Acute Myocardial Infarction with Lung Cancer during Treatment with Gefitinib: the Possibility of Gefitinib-Induced Thrombosis

administration of gefi tinib was then started. A good response was observed but with a grade 1–2 skin adverse toxicity ( table 1 , period A). Two months later she complained of severe fatigue, and electrocardiography (ECG) revealed ischemic changes ( table 1 , period B). She was diagnosed with acute myocardial infarction. Therefore, the administration of gefi tinib was halted. On admission day, ECG revealed sinus rhythm with an ST elevation in leads V 1–3 and a T wave inversion in leads V 3–6 ( fi g. 1 ). However, there were neither changes in ECG fi ndings nor abnormalities in laboratory tests over the next 24 h ( table 1 , period C). On the other hand, echocardiographic fi ndings were consistent with a diagnosis of myocardial infarction in the left anterior descending area. After 2 weeks’ observation, the administration of gefi tinib was restarted under the continued treatment with aspirin ( table 1 , period D). Following about 2 weeks’ administration of gefi tinib, a minor response of the lung cancer was observed. An analysis of platelet aggregation, stimulated by ADP or collagen before and after 2 weeks of receiving gefi tinib, was performed. Both ADP and collagen-induced aggregations were suppressed before the restart of gefi tinib. However, both the aggregations exhibited a tendency towards enhancement after the restart of gefi tinib.