Abstract 897: Etiology of Chronic Total Coronary Occlusions Assessed by in Vivo Intravascular Ultrasound Analysis
Background- Histopathologically, chronic total occlusions (CTOs) most often arise from thrombotic occlusion, followed by thrombus organization and tissue aging. However, these etiologic mechanisms of CTOs have not been well studied in vivo.
Methods and Results- A CTO was defined as an obstruction of a native coronary artery with Thrombosis In Myocardial Infarction 0 antegrade flow and the duration of occlusion >4 weeks. From October 2002 to April 2008, 39 de novo CTO lesions (38 pts) were successfully recanalized and intravascular ultrasound (IVUS) imaging was performed only after crossing with a guidewire or pre-dilatation with a 1.5–2.0mm balloon. CTO was located in RCA in 56%, LAD in 28%, and LCX in 15%; the length of the CTO was 13.7±15.0mm. In 9 of the 39 lesion (23%), 12 ruptured plaques were observed; 9/12 ruptured plaques (75%) were located within the CTO segment or just proximal to the segment. In addition, 18 echolucent plaques were observed in 15 of the 39 lesions (38%). Therefore, 51% of the CTO lesions had either a ruptured and/or an echolucent plaque. CTO lesions with ruptured plaque had angiographic stain within the CTO segment more frequently than CTO lesions without ruptured plaque (33% vs 3%, P=0.03). Finally, 8 of 39 lesions (21%) had an appearance of superficial thrombus with underlying hyperechoic plaque; CTO lesions with layered plaque/thrombus had longer length of occluded segment lengths compared to the CTO lesions without layered plaque/thrombus (25.3±24.7 vs 10.5±9.3mm, P=0.01).
Conclusions- These novel in vivo IVUS findings add further evidence that ruptured plaque and/or thrombotic events contribute to the onset and extension of CTOs in a significant number of patients. Therefore, the pathogenesis of CTO may be an acute coronary syndrome with rupture and thrombosis of a vulnerable plaque in a significant number of patients.