Thin-Cap Fibroatheroma Rupture Is Associated With a Fine Interplay of Shear and Wall Stress

Pedrigi, Ryan M.; Silva, Ranil de; Bovens, Sandra M.; Mehta, Vikram V.; Petretto, Enrico; Krams, Rob

doi:10.1161/atvbaha.114.303426

Cited by 55 publications

(39 citation statements)

References 63 publications

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“…Currently, only vessel geometry and blood pressure can be obtained through catheter-based technologies, but not vessel stiffness [3]. Our results show that vessel stiffness can be determined using Brillouin spectroscopy.…”

Section: Discussionmentioning

confidence: 92%

Quantification of plaque stiffness by Brillouin microscopy in experimental thin cap fibroatheroma

Antonacci

Pedrigi

Kondiboyina

et al. 2015

J. R. Soc. Interface.

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Plaques vulnerable to rupture are characterized by a thin and stiff fibrous cap overlaying a soft lipid-rich necrotic core. The ability to measure local plaque stiffness directly to quantify plaque stress and predict rupture potential would be very attractive, but no current technology does so. This study seeks to validate the use of Brillouin microscopy to measure the Brillouin frequency shift, which is related to stiffness, within vulnerable plaques. The left carotid artery of an ApoE 2/2 mouse was instrumented with a cuff that induced vulnerable plaque development in nine weeks. Adjacent histological sections from the instrumented and control arteries were stained for either lipids or collagen content, or imaged with confocal Brillouin microscopy. Mean Brillouin frequency shift was 15.79 + 0.09 GHz in the plaque compared with 16.24 + 0.15 ( p , 0.002) and 17.16 + 0.56 GHz ( p , 0.002) in the media of the diseased and control vessel sections, respectively. In addition, frequency shift exhibited a strong inverse correlation with lipid area of 20.67 + 0.06 ( p , 0.01) and strong direct correlation with collagen area of 0.71 + 0.15 ( p , 0.05). This is the first study, to the best of our knowledge, to apply Brillouin spectroscopy to quantify atherosclerotic plaque stiffness, which motivates combining this technology with intravascular imaging to improve detection of vulnerable plaques in patients.

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Section: Discussionmentioning

confidence: 92%

Quantification of plaque stiffness by Brillouin microscopy in experimental thin cap fibroatheroma

Antonacci

Pedrigi

Kondiboyina

et al. 2015

J. R. Soc. Interface.

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“…Plaque rupture itself also depends on wall strain. In particular, regions of low shear stress but high strain appear to be at greatest risk, presumably because of the combination of vulnerable plaque and high strain (80). Microcalcification within a thin fibrous cap can also increase the risk of rupture, probably because of compliance mismatch, which generates regions of especially high strain (81).…”

Section: Plaque Progression and Remodelingmentioning

confidence: 99%

Endothelial fluid shear stress sensing in vascular health and disease

Baeyens

Bandyopadhyay

Coon

et al. 2016

Journal of Clinical Investigation

446

407

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“…However, residual stresses are not currently quantifiable in vivo, and although endothelial shear stress may affect plaque development, it is 10 −5 times smaller than PSS and unlikely induce plaque rupture. 25 …”

Section: Brown Et Al Plaque Stress and Macementioning

confidence: 99%

Plaque Structural Stress Estimations Improve Prediction of Future Major Adverse Cardiovascular Events After Intracoronary Imaging

Brown

Zhang

Calvert

et al. 2016

Circ: Cardiovascular Imaging

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A therosclerosis is a multifocal disease, with myocardial infarction (MI) remaining a leading cause of morbidity and mortality. Around two thirds of all spontaneous thrombotic coronary events resulting in MI or sudden cardiac death are caused by rupture of an atheromatous plaque.1,2 Repeated cycles of subclinical rupture and repair also underlie rapid plaque growth, 3 leading to luminal encroachment and symptoms of progressive angina. Morphologically, ruptured plaques exhibit large necrotic lipid cores, thin overlying fibrous caps, and evidence of microcalcification. 4 The precursor lesion for rupture, termed a thin-cap fibroatheroma (TCFA), displays several of these compositional features. 4 However, prospective studies have shown that future clinical event rates attributable to high-risk plaques were <10% for 3 years, 5 highlighting that novel, non-imaging-based markers are required to improve plaque-based risk stratification. See Editorial by Stone and Coskun See Clinical PerspectivePlaque rupture occurs when the plaque structural stress (PSS) exceeds the material strength of the tissue. 6 Autopsy studies have shown that PSS is increased after plaque rupture and that the location of peak PSS can accurately predict 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). 9-11 Although direct in vivo measurement of PSS is currently impos...

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Thin-Cap Fibroatheroma Rupture Is Associated With a Fine Interplay of Shear and Wall Stress

Cited by 55 publications

References 63 publications

Quantification of plaque stiffness by Brillouin microscopy in experimental thin cap fibroatheroma

Quantification of plaque stiffness by Brillouin microscopy in experimental thin cap fibroatheroma

Endothelial fluid shear stress sensing in vascular health and disease

Plaque Structural Stress Estimations Improve Prediction of Future Major Adverse Cardiovascular Events After Intracoronary Imaging

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