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LETTER

Failure of APSAC Thrombolysis

right arrow Mark J. Binette and Frank A. Agnone Jr.

1 October 1993 | Volume 119 Issue 7 Part 1 | Page 637


TO THE EDITOR:

We observed a 67-year-old white woman who was hospitalized for chest pain and electrocardiographic changes consistent with a posterior myocardial infarction. She received 30 units of anisoylated plasminogen streptokinase activator complex (APSAC) intravenously over 5 minutes. She subsequently completed a myocardial infarction without evidence of reperfusion by standard criteria. No laboratory evidence of a systemic lytic state was found, and cardiac catheterization showed a 100% proximal circumflex artery occlusion with a suggestion of luminal thrombus. There were no collaterals to the infarction zone, and a ventriculogram showed akinesis of the posterior wall.

On hospital day 2, the patient developed a fever, and a chest radiograph showed a right lower lobe infiltrate. Sputum culture results were positive for Streptococcus pneumoniae infection, and therapy was initiated. It was suggested that circulating antistreptococcal antibodies, which formed during the subclinical stages of her pneumonia, may have interfered with the action of APSAC, thus resulting in failure of thrombolysis. For this reason, the patient's blood stored in the laboratory at admission was sent for further studies. As expected, her antistreptolysin O, antistreptokinase, and antistreptococcal deoxyribonuclease B titers were markedly elevated, confirming the presence of circulating antistreptococcal antibodies at the time of hospitalization.

Failure of streptokinase to reperfuse the occluded coronary vessels in the presence of antistreptokinase antibodies has been documented [1, 2]. Several investigators have noted a nonlytic state after administration of APSAC but have only postulated the presence of circulatory antistreptokinase antibodies [3, 4]. Our findings suggest that APSAC, like its parent drug streptokinase, is susceptible to neutralization by antistreptokinase antibodies and that the same precautions for the use of streptokinase in the face of recent streptococcal infection or streptokinase use should also be applied to the use of APSAC.


References
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1. Lew AS, Neer T, Rodriquez L, Geft I, Prediman SK, Ganz W. Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody. J Am Coll Cardiol. 1984; 4:183-5.

2. Sanjeev J, Morris G. Antistreptokinase titres after intravenous streptokinase. Lancet. 1990; 335:184-5.

3. Brugemann J, van der Meer J, Takens BH, Hillege H, Lie KI. A systemic non-lytic state and local thrombolytic failure of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) in acute myocardial infarction. Br Heart J. 1990; 64:355-8.

4. Rothbard RL, Anderson JL, Fitzpatrick PG, Hakworthy RA, Sorensen SG, Marder VJ. Tolerance and complications in a multicenter trial of intravenous APSAC and intracoronary streptokinase in acute myocardial infarction. Clin Cardiol. 1990; 13(Suppl 5):V11-4, V27-32.

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