Relationship of renin, angiotensin II and atrial natriuretic factor to clinical status in the early post-infarct period in patients with left ventricular dysfunction

The vasoconstrictor and cardiotoxic effects of angiotensin II may be particularly harmful in the early post-infarct period but could be partially offset by the release of atrial natriuretic factor. We studied the relationship of renin, angiotensin II and atrial natriuretic factor to clinical status in the first 72 h after infarction in 36 patients not requiring treatment with diuretics on clinical grounds. Since these patients were treated with streptokinase, 16 non-thrombolysed patients were included to control for the acute effects of streptokinase on plasma hormones. Streptokinase caused transient fluctuations in plasma renin and atrial natriuretic factor but did not limit the subsequent development of supranormal hormone levels. Streptokinase-treated patients were divided on the basis of the highest recorded Killip class. Activation of the renin angiotensin system occurred only in those patients in Killip class 2 (n=11), was maximal at 24-72 h and was proportional to the extent of left ventricular dysfunction. Plasma levels of atrial natriuretic factor were elevated on admission, even in patients in Killip class 1 (n=25), but declined within an hour before rising again to supranormal levels at 24-72 h. Cumulative release of renin and angiotensin II, but not atrial natriuretic factor, were significantly greater in patients in Killip class 2. Heart rate was greater in Killip class 2 at 24 and 72 h but there was no difference in mean arterial pressures. We conclude that the renin angiotensin system is activated in the early post-infarction phase, but only in patients in Killip class 2, possibly as a result of increased sympathetic activity and reduced renal perfusion. Release of atrial natriuretic factor is less dependent on left ventricular dysfunction and follows a biphasic pattern, irrespective of streptokinase treatment.