Heterogeneity of Plaque Structural Stress Is Increased in Plaques, Leading to MACE
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Coronary events are caused by culprit plaque destabilization leading to acute coronary events and sudden cardiac death. Preventing or predicting such events by being able to locate culprit plaques before they go on to cause clinical symptoms would be a major advance for the cardiology community and potentially benefit millions of patients. To date intravascular imaging studies such as the PROSPECT study which performed virtual histology intravascular ultrasound (VH-IVUS) of non-culprit plaques at the time of percutaneous coronary intervention and followed patients for future events have shown plaques with a minimal luminal area (MLA) 4.0 mm2, plaque burden (PB) ³70% at the MLA, and the presence of virtual histology thin-cap fibroatheroma (VH-TCFA) were independent predictors of nonculprit (NCL) future major adverse cardiovascular events (MACE) over a 3-year period. While of interest the predictive value of such information in limited given that < 10% of such plaques led to major adverse cardiac events. Here Costopoulos et al. investigate whether the use of plaque structural stress (PSS, reported in Kpa), the stress located inside a plaque due to plaque structure and composition, might improve the ability of imaging to predict high-risk plaques using a dataset from the PROSPECT trial. PSS is increased in the minimal lumen area regions of NCL major adverse cardiovascular events (MACE) versus no MACE plaques for all plaques (PSS: 112.1 ± 5.5 kPa vs. 90.4 ± 3.3 kPa, respectively; p = 0.001) and virtual histology thin-cap fibroatheromas (VH-TCFAs) (PSS: 119.2 ± 6.6 kPa vs. 95.8 ± 5.0 kPa, respectively; p = 0.005). They report that PSS is increased in the peri-MLA regions of plaques that lead to MACE and that longitudinal heterogeneity is markedly increased in MACE plaques. While these data add to a long established paradigm that PSS is associated with progression of atherogenesis, the additive value of such biomechanical information remains uncertain and has not been tested in prospective trials.
OBJECTIVES
This study sought to determine if plaque structural stress (PSS) and other plaque stress parameters are increased in plaques that cause future major adverse cardiovascular events (MACE) and if incorporating these parameters improves predictive capability of intravascular ultrasonography (IVUS).
BACKGROUND
Less than 10% of coronary plaques identified as high-risk by intravascular imaging result in subsequent MACE. Thus, more specific measurements of plaque vulnerability are required for effective risk stratification.
METHODS
Propensity score matching in the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study plaque cohort resulted in 35 nonculprit lesions (NCL) associated with future MACE and 66 matched NCL that remained clinically silent. PSS was calculated by finite element analysis as the mechanical loading within the plaque structure in the periluminal region.
RESULTS
PSS was increased in the minimal luminal area (MLA) regions of NCL MACE versus no MACE plaques for all plaques (PSS: 112.1 ± 5.5 kPa vs. 90.4 ± 3.3 kPa, respectively; p = 0.001) and virtual histology thin-cap fibroatheromas (VH-TCFAs) (PSS: 119.2 ± 6.6 kPa vs. 95.8 ± 5.0 kPa, respectively; p = 0.005). However, PSS was heterogeneous over short segments, and PSS heterogeneity index (HI) was markedly greater in NCL MACE than in no-MACE VH-TCFAs (HI: 0.43 ± 0.05 vs. 0.29 ± 0.03, respectively; p = 0.01). Inclusion of PSS in plaque assessment improved the identification of NCLs that led to MACE, including in VH-TCFAs (p = 0.03) and plaques with MLA ≤4 mm2 (p = 0.03). Incorporation of an HI further improved the ability of PSS to identify MACE NCLs in a variety of plaque subtypes including VH-TCFA (p = 0.001) and plaques with MLA ≤4 mm2 (p = 0.002).
CONCLUSIONS
PSS and variations in PSS are increased in the peri-MLA regions of plaques that lead to MACE. Moreover, longitudinal heterogeneity in PSS is markedly increased in MACE plaques, especially VH-TCFAs, potentially predisposing to plaque rupture. Incorporation of PSS and heterogeneity in PSS may improve the ability of IVUS to predict MACE.
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