Long-term haemodynamic results and exercise capacity were studied in 34 patients with tetralogy of Fallot (24 men and 10 women) repaired 10.0 +/- 4.9 (mean +/- SD) years previously and compared to 34 healthy matched controls. All subjects were studied by resting spirometry, echocardiography and a symptom limited treadmill exercise test (modified Bruce protocol). The maximal oxygen consumption was 38.2 +/- 8.0 ml.kg-1.min-1 in patients and 48.1 +/- 8.1 ml.kg-1.min-1 in the control group (P < 0.001). Reduced maximal oxygen consumption was found in patients with low vital capacity (VC) and pulmonary regurgitation (PR). The ventilatory anaerobic threshold (VAT) was 23.8 +/- 0.6 ml.kg-1.min-1 and 29.9 +/- 0.6 ml.kg-1.min-1 in patients and controls, respectively (P < 0.001). VC was 3.4 +/- 1.21 in patients and 4.0 +/- 1.31 in controls (P < 0.02). In the patients, maximal ventilation was reduced and at submaximal exercise, the breathing frequency increased. Heart rates during exercise were similar in patients and controls. Tricuspid regurgitation (TR) was detected in 20 patients (58.8%); however, the exercise capacity was not reduced. Thus, impaired exercise capacity in tetralogy of Fallot is partly due to reduced resting lung function, pulmonary regurgitation and low ventilatory anaerobic threshold.

We compared the levels of various metabolic indicators in arterial and venous forearm blood during maximal treadmill leg exercise, and the subsequent 9 min in nine volunteers aged 31-56 years. At maximal exercise plasma lactate was 13.2 +/- 3.1 mmol l-1 arterially, while venous was 41% lower, but increased more than arterial after exercise. There was a linear relationship between arterial and venous samples during and after exercise, but not at baseline. Plasma pyruvate increased on the arterial side from 49 +/- 8 to 172 +/- 30 mumol l-1 at maximal exercise, maximal venous was 21% lower. Free fatty acids were not different at rest, but decreased during exercise by 52 and 38% on the arterial and venous side. There was no relationship between arterial and venous levels. Changes in these three variables occurred significantly earlier on the arterial side. Arterial cyclic AMP rose from 97.3 +/- 28.4 to 262.7 +/- 67.5 nmol l-1 from rest to exercise, and was linearly inversely related to the decrease in free fatty acids. The mean venous pH was lower than arterial at rest, but was the same as arterial at maximal exercise and after. Thus, venous plasma lactate and pyruvate, but not free fatty acids, are linearly related to arterial measurements during maximal exercise, while pH is identical. Non-working muscle modifies exercise-induced changes, and therefore venous and arterial forearm blood sampling give more information than either alone.

It has recently been claimed that lack of sodium in nonionic contrast media may increase the risk of ventricular arrhythmias during coronary angiography. Thus. the influence of sodium addition to the nonionic contrast medium iohexol was studied in 75 patients with severe coronary heart disease. The study design was randomized, parallel and double-blind, and iohexol was given either with or without addition of NaCl (28 mmol/l). Both formulations induced a transient drop in arterial blood pressure, and prolongation of the QT interval and QRS duration at 10 s only (p

It has recently been suggested that the addition of sodium to low osmolality contrast media may reduce the incidence of ventricular fibrillation and conduction disturbances during coronary angiography. In a randomized, double blind study of 30 patients undergoing coronary angiography we therefore examined the electrophysiological and hemodynamic effects of the two low osmolality contrast media-ioxaglate (with sodium) and iohexol (without sodium). Standard ECG, aortic blood pressure, and His bundle electrocardiogram were recorded. The contrast media were well tolerated and no serious arrhythmias were observed. Both induced a transient decrement in systolic blood pressure and reduction in heart rate 10 s following contrast injection (all P less than 0.01). Ioxaglate prolonged the QT interval at 10 s (P less than 0.01) and also when analysed for the whole observation period (120 s) (P less than 0.05), whereas iohexol did not cause any significant changes in the QT-interval. The AH-interval was prolonged by ioxaglate at 10 s (P less than 0.01), but not altered by iohexol. Thus, other factors than osmolality and sodium content might contribute to QT prolongation, since only the contrast agents with sodium (ioxaglate) induced QT prolongation in this study.