To ascertain the effect of anabolic steroids (AS) on left ventricle size and function, M-mode and 2D echocardiographic evaluation was carried out in 14 body builders at the end of a phase of AS self-administration (8 +/- 3 weeks, mean +/- S.D.) and after a period (9 +/- 2 weeks, mean +/- S.D.) of drug withdrawal, as well as in 14 other body builders who had never made use of AS, and in 14 sedentary individuals. All the subjects were also examined anthropometrically. Ventricular septal thickness index was slightly greater in athletes using AS, compared to the other two groups (p less than 0.05), while left ventricle mass, the end-diastolic volume indexes and isovolumetric relaxation time, (a parameter of left ventricle diastolic function) were significantly increased (p less than 0.001) as well as the fat free mass (FFM), a marker of skeletal muscle mass. The non-users showed no differences in echocardiographic parameters, compared to sedentary controls. During the off treatment phase, the percentage of adipose mass increased and FFM decreased, while echocardiographic parameters did not vary significantly from on treatment values. The findings indicate that AS can induce an unfavourable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase. These modifications tend to persist following a short period of drug withdrawal.

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All patients were in sinus rhythm at the time of the electrophysiologic study, and cardioactive drugs were discontinued at least 48 hours before. The study was performed with patients in the resting, postabsorptive, nonsedated state. All patients gave informed written consent. Two #6F bipolar electrode catheters were passed percutaneously via the femoral veins into the right heart; the first was positioned in the high right atrium for the PRAS and the second was advanced to the tricuspid orifice to record His bundle activity according to the method of Scherlag et al.25 Single premature atrial stimuli were delivered after every eighth spontaneous beat at progressively decreasing 10-msec coupling intervals until the atrioventricular (AV) nodal or ventricular specialized conduction system effective refractory period (ERP) was reached. We used the bipolar atrial electrogram as the trigger signal. Stimuli were approximately twice diastolic threshold, 2.5 msec in duration and elicited by a programmable digital stimulator (El Desi CD 6). The PRAS was performed during spontaneous sinus rhythm and not during atrial driving because in this way it is easier to find the refractoriness of the HisPurkinje system. The His bundle electrogram, the surface ECG (leads I, II, III and V1), and the frontal, horizontal and left sagittal planes of VCG (Frank method)26 were simultaneously recorded during PRAS, using an eight-channel direct writing recorder (Elema Schonander Mingograf 81) at a paper speed of 50 or 100 mm/sec and an ICR 1001 Instant VCG vec-

Fifty-eight patients (29 M, 29 F, mean age 60.8 +/- 16 years) with unexplained syncope at the end of a complete clinical and electrophysiological evaluation, were followed for a mean period of 36.6 +/- 20.5 months (median: 30.5 months). Structural heart disease was present in 32 patients (55.2%). The standard ECG was normal in 24 (41.4%) and showed sinus bradycardia (greater than 40 m-1) and/or first degree AV block and/or intraventricular conduction disturbances in 29 patients (50%). During follow-up, recurrences of syncope were observed in 11 of 43 untreated patients (25.6%), three of seven electrically treated patients (42.9%) and two of eight pharmacologically treated patients (25%). The cause of these recurrences was cardiac in one (1.7%), non-cardiac in 10 (17.2%) and remained undetermined in five (8.6%). Sudden death occurred in only one patient (1.7%), who was receiving chronic amiodarone therapy. These results indicate that (1) syncopal recurrences may occur in an appreciable percentage of patients with unexplained syncope and a negative electrophysiologic study during a relatively long-term follow-up, (2) syncopal recurrences, when they occur, are generally due to a non-cardiac cause, (3) sudden death is an occasional and rare event in this patient population and (4) empirical prophylactic treatment with a permanent pacemaker or antiarrhythmic drugs does not usually prevent complications during the follow-up.