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Atrial fibrillation in patients with Wolff-Parkinson-White (WPW) syndrome may lead to syncope, ventricular fibrillation, and sudden death. In a follow-up study of 241 patients with WPW syndrome in a relatively unselected population, 26 patients had documented atrial fibrillation (11%). These patients were followed up after 1-37 years (median 11 years; mean 15 years). During this period, 2 of 26 died suddenly. These 2 patients had the shortest RR interval during spontaneous atrial fibrillation (less than or equal to 220 msec), greater than or equal to 1 episodes of syncope, and a persistent delta wave in all available electrocardiograms. In comparison, sudden or tachycardia-related death was seen in 4 of the 241 patients. This difference is not statistically significant. Thus, atrial fibrillation of 26 patients with WPW syndrome was surprisingly well tolerated in our follow-up study with only 2 sudden deaths.

Background Despite the efficacy of warfarin sodium therapy for stroke prevention in atrial fibrillation, many physicians hesitate to prescribe it to elderly patients because of the risk for bleeding complications and because of inconvenience for the patients. Methods The Second Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulation Study was a randomized, controlled trial examining the following therapies: warfarin sodium, 1.25 mg/d; warfarin sodium, 1.25 mg/d, plus aspirin, 300 mg/d; and aspirin, 300 mg/d. These were compared with adjusted-dose warfarin therapy (international normalized ratio of prothrombin time [INR], 2.0-3.0). Stroke or a systemic thromboembolic event was the primary outcome event. Transient ischemic attack, acute myocardial infarction, and death were secondary events. Data were handled as survival data, and risk factors were identified using the Cox proportional hazards model. The trial was scheduled for 6 years from May 1, 1993, but due to scientific evidence of inefficiency of low-intensity warfarin plus aspirin therapy from another study, our trial was prematurely terminated on October 2, 1996. Results We included 677 patients (median age, 74 years). The cumulative primary event rate after 1 year was 5.8% in patients receiving minidose warfarin; 7.2%, warfarin plus aspirin; 3.6%, aspirin; and 2.8%, adjusted-dose warfarin (P=.67). After 3 years, no difference among the groups was seen. Major bleeding events were rare. Conclusions Although the difference was insignificant, adjusted-dose warfarin seemed superior to minidose warfarin and to warfarin plus aspirin after 1 year of treatment. The results do not justify a change in the current recommendation of adjusted-dose warfarin (INR, 2.0-3.0) for stroke prevention in atrial fibrillation.

Summary A description is given of an eight-year-old boy with extrasystoles, seizures of muscular weakness, and multiple developmental anomalies (dwarfism, scaphocephalic skull, hypertelorism, bilateral ptosis, low-set ears, broad nose, mandibular hypoplasia, aplasia of a number of teeth, defect of both the soft and osseous palate, inward bending of the fifth fingers, single transverse palmar crease of both hands, and cryptorchidism). These findings suggest a specific syndrome, but no similar description was found in the literature. The investigations disclosed no signs of either a chromosomal, a neuromuscular, or an endocrine disease.

The number of antiarrhythmic drugs has increased greatly during the last three decades. From the triad of digitalis, quinidine and procainamide in 1951 to now a multitude of drugs. The purpose of the present paper is to assess the therapeutical potentials of this large armory of drugs. Focus will be on long-term prophylaxis of symptomatic paroxysmal tachycardia and fibrillation with a few comments on the treatment of ventricular extrasystole.

Plasma renin activity in the brachial artery and in the renal vein together with arterial noradrenaline Concentration were determined repeatedly during and after 10 min of dynamic exercise in eight cardiac patients. Arterial renin increased slightly during exercise and gradually returned to control level after exercise. Renal vein renin increased markedly during exercise and returned to the resting value immediately after exercise, similarly to the changes in plasma noradrenaline and heart rate. A close temporal relationship between the changes in the renal veno-arterial renin difference, plasma noradrenaline and heart rate strongly suggests that the sympathetic nervous system is a major determinant of renin release in man during exercise.