Why the study?
Does intravenous streptokinase reduce plasma atrial natriuretic peptide concentrations in patients with acute myocardial infarction?
Does intravenous streptokinase reduce plasma atrial natriuretic peptide concentrations in patients with acute myocardial infarction?
Treatment with intravenous streptokinase in acute myocardial infarction is associated with normalized plasma atrial natriuretic peptide levels, suggesting a beneficial short-term hemodynamic effect.
Streptokinase-associated lower ANP in AMI may suggest hemodynamic benefit; hypothesis-generating and should not change practice without randomized confirmation.
Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.
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Phillips et al. (1989) studied this question.