title: Recurrent Acute Myocardial Infarction in a Patient with Severe Coronary Artery Ectasia: Implication of Antithrombotic Therapy.
abstract: BACKGROUND Acute myocardial infarction (AMI) can be caused not only by plaque rupture/erosion, but also by many other mechanisms. Thromboembolism due to atrial fibrillation and coronary thrombosis due to coronary artery ectasia are among the causes. Here we report on a case of recurrent myocardial infarction with coronary artery ectasia. CASE REPORT Our case was a 78-year-old woman with hypertension. Within a one-month interval, she developed AMI twice at the distal portion of her right coronary artery along with coronary artery ectasia. On both events, emergent coronary angiography showed no obvious organic stenosis or trace of plaque rupture at the culprit segment after thrombus aspiration. After the second acute event, we started anticoagulation therapy with warfarin to prevent thrombus formation. In the chronic phase, we confirmed, by using coronary angiography, optimal coherence tomography and intravascular ultrasound, that there was no plaque rupture and no obvious thrombus formation along the coronary artery ectasia segment of the distal right coronary artery, which suggested effectiveness of anticoagulant. Furthermore, by Doppler velocimetry we found sluggish blood flow only in the coronary artery ectasia lesion but not in the left atrium which is generally the main site of systemic thromboembolism revealed by transesophageal echocardiography. CONCLUSIONS These results suggest that the two AMI events at the same coronary artery ectasia segment were caused by local thrombus formation due to local stagnant blood flow. Although it has not yet been generally established, anticoagulation therapy may be effective to prevent thrombus formation in patients with coronary artery ectasia regardless of the prevalence of atrial fibrillation.
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tomioka
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Takeuchi
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Ito
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Shioiri
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Jiro
authors.initials: J
authors.lastname: Koyama
authors.affiliation: Department of Cardiology, South-Miyagi Medical Center, Shibata, Miyagi, Japan.
authors.forename: Kanichi
authors.initials: K
authors.lastname: Inoue
mesh_terms: D000368:Aged; D003328:Coronary Thrombosis / Q000150:complications* / Q000175:diagnosis / Q000628:therapy*; D003331:Coronary Vessels / Q000473:pathology*; D004108:Dilatation, Pathologic / Q000150:complications; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy
chemical_list: D005343:Fibrinolytic Agents