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Disruption of In-Stent Neointima Causing Acute Mycoardial Infarction
May 2006
Case Presentation. A 25-year-old male presented with an acute anterior myocardial infarction and was referred for immediate primary percutaneous coronary intervention. His cardiovascular risk factors included smoking, hypercholesterolemia, obesity and a positive family history of ischemic heart disease. Of note, he had no history of cocaine use. At coronary angiography, he had a totally occluded left anterior descending artery just beyond the first diagonal branch, but no significant coronary artery disease elsewhere. A 3.5 x 23 mm Tetra™ coronary stent (Guidant Corp, Indianapolis, Indiana) was deployed at 12 atmospheres, after balloon predilatation, with an excellent angiographic result and TIMI 3 flow. At discharge, he was receiving aspirin, clopidogrel (1 month), ramipril, simvastatin and metoprolol. Furthermore, there was no detectable prothrombotic disorder on this admission, with assays for protein C and S, antithrombin III, lupus anticoagulant, serum homocysteine and plasminogen activator inhibitor 1 all within the laboratory normal ranges.
He returned with another anterior myocardial infarction 3 months later, having had no symptoms of angina pectoris since discharge, and having given up smoking. Reteplase (F. Hoffmann-La Roche Ltd, Basel, Switzerland) was administered with resolution of his chest pain and precordial ST-segment elevation. He had no angina in hospital, but returned for coronary angiography prior to discharge. Within the coronary stent an ulcerated plaque (panels A and B) was identified. Intravascular ultrasound examination revealed a ruptured neointima within the stent (panel C), with definable shoulders (yellow arrows, panel D), ruptured core and associated ulcerated region (yellow asterisk, panel D). There was only minor in-stent restenosis, and as such, further coronary intervention was deferred. The patient was discharged on a combination of aspirin and warfarin.
It is uncommon for myocardial infarction to occur late after a percutaneous coronary intervention with stent placement due to pathology at the stent site. This is the first such description of an acute coronary syndrome presenting due to a disruption within the neointima associated with noncritical in-stent restenosis. The pathobiology of the process in this case is unclear.
