiolog- ic evaluation in five cases revealed block distal to the AV node in each,5aK8 despite normal HV intervals at rest in three cases, as in our case No. 3. Our findings are consistent with a primary conduction tissue etiology of exercise-induced AV block, but since none of our patients underwent coronary angiography, occult ischemia cannot be excluded. Infranodal conduction is relatively unaffect- ed by changes in autonomic tone, and in diseased tissue it may decrease during exercise as effective refractory peri- ods increase. In contrast, conduction within the AV node generally increases with the increased sympathetic and decreased parasympathetic effects of exercise, and in normal tissue these changes offset the decremental AV nodal conduction found with nonphysiologic changes in rate alone, as occurs with atria1 pacing. However, exercise- induced abnormal conduction in the AV node might result from ischemia, despite autonomic regulation. At least one case of exercise-related AV block has been associated with ST segment depression,4 but the site of block in this case was not documented. REFERENCES 1. 2. 3. 4. 5. Moulopoulos SD, Anthopoulos LP. Reversible atrio-ventricu- lar conduction changes during exercise. Acta Cardiologica 1968;23:352-66. Moulopoulos SD, Darsinos J, Sideris DA. Atrioventricular block response to exercise and intraventricular conduction at rest. Br Heart J 1972;34:998-1004. Bakst A, Goldberg B,‘Schamroth L. Significance of exercise- induced second degree atrioventricular block. Br Heart J 1975;37:984-6. Rozanski JJ, Castellanos A, Sheps D, Pozen R, Myerberg RJ. Paroxysmal second-degree atrioventricular block induced by exercise, Heart Lung 1980;887-90. Freeman G, Hwang MH, Danoviz J, Moran JF, Gunnar RM. Exercise induced “Mobitz type II” second degree AV block in Brief Communications 1317 a patient with chronic bifascicular block (right bundle branch block and left anterior hemiblock). J Electrocardiol 1984; 17:409-12. Woelfel AK, Simpson RJ, Gettes LS, Foster JR. Exercise- induced distal atrioventricular block. J Am Co11 Cardiol 1983;2:578-81. Gilchrist AR. Clinical aspects of high-grade heart block. Scott Med J 1958;3:53-75. Kalusche D, Roskamm H. Tachycardia-dependent second degree AV-block in a patient with right bundle branch block. J Electrocardiol 1987;20:169-75. Successful use of flecaktida in atrial fibrlltatkm with rapid vmtriiulert rate in the Wolff-Parkinson-White syndrome Harry J. G. M. Crijns, M.D., Peter den Heijer, M.D., Leendert M. van Wijk, M.D., and K. I. Lie, M.D. Groningen, The Netherlands Atria1 fibrillation occurring in patients with the Wolff- Parkinson-White syndrome is a potentially life-threaten- ing arrhythmia because it may lead to ventricular fibrilla- tion.’ Ajmaline and procainamide have proven to be the drugs of choice in this condition. Flecainide, a relatively new class Ic antiarrhythmic drug, proved to be effective in ventricular arrhythmias.2 Up to now only few data have been published on the acute clinical effects of flecainide in the Wolff-Parkinson-White syndrome complicated by atria1 fibrillation. In the electrophysiology laboratory, the influence of this drug on the properities of the accessory pathway (AP) in patients with atrial fibrillation (AF) has been studied extensively.3-5 However, electrophysiologic testing cannot always predict the outcome of a drug when it is used in the clinical situation. In these circumstances, increased sympathetic activity may, for example, cause deleterious changes in electrophysiologic parameters.6r7 As a consequence, antiarrhythmic drugs may be less effective clinically when compared to the laboratory situation. Therefore we report the clinical use of intravenous flecain- ide in two patients with the Wolff-Parkinson-White syn- drome who were admitted with sustained AF with a rapid ventricular rate. Patient No. 1. A al-year-old man was admitted to the hospital because of palpitations and dizziness on standing. These symptoms existed for several hours and had previ- ously occurred in short paroxysms. On admission, he had a rapid irregular pulse and the supine blood pressure was 120/80 mm Hg. The ECG showed an irregular tachycardia with a mean ventricular rate of 280 beats/min. The QRS complexes were wide due to maximal preexcitation, and From the Department of Cardiology, University Hospital Groningen. Reprint requests: Harry J. G. M. Crijns, M.D., University Hospital Gronin- gen, Oostersingel 59, 9713 EZ Groningen, The Netherlands.