Aim of the present study was to evaluate 24 h electrocardiographic recording in 30 top athletes, 30 athletic students and 30 sedentary control subjects. Each group consisted of 15 males and 15 females and were matched for age (about 24 years). Training was not allowed during the recording. Top athletes had the lowest diurnal and nocturnal heart rate, but the difference between top athletes and athletic students was far less pronounced than between athletic students and controls. This may indicate that bradycardia reaches a lower limit with moderate degrees of training. Atrioventricular (AV) block II was found in 3 top athletes and 4 athletic students and in none of the subjects, the longest pause being 2.4 s in both athletic groups. Most episodes occurred during night and nearly all were Mobitz type I. In all cases of AV block II the QRS complexes were narrow and AV block III did not occur. SA block was found in 3 top athletes, 1 athletic student and 1 control subject, the longest pause being 3.1, 2.9 and 1.9 s, respectively. Ventricular premature beats were rare in all groups and complex ventricular arrhythmias were not found. Half of the subjects were in Lown class 0, the other half in Lown class 1. Supraventricular premature beats were also scarce and most frequent in top athletes, followed by athletic students and sedentary controls (2.0, 1.0, 0.7 beats/h, respectively).

Continuous ECG recording has been carried out for at least 24 h in 27 patients suffering from cluster headache. During the study a total of 84 attacks occurred in 25 of the 27 patients who took part. A computerized analysis of the heart rate changes accompanying attacks showed the following: (i) an increase in heart rate at the onset of attacks; the degree of this increase being dependent on the heart rate before attacks, (ii) a relative decrease in heart rate and increased variations in heart rate during attacks, (iii) a relative increase in heart rate at the end of attacks, and (iv) a relative decrease in heart rate after attacks. Five patients (18.5%) showed ECG rhythm disturbances: two frequent premature ventricular beats, one transient attacks of atrial fibrillation, one first degree atrio-ventricular block, and one patient sinoatrial block.

Thirty top level athletes, 30 athletic students and 30 sedentary controls underwent electrocardiographic and echocardiographic investigation. Resting ECG in athletes showed increased indices of hypertrophy compared to controls. The echocardiographic examination demonstrated an increase in left ventricular mass (LVM) of 47% in top athletes and 23% in athletic students compared to controls. The relationship between wall thickness and diameter was similar in all groups, as were parameters of systolic and diastolic left ventricular function at rest. There was no correlation between LVM assessed by echocardiography and ventricular ectopic activity assessed by Holter monitoring in this normotensive population. Highly significant correlations between ECG and echocardiographic parameters of hypertrophy were demonstrated.

The aim of the present investigation is to study digitoxin and digoxin protein binding in patients with normal renal and hepatic function, in patients with uremia, and in patients under treatment with hemodialysis for renal failure. The binding of digitoxin and cardioactive metabolites to serum proteins was studied using equilibrium dialysis (an in vitro chemical assay) alone and in combination with a modified 86Rb method. The following values for protein binding were found: DT-3 (digitoxin), 95.7%; DT-2 (digitoxigenin-bis-digitoxoside), 96.5%; DT-1 (digitoxigenin-mono-digitoxoside), 98.7%; DT-0 (digitoxigenin), 92.7%; DG-3 (digoxin), 21.2%; DG-2 (digoxigenin-bis-digitoxoside), 16.3%; DG-1 (digoxigenin-mono-digitoxoside), 18.5%; and DG-0 (digoxigenin), 13.3%. In vitro addition of procainamide, phenytoin, heparin, and rifampicillin did not influence the in vitro binding of digitoxin. Protein binding of digitoxin showed small individual variations in patients with normal renal and hepatic function. Uremia per se did not influence the in vitro binding of digitoxin. There were marked changes in digitoxin and digoxin protein binding during an 8-hr hemodialysis, digitoxin binding decreasing from 97.1% to 93.7% (p less than 0.0025) and digoxin binding from 23.5% to 15.4% (p less than 0.05). In the uremic patient the metabolic pattern of digitoxin tended toward a decrease in protein-bound metabolites.