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Successful thrombolysis with intracoronary administration of tissue plasminogen activator in an infant with Kawasaki disease
  1. Hitoshi Horigome,
  2. Toshio Sekijima,
  3. Tomoyuki Miyamoto
  1. Department of Pediatrics, Institute of Clinical Medicine, University of Tsukuba, 1–1–1 Tennodai, Tsukuba 305, Japan
  1. Dr Horigome.

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We present the case of a 3 month old male Japanese infant who developed a myocardial infarction a month after the onset of Kawasaki disease. An electrocardiogram showed abnormal Q waves in leads V1 through V4. He was referred to our department eight days after the onset of myocardial infarction. Echocardiography on admission revealed giant left coronary aneurysms with massive thrombus in the lumen. Therapy with intravenous urokinase (5000 U/kg three times daily), heparin, and oral warfarin for one week failed to induce thrombolysis. A coronary angiogram revealed that a large thrombus occluded much of the lumen of the left anterior descending artery (fig 1A). A bolus dose of 50 000 U/kg of intracoronary tissue plasminogen activator (tPA) was administered into the left coronary artery over 10 minutes, but no change in the size of the thrombus was observed. The dose of tPA was increased to 80 000 U/kg. An angiogram 15 minutes later and an echocardiogram six hours later showed little change in the size of thrombus. However, the thrombus began to regress 24 hours after administration of tPA and completely disappeared within 48 hours, indicated by echocardiography. Coronary angiography performed one week after treatment (fig 1B) showed that the peripheral coronary blood flow was restored. No complications occurred.

Figure 1

Selective left coronary arteriograms in the right anterior oblique view obtained before (A) and one week after (B) the intracoronary administration of tissue plasminogen activator (tPA). (A) Note the giant aneurysm (maximal diameter 11 mm) involving the left main trunk, the left anterior descending artery, and the left circumflex artery. A large thrombus observed as a negative shadow in the aneurysm (white arrow) occluded a large part of the lumen. Blood slowly passed through the circumferential slit of the lumen to reach the peripheral left anterior descending artery. (B) The large thrombus was completely dissolved. The washout of contrast medium was delayed, taking more than five seconds in the aneurysm. The peripheral left anterior descending artery, which could not be visualised in this phase, was later shown to be patent.


Thrombotic occlusion of large coronary aneurysms is the principal cause of myocardial infarction and death in patients with Kawasaki disease.1 Intravenous tPA and intracoronary urokinase have been used to achieve thrombolysis in Kawasaki disease patients with or without myocardial infarction,2 ,3 but clinical experience with intracoronary tPA in infants is limited.4 In the present case intracoronary administration of tPA 15 days after the onset of myocardial infarction successfully induced thrombolysis, although the huge thrombus did not dissolve completely until 48 hours after treatment. A similarly delayed thrombolytic effect was previously observed in another infant with Kawasaki disease.4 The reason for the delayed effect of tPA in patients with Kawasaki disease is not known, but it is possible that the thrombus in the present and the previous case may have been too large to dissolve rapidly. The results in the present patient demonstrate that intracoronary tPA is a safe and effective thrombolytic agent, even in early infancy.