Journal of interventional cardiology · 2010
Role of a streamer-like coronary thrombus in the genesis of unstable angina.
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Uchida Yasumi, Uchida Yasuto, Kanai Masahito, Sakurai Takeshi, Oshima Tomomitsu, Shirai Seiichiro
Аннотация
INTRODUCTION: It is generally believed that the coronary occlusion occurs at the site of plaque disruption in acute coronary syndromes. An exceptional mechanism of coronary occlusion, namely a streamer-like thrombus (SLT) originating in a nonstenotic lesion extended distally to obstruct a just distal nondisrupted stenotic segment, was found by angioscopy in patients with unstable angina (UA). This study was carried out to examine the incidence of this phenomenon and its relationship to the subtypes of UA.
METHODS: The culprit coronary artery was investigated by angioscopy in successive 48 patients (mean +/- SE age, 61.0 +/- 2.3 years; 10 females and 38 males) with UA.
RESULTS: SLT originating in a nonstenotic lesion extended distally, and obstructed the just distal most stenotic segment (DMSS) by its tail in 11 patients (eight with class III and three with class II according to Braunwald's classification). Recurrent anginal attacks were observed in all. The nonstenotic lesion in which the SLT originated was a disrupted yellow plaque in most cases. The SLT was frequently red and yellow in a mosaic pattern, indicating a mixture of fresh thrombus and plaque debris. The plaques that constructed the DMSS were not disrupted. Angiographically, the SLT was not detectable and the entry of the DMSS showed a "tapering" configuration.
CONCLUSIONS: Obstruction of the DMSS by the tail of SLT originating in a nonstenotic lesion is another mechanism of UA. Therefore, treatment of both the nonstenotic lesion and DMSS is needed to prevent recurrent thrombus formation and consequent reattacks.
METHODS: The culprit coronary artery was investigated by angioscopy in successive 48 patients (mean +/- SE age, 61.0 +/- 2.3 years; 10 females and 38 males) with UA.
RESULTS: SLT originating in a nonstenotic lesion extended distally, and obstructed the just distal most stenotic segment (DMSS) by its tail in 11 patients (eight with class III and three with class II according to Braunwald's classification). Recurrent anginal attacks were observed in all. The nonstenotic lesion in which the SLT originated was a disrupted yellow plaque in most cases. The SLT was frequently red and yellow in a mosaic pattern, indicating a mixture of fresh thrombus and plaque debris. The plaques that constructed the DMSS were not disrupted. Angiographically, the SLT was not detectable and the entry of the DMSS showed a "tapering" configuration.
CONCLUSIONS: Obstruction of the DMSS by the tail of SLT originating in a nonstenotic lesion is another mechanism of UA. Therefore, treatment of both the nonstenotic lesion and DMSS is needed to prevent recurrent thrombus formation and consequent reattacks.