Abstract 10375: Rupture of Non-Thin Cap Fibroatheroma in Culprit Lesions of Acute ST Elevation Myocardial Infarction: A Virtual Histology Intravascular Ultrasound analysis
We assessed ruptured plaques with Virtual Histology Intravascular Ultrasound (VH-IVUS) in 150 pts with acute ST elevation myocardial infarction (STEMI).
Methods and Results: VH-thin-capped fibroatheromas (VH-TCFAs) TCFAs were defined as necrotic core (NC) >10% of plaque area, plaque burden >40%, and NC in contact with the lumen for ≥3 image slices. Remodeling index (RI) was lesion/reference external elastic membrane >1.05. Plaque rupture was present in 69 pts and divided into 2 groups: VH-TCFA (33 pts) and non-VH-TCFA (36 pts). 61% (42/69) of ruptured plaques were located in the proximal 30mm of a coronary artery. Vessel size, lesion length, plaque burden, minimal lumen area (MLA), and frequency of positive remodeling (57% [19/33] vs 55% [20/36], p=0.410) were similar in VH-TCFA vs non-VH-TCFA (Table). However, there were larger ruptured cavities and larger necrotic core areas within the rupture sites of VH-TCFAs compared to non-VH-TCFAs (p=0.021) while fibrofatty plaque areas were greater in non-VH TCFAs (p=0.004). Ruptured plaque cavity size correlated with distal reference lumen area (r=0.626, p=0.0002), MLA (r=0.422, p=0.018), and plaque area (r=0.26, p=0.05).
Conclusions: Not all culprit lesion plaque ruptures in STEMI patients occur as a result of TCFA rupture; a prominent fibrofatty plaque, especially in a proximal vessel, may be another form of vulnerable plaque.
- Vulnerable plaque
- Myocardial infarction, STEMI
- Intravascular ultrasound/Doppler
- Plaque rupture
- Acute coronary syndromes
- © 2010 by American Heart Association, Inc.