Serial determination of plasma catecholamines in myocardial infarction.

SUMMARY By the use of a precise and sensitive double-isotope derivative technic, plasma cate-cholamine concentration was measured at 2-hour intervals in 10 patients during the first 48 hours of myocardial infarction. Plasma catecholamine concentration was elevated in most patients, but to an extremely variable degree. In each patient, however, the values were rather stable during the study period. High levels of plasma catecholamines were correlated to the clinical state of the patients. Patients who received antiarrhythmic treatment on admission to the hospital had higher values than untreated patients. There was no temporal correlation between plasma catecholamine concentration and ventricular arrhythmias. In contrast to the plasma catecholamine level, the heterotopic ventricular activity declined spontaneously in the untreated patients within the study period. It is emphasized that the plasma catecholamine concentration in patients with acute myocardial infarction is considerably lower than the level necessary to produce arrhythmias in experimental myocardial infarction. Words: Plasma norepinephrine Ventricular ectopic beat Double-isotope technic Ventricular tachycardia IT IS GENERALLY accepted that the urinary excretion of catecholamines1-6 and the plasma catecholamine levels7-10 are elevated in most patients during the acute stage of myocardial infarction. A high level of catecholamines appears to be associated with the clinical state of the patient, and especially with heart failure.4-10 Catecholamine excretion is also elevated in congestive heart failure unrelated to myocar-dial infarction.1' Studies of urinary catecholamine excretion have shown that arrhythmias occur most frequently in patients with high excretion 846 rates.4 6 Such patients, in addition, often show varying degrees of heart failure. However, McDonald et al.8 found raised norepinephrine levels in patients with early ventricular arrhythmias independent of the presence or absence of pulmonary venous congestion. Siggers et al.9 found a relationship only between peak levels of epinephrine and ventricular arrhythmias but not with mean values of norepinephrine and epinephrine, nor with peak norepinephrine levels. The aforementioned studies are based on estimations of urinary excretion of catechola-mines or a few plasma determinations in the individual patients within the first 1 or 2 days of myocardial infarction where significant arrhythmias are likely to occur. More information about the role of elevated plasma catecholamine levels in the development of cardiac arrhythmias might be obtained by studying more closely the temporal