Data from ambulatory electrocardiographic recording in 35 highly trained endurance athletes and in 35 non-athletic controls of similar ages are given. The minimal, mean hourly, and maximal heart rates were significantly lower in the athletes. Thirteen athletes (37 . 1%) but only two controls (5 . 7%) had sinus pauses exceeding 2 . 0 seconds. First degree atrioventricular block was observed in 13 athletes (37 . 1%) and five controls (14 . 3%), second degree Wenckebach type block in eight athletes (22 . 9%) and two controls (5 . 7%), and second degree block with Mobitz II-like pattern in three athletes (8 . 6%) and no control. All athletes with Mobitz II-type pattern also had first degree and Wenckebach-type second degree atrioventricular block. The behavior of sinus rate on development of atrioventricular block varied, not only interindividually but also intraindividually, from absence of change to an increase or decrease in most subjects in both study groups. A decrease in sinus rate on appearance of atrioventricular block was found constantly in only two athletes and one control. Atrioventricular dissociation with junctional rhythm occurred in seven athletes (20%) and with ventricular rhythm in one athlete. Neither of these phenomena was seen in the group of controls. The athletes had slightly fewer ventricular extrasystoles than controls, and no athlete had ventricular tachycardia, whereas two controls had ventricular tachycardia.

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The electrocardiogram and the urinary excretion of catecholamines and metanephrines, plasma corticosteroids, blood sugar, NEFA, serum cholesterol, serum triglycerides, SGOT, SGPT, SLDH, SCPK, serume lectrolytes, and serum lactic acid have been measured in 20 patients with subarachnoid haemorrhage, including 6 patients with earlier known arterial hypertension, from their admission to the hospital up to their discharge or death. Electrocardiographic abnormalities were seen in all patients during the follow-up time. Electrocardiographic changes appeared most often at admission or on the first hospital day. An abnormal U wave was the change more often seen (13 patients).'Next in frequency was QT interval prolongation (II patients), and ST depression was seen in zopatients. SVx + RV5 exceeded 35 mm in 8 patients. The other abnormalities were T wave flattening and/or inversion, large P wave, ST elevation, prolonged PQ interval, atrial fibrillation, sinus bradycardia and tachycardia, and ventricular extrasystoles. Twelve patients survived the disease: in 8 of them the electrocardiogram returned to normal during the follow-up. The persisting abnormalities in electrocardiograms of the 4 other survivors were abnormal U wave in 3 patients, large P wave in 2, ST elevation in I, ST depression in I, sinus bradycardia in I, and sinus tachycardia in I. No clear, uniform correlation could be found between any single laboratory finding and electrocardiographic abnormalities. Since Byer, Ashman, and Toth (I947) reported large upright T waves and QT interval prolongation in the electrocardiogram of a patient with subarachnoid haemorrhage, many papers have been published reporting various *, changes tin the electrocardiograms of patients with subarachnoid haemorrhage (Hersch,

kg. of body weight intravenously, in three of the subjects receiving Lyndiol, one of those taking Orgametril, and in all the Mestranol subjects.

Ambulatory electrocardiographic recordings were obtained from 35 male athletes between 14 and 16 years old, and from 35 male non-athlete controls of the same ages, in order to determine the effects of regular physical training on cardiac electrical activity. In the young athletes, the heart rates were significantly (P less than 0.01) lower than in the nonathletes. Sinus intervals over 2.00 s were present in five athletes (14%) and one control (3%). First-degree atrioventricular block was detected in eight athletes (23%) and four controls (11%), and second-degree block was detected in seven athletes (20%) and one control (3%) (P less than 0.05). Ventricular premature beats were present in 60% of athletes and 57% of controls. The bradycardia in athletes did not predispose to ventricular ectopic activity, since heart rates at the times of occurrence of extrasystoles were higher in athletes than in controls. Even after two years of regular physical training there are significant differences in sinus nodal function and atrioventricular conduction as between young athletes and controls.