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Background: Data from broad populations have established associations between incidental carotid plaque and vascular events. Among people living with HIV (PLWHIV), the risk of vascular events is increased; however, whether incidental carotid plaque is increased and there is an association between incidental carotid plaque, plaque characteristics, and vascular events among PLWHIV is unclear., Methods and Results: Data from the multi-institutional Research Patient Data Registry were used. Presence and characteristics (high-risk plaque, including spotty calcification and low attenuation) of carotid plaque by computerized tomography among PLWHIV without known vascular disease were described. Data were compared with uninfected controls similar in age, sex, and cardiovascular risk factors, including diabetes mellitus, hyperlipidemia, and cigarette smoking to cases. Primary outcome was an atherosclerotic cardiovascular disease event, and secondary outcome was ischemic stroke. Cohort consisted of 209 PLWHIV (45±10 years, 72% male) and 168 controls. Using computerized tomography, PLWHIV without vascular disease had higher rates of any carotid plaque (34% versus 25%; P =0.04), noncalcified (18% versus 5%; P <0.001) and high-risk plaque (25% versus 16%; P =0.03). Over a follow-up of 3 years, 19 atherosclerotic cardiovascular disease events (9 strokes) occurred. Carotid plaque was independently associated with a 3-fold increase in atherosclerotic cardiovascular disease events among PLWHIV (hazard ratio, 2.91; confidence interval, 1.10-7.7, P =0.03) and a 4-fold increased risk of stroke (hazard ratio, 4.43; confidence interval, 1.17-16.70; P =0.02); high-risk plaque was associated with a 3-fold increased risk of atherosclerotic cardiovascular disease events and a 4-fold increased risk of stroke., Conclusions: There is an increase in incidental carotid plaque, noncalcified plaque, and high-risk plaque among PLWHIV, and the presence and characteristics of carotid plaque are associated with subsequent vascular events., (© 2017 American Heart Association, Inc.)

Background: Although plaque rupture is responsible for most myocardial infarctions, few high-risk plaques identified by intracoronary imaging actually result in future major adverse cardiovascular events (MACE). Nonimaging markers of individual plaque behavior are therefore required. Rupture occurs when plaque structural stress (PSS) exceeds material strength. We therefore assessed whether PSS could predict future MACE in high-risk nonculprit lesions identified on virtual-histology intravascular ultrasound., Methods and Results: Baseline nonculprit lesion features associated with MACE during long-term follow-up (median: 1115 days) were determined in 170 patients undergoing 3-vessel virtual-histology intravascular ultrasound. MACE was associated with plaque burden ≥70% (hazard ratio: 8.6; 95% confidence interval, 2.5-30.6; P<0.001) and minimal luminal area ≤4 mm(2) (hazard ratio: 6.6; 95% confidence interval, 2.1-20.1; P=0.036), although absolute event rates for high-risk lesions remained <10%. PSS derived from virtual-histology intravascular ultrasound was subsequently estimated in nonculprit lesions responsible for MACE (n=22) versus matched control lesions (n=22). PSS showed marked heterogeneity across and between similar lesions but was significantly increased in MACE lesions at high-risk regions, including plaque burden ≥70% (13.9±11.5 versus 10.2±4.7; P<0.001) and thin-cap fibroatheroma (14.0±8.9 versus 11.6±4.5; P=0.02). Furthermore, PSS improved the ability of virtual-histology intravascular ultrasound to predict MACE in plaques with plaque burden ≥70% (adjusted log-rank, P=0.003) and minimal luminal area ≤4 mm(2) (P=0.002). Plaques responsible for MACE had larger superficial calcium inclusions, which acted to increase PSS (P<0.05)., Conclusions: Baseline PSS is increased in plaques responsible for MACE and improves the ability of intracoronary imaging to predict events. Biomechanical modeling may complement plaque imaging for risk stratification of coronary nonculprit lesions., (© 2016 American Heart Association, Inc.)