Effect of the Kallikrein Inhibitor Aprotinin on Myocardial Ischemia and Necrosis in Man

Cecefia-Seldner, Felipe A.; Villarreal, Jorge
July 1980
Angiology;Jul1980, Vol. 31 Issue 7, p488
Academic Journal
The effect of administration of aprotinin, a serine esterase inhibitor capable of inactivating kallikrein, on the extent and severity of acute myocardial ischemic injury and subsequent necrosis, was studied in 25 patients. Another group of 25 patients who did not receive aprotinin served as a control group. We administered 100,000 kallikrein inhibitor units (KIU) of aprotinin as a bolus dose, followed by a continuous infusion (4 ml/min) that contained 10,000 KlU/kg in 240 ml of dextrose/water solution, to all 25 patients admitted to the hospital within 30 to 60 minutes after the onset of acute myocardial ischemia. To measure the effect of aprotinin, three parameters were studied; the sum of S-T segment elevations (2ST), the development of Q waves, and the prediction of infarct size by measuring the disappearance rate of creatine phosphokinase (MB CPK isoenzyme). The average EST in the treated group decreased from 40.5 ± 7.00 mv to 12.95 ± 4.60 mv (P < 0.01); in contrast the control group's ΣST did not change significantly, from 54.25 ± 8.02 to 51.7 ± 6.8. Deeper Q waves evolved in the control group compared to the treated group: AQ (6 hours) = 1.0 ST (15 min) + 1.19 (25 patients, r = 0.78); and in the treated group ΔQ (6 hours) = 0.66 ST (15 min) + 0.91 (25 patients, r = 0.65) (P < 0.025). In the control group the estimated infarct size was 57.4 ± 4 CPK-gram-equivalents (CPK-g-Eq). There was significantly less damage in the treated group: 19 ± 2 CPK-g-Eq (P < 0.01). Thus we conclude that aprotinin diminishes myocardial damage.


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