To determine whether acute myocardial ischaemia induced by dynamic exercise can lead to changes in plasma levels of atrial natriuretic factor, we performed symptom-limited bicycle electrocardiographic tests in 20 males with recent acute myocardial infarction and in 8 control males. Ten patients developed exercise-induced myocardial ischaemia and 10 patients did not. There were no significant differences between the two groups with regard to age, site of myocardial infarction, urinary sodium, atrial sizes, radionuclide left ventricular ejection fraction, workload, baseline and peak-exercise heart rate, baseline and peak-exercise rate-pressure product, duration of exercise. Also baseline atrial natriuretic factor concentrations were similar in both groups (ischaemic patients: 34.51 ± 15.73 pg/ml; nonischaemic patients: 27.17 ± 8.74 pg/ml, NS), while peak-exercise atrial natriuretic factor concentrations were higher in patients with exercise-induced myocardial ischaemia (112.31 ± 35.5 pg/ml) than in the others (80.46 ± 23.43 pg/ml) (P < 0.05). After 15 minutes of recovery, plasma atrial natriuretic factor levels were still raised only in the ischaemic patients (63.3 ± 15.44 pg/ml, P < 0.01), returning to baseline after 30 minutes in both groups. In control subjects, the behaviour of atrial natriuretic factor resembled that of the patients without exercise-induced ischaemia, with a significant increase at peak-exercise (from baseline levels of 23.1 ± 10.5 pg/ml to peak-exercise levels of 91.3 ± 14.5 pg/ml, P < 0.0005) and a rapid return to baseline levels after 15 minutes of recovery (28.5 ± 10.6 pg/ml, NS). Plasma atrial natriuretic factor levels were significantly higher in patients with exercise-induced myocardial ischaemia than in controls both at peak-exercise (P < 0.05) and after 15 minutes of recovery (P < 0.01). In conclusion, our data confirm that plasma atrial natriuretic factor levels increase during exercise in patients after acute myocardial infarction. Furthermore, atrial natriuretic factor levels increase to a larger extent in patients developing exercise-induced myocardial ischaemia, also showing a delayed return to baseline as compared either to nonischaemic patients or to control subjects. This particular behaviour could be due to the onset of left ventricular dysfunction depending on myocardial ischaemia or to the direct stimulatory effect of myosite hypoxia on the release of atrial natriuretic factor. © 1992.
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