['Post-mortem pathological studies have shown that a "vulnerable" plaque is the dominant patho-physiological mechanism responsible for acute coronary syndromes (ACS). One way to improve our understanding of these plaques in vivo is by using histological "surrogates" created by intravascular ultrasound derived virtual histology (IVUS-VH). Our aim in this analysis was to determine the relationship between site-specific differences in individual plaque areas between ACS plaques and stable plaques (SP), with a focus on remodelling index and the pattern of calcifying necrosis.', 'IVUS-VH was performed before percutaneous intervention in both ACS culprit plaques (CP) n=70 and stable disease (SP) n=35. A total of 210 plaque sites were examined in 105 lesions at the minimum lumen area (MLA) and the maximum necrotic core site (MAX NC). Each plaque site had multiple measurements made including some novel calculations to ascertain the plaque calcification equipoise (PCE) and the calcified interface area (CIA). CP has greater amounts of positive remodelling at the MLA (RI@MLA): 1.1 (±0.17) vs. 0.95 (±0.14) (P<0.001); lower values for PCE 30% vs. 54% (P<0.001) but a higher CIA 5.38 (±2.72) vs. 3.58 (±2.26) (P=0.001). These features can provide discriminatory ability between plaque types with area under the curve (AUC) measurements between 0.65-0.86. The cut-off values with greatest sensitivity and specificity to discriminate CP morphologies were: RI @ MLA >1.12; RI @ MAX NC >1.22; PCE @ MLA <47.1%; PCE @MAX NC <47.3%; CIA @ MLA >2.6; CIA @ MAX NC >3.1.'] Does site-specific intravascular ultrasound analysis of remodelling index and calcified necrosis patterns reveal novel blueprints for coronary plaque instability?