The QT interval of the electrocardiogram is prolonged in right and left bundle-branch block. Since the QT interval is not prolonged outside the normal range due to myocardial disease alone, this lengthening of the QT interval is due to the conduction defect and is probably due to delayed depolarization (and thus August, 1972. bundle-branch block, and 126 electrocardiograms indicating right bundle-branch block were examined during a 9-month period at two busy general hospitals. They were obtained by examination of all electrocardiograms with a QRS>o I2 sec. The criteria used in selecting cases of bundle-branch block were those of Lipman and Massie (I965). Thus the QRS was at least OI4 sec; there was delayed onset of intrinsicoid deflection over the affected ventricle ( >o-o6 sec) with the initial o004 sec shown as a positive deflection in leads over the unaffected ventricle and the terminal 0 04 sec shown as a negative deflection in these leads.In 55 electrocardiograms with left bundle-branch block and 33 electrocardiograms with right bundlebranch block there were electrocardiographic changes which were not due to bundle-branch block, such as those of myocardial infarction or arrhythmias such as atrial fibrillation; in some, drugs known to affect the QT had been given or the heart rates were in excess of i5o/minute or below 40/minute. These cases were excluded because of the possible effect of such factors on the QT and the difficulty of determining the QT at the extremes of heart rate (Lepeschkin, I955). To eliminate any error due to age or sex these details were recorded for each patient.The cycle length (C), the QT, the QRS, and the PR interval were measured for each electrocardiogram to an accuracy of ± 0 02 sec. All the leads were examined and the mean of the longest and shortest measurements of the QT in these leads and the longest measurement of the QRS in any lead were recorded (Grant, I970); the PR was measured in the same lead as the QRS. The ST interval (the measurement from the end of the S wave to the end of the T wave) was calculated from the differ-

The relation of lipid metabolism to nitrogen balance was studied in patients having undergone abdominal surgery and was compared with control subjects who had fasted for a similar period. The patients had lower circulating concentrations of glycerol, non-esterified fatty acids and ketone bodies. There were inverse correlations between blood alanine and ketone body concentrations in both patients (r = -0.64, P less than 0.01) and controls (r = -0.58, P less than 0.01). Nitrogen excretion by patients (12.7 mmol/kg body weight/day +/- 1.4 s.e. mean) was greater than by controls (9.2 mmol kg(-1)d(-1) +/- 0.8, P less than 0.05), but a more marked difference was noted for urinary methyl histidine excretion of 5.1 +/- 0.5 mmumol kg(-1) d(-1) by patients and only 2.5 +/- 0.3 mumol kg(-1) d(-1) by controls (P less than 0.01), a disparity indicative of more active protein turnover after surgery.

Comparisons of isonitrogenous supplements (1.2 g N) of essential amino acids and five keto acid analogues with four essential amino acids were made in seven patients with stable chronic renal failure (creatinine clearance, 4.6 to 16 ml/min) on moderately protein-restricted diets (4.60 to 7.8 g N per day). Full nitrogen balance data on the four patients who have already completed studies lasting 24 weeks are presented. No benefits of keto acid over amino acid supplements were observed. Two transient episodes of hypercalcemia occurred during keto acid treatment. There was no improvement of renal function with keto acids. Also, no carry-over effects were seen after keto acid treatment. It is concluded that any beneficial effects of keto acids in patients with chronic renal failure are only likely to occur in those taking a diet of less than 30 g protein daily.

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