LETTER
Failure of APSAC Thrombolysis
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.
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.
About Letters
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
Include no more than 300 words of text, three authors, and five references
Type with double-spacing
Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.