The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Jolanda J Wentzel - One of the best experts on this subject based on the ideXlab platform.
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Abstract 126: Are Carotid Plaques With IntraPlaque Hemorrhage Different in Plaque Size, Distribution and Shear Stress?
Arteriosclerosis Thrombosis and Vascular Biology, 2014Co-Authors: Zaid A. M. Kassar, Frank J. H. Gijsen, Mariana Selwaness, Lambert Speelman, Merih Cibis, Anouk C. Van Dijk, Anton F. W. Van Der Steen, Aad Van Der Lugt, Jolanda J WentzelAbstract:Introduction: IntraPlaque hemorrhage (IPH) is associated with risk at ischemic stroke. In addition, Plaques that contain IPH show accelerated Plaque growth, which might affect the local shear stress (SS) distribution over the Plaque. Blood flow induced SS is known to be involved in the development and destabilization of atherosclerotic Plaques. It is unknown whether the SS distribution over Plaques with IPH differs from Plaques without IPH and whether SS is involved in Plaque progression/destabilization of Plaques with IPH. We compared the Plaque size, distribution and SS over Plaques with and without IPH in symptomatic patients. Methods: 38 patients with a recent (
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Shear stress and advanced atherosclerosis in human coronary arteries
Journal of Biomechanics, 2012Co-Authors: Frank J. H. Gijsen, Alina Van Der Giessen, Anton F. W. Van Der Steen, Jolanda J WentzelAbstract:Abstract The role of low and oscillating shear stress as a key factor for localizing early atherosclerotic Plaques is generally accepted. Once more advanced Plaques protrude into the lumen, the shear stress they are exposed to changes. The influence of shear stress on Plaque composition in advanced atherosclerosis is not fully understood. In this review, we discuss our recent studies on the relationship between shear stress and Plaque composition and the location of Plaque rupture in human coronary arteries. We have shown that elevated shear stress levels can be found over Plaques inducing only mild luminal narrowing and are not subjected to treatment. Regional exposure of certain Plaque regions to high shear stress is therefore a condition that will pertain for a prolonged period of time. We have also shown that in more advanced atherosclerosis the necrotic core experiences higher shear stress. Low shear stress Plaque regions can be found downstream of the Plaque and are stiffer. High shear stress Plaque regions can be found either at the upstream, shoulder or cap region of the Plaque and are softer. The Plaque regions with the highest strain levels are the regions that are exposed to the highest shear stress. The high shear stress Plaque regions are the only Plaque regions that get softer over time. Finally, high shear stress is also associated with the location of Plaque rupture in non-culprit lesion in human coronary arteries. Combining our findings with data from literature, we can conclude that advanced coronary Plaques grow in the distal regions. The distal Plaque regions are exposed to low shear stress, are stiffer and have a stable Plaque phenotype. The regions exposed to high shear stress are softer, and are associated with vulnerable Plaque features.
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current diagnostic modalities for vulnerable Plaque detection
Current Pharmaceutical Design, 2007Co-Authors: Johannes A Schaar, Patrick W Serruys, Evelyn Regar, Frits Mastik, Jolanda J Wentzel, Frank J. H. Gijsen, A F W Van Der StehenAbstract:Rupture of vulnerable Plaques is the main cause of acute coronary syndrome and myocardial infarction. Identification of vulnerable Plaques is therefore essential to enable the development of treatment modalities to stabilize such Plaques. Several diagnostic methods are currently tested to detect vulnerable Plaques. Angiography has a low discriminatory power to identify the vulnerable Plaque, but does provide information about the entire coronary tree and serves as guide for invasive imaging techniques and therapy. Angioscopy offers a direct visualization of the Plaque surface and intra- luminal structures like thrombi and tears. However, angioscopy is difficult to perform, invasive and only the proximal part of the vessels can be investigated. IVUS (intravascular ultrasound) provides some insight into the composition of Plaques. The detection of vulnerable Plaques is mainly based on series of case reports with a lack of prospectivity and follow- up. Palpography, an IVUS derived technique, reveals information, which is not recognizable in IVUS. It can differentiate between deformable and non-deformable tissue, which enables the technique to detect vulnerable Plaques with a positive predictive value. The clinical value of palpography is currently under investigation. Thermography assesses the temperature heterogeneity as an indicator of the metabolic state of the Plaque. A coincidence of temperature rise and localization of vulnerable Plaque was suggested. OCT (optical coherence tomography) can provide images with ultrahigh resolution utililizing the back-reflection of near-infrared light from optical interfaces in tissue. Drawbacks are the low penetration depth into tissue and the absorbance of light by blood. Raman spectroscopy can provide quantification about the molecular composition of the Plaque. Long acquisition time, the low penetration depth and light absorbance by blood limit the performance of the technique. Another light emitting technique is NIR (near infrared spectroscopy), which identifies lipid loaded Plaques and is tested currently in clinical trials. Non-invasive MRI (magnetic resonance imaging) and multislice spiral computed tomography (MSCT), with their excellent ability to identify lipid-rich tissue, have been utilized to characterize potentially vulnerable Plaques foremost in non-moving structures like the carotid arteries. Due to the resolution of the techniques small Plaque structure cannot be assessed. The role of non-invasive imaging in vulnerable Plaque detection is currently under investigation. Several invasive and non-invasive techniques are currently under development to assess the vulnerable Plaque. Most of the techniques show exiting features, but none have proven their value in an extensive in vivo validation and all have a lack of prospective data.
Renu Virmani - One of the best experts on this subject based on the ideXlab platform.
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mechanisms of Plaque formation and rupture
Circulation Research, 2014Co-Authors: Jacob F Bentzon, Renu Virmani, Fumiyuki Otsuka, Erling FalkAbstract:Atherosclerosis causes clinical disease through luminal narrowing or by precipitating thrombi that obstruct blood flow to the heart (coronary heart disease), brain (ischemic stroke), or lower extremities (peripheral vascular disease). The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Atherosclerosis is a lipoprotein-driven disease that leads to Plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification. After decades of indolent progression, such Plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary syndrome. Most often, the culprit morphology is Plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material. The permissive structural requirement for this to occur is an extremely thin fibrous cap, and thus, ruptures occur mainly among lesions defined as thin-cap fibroatheromas. Also common are thrombi forming on lesions without rupture (Plaque erosion), most often on pathological intimal thickening or fibroatheromas. However, the mechanisms involved in Plaque erosion remain largely unknown, although coronary spasm is suspected. The calcified nodule has been suggested as a rare cause of coronary thrombosis in highly calcified and tortious arteries in older individuals. To characterize the severity and prognosis of Plaques, several terms are used. Plaque burden denotes the extent of disease, whereas Plaque activity is an ambiguous term, which may refer to one of several processes that characterize progression. Plaque vulnerability describes the short-term risk of precipitating symptomatic thrombosis. In this review, we discuss mechanisms of atherosclerotic Plaque initiation and progression; how Plaques suddenly precipitate life-threatening thrombi; and the concepts of Plaque burden, activity, and vulnerability.
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a pathobiologic link between risk factors profile and morphological markers of carotid instability
Atherosclerosis, 2010Co-Authors: Alessandro Mauriello, Renu Virmani, Giuseppe Sangiorgi, Santi Trimarchi, David R Holmes, Frank D Kolodgie, David G Piepgras, Giulia Piperno, Doriana Liotti, Jagat NarulaAbstract:Abstract Objective Although cardiovascular risk factors have been strongly linked to carotid intimal-media thickness, their association with Plaque progression towards instability is poorly understood. We evaluated a large database of endarterectomy specimens removed from symptomatic and asymptomatic patients to determine the correlation between major cardiovascular risk factors and carotid Plaque morphology. Methods Incidence of thrombotic, vulnerable and stable Plaques together with the degree of Plaque inflammatory infiltration was evaluated in 457 carotid atherosclerotic lesions. Clinical records were reviewed in all cases for risk factors profile. Results Thrombotic Plaques were more frequently observed in patients affected by stroke (66.9%) as compared to TIA (36.1%) and asymptomatic patients (26.8%, p 5 with vulnerable and thrombotic carotid Plaques. Hypertension (p = 0.001), hypercholesterolemia (p = 0.05) and low HDL-C (p = 0.001) significantly also correlated with the presence of high inflammatory infiltrate of the Plaque. When multivariate analysis was restricted to asymptomatic patients, hypertension (p = 0.009, OR 2.29), low HDL-cholesterol (p = 0.01 OR 2.21) and the ratio of total to HDL-C >5 (p = 0.03, OR 2.07) were confirmed to be the risk factors most significantly associated to unstable Plaques. The relative risk to carry an unstable Plaque for asymptomatic patients with high Framingham Risk Score as compared with those with low risk score was 2.06 (95% C.I., 1.26–3.36). Conclusions The present histopathological study identifies risk factors predictive of increased risk of carotid Plaque rupture and thrombosis. Asymptomatic patients with high risk factors profile may constitute a specific target to reduce the likelihood of cerebrovascular accidents even in the presence of non-flow-limiting Plaque.
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coronary risk factors and Plaque morphology in men with coronary disease who died suddenly
The New England Journal of Medicine, 1997Co-Authors: Allen P Burke, Andrew Farb, Youhui Liang, John E Smialek, Gray T Malcom, Renu VirmaniAbstract:Background Cigarette smoking and abnormal serum cholesterol concentrations are risk factors for acute coronary syndromes, but the underlying mechanisms are poorly understood. We studied whether cigarette smoking and abnormal cholesterol values may precipitate acute coronary thrombosis and sudden death resulting from either rupture of vulnerable coronary Plaques or erosion of Plaques. Methods We examined the hearts of 113 men with coronary disease who had died suddenly and also analyzed their coronary risk factors. We found an acute coronary thrombus in each of 59 men, and severe narrowing of the coronary artery by an atherosclerotic Plaque without acute thrombosis (stable Plaque) in 54. Cases of acute thrombosis were divided into two groups: 41 resulting from rupture of a vulnerable Plaque (a thin fibrous cap overlying a lipid-rich core), and 18 resulting from the erosion of a fibrous Plaque rich in smooth-muscle cells and proteoglycans. Vulnerable Plaques that had not ruptured were counted in each heart....
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coronary Plaque erosion without rupture into a lipid core a frequent cause of coronary thrombosis in sudden coronary death
Circulation, 1996Co-Authors: Andrew Farb, Allen P Burke, Anita L Tang, Youhui Liang, Poonam Mannan, John E Smialek, Renu VirmaniAbstract:Background Coronary thrombosis has been reported to occur most frequently in lipid-rich Plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of extracellular lipid. However, the frequency of coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown. In this study, we compared the incidence and morphological characteristics of coronary thrombosis associated with Plaque rupture versus thrombosis in eroded Plaques without rupture. Methods and results Fifty consecutive cases of sudden death due to coronary artery thrombosis were studied by histology and immunohistochemistry. Plaque rupture of a fibrous cap with communication of the thrombus with a lipid pool was identified in 28 cases. Thrombi without rupture were present in 22 cases, all of which had superficial erosion of a proteoglycan-rich Plaque. The mean age at death was 53 +/- 10 years in Plaque rupture cases versus 44 +/- 7 years in eroded Plaques without rupture (P Conclusions Erosion of proteoglycan-rich and smooth muscle cell-rich Plaques lacking a superficial lipid core or Plaque rupture is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the present study. These lesions are more often seen in younger individuals and women, have less luminal narrowing and less calcification, and less often have foci of macrophages and T cells compared with Plaque ruptures.
Frank J. H. Gijsen - One of the best experts on this subject based on the ideXlab platform.
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Calcifications in atherosclerotic Plaques and impact on Plaque biomechanics
Journal of biomechanics, 2019Co-Authors: Hilary E. Barrett, Frank J. H. Gijsen, Kim Van Der Heiden, Eric Farrell, Ali C. AkyildizAbstract:Abstract The catastrophic mechanical rupture of an atherosclerotic Plaque is the underlying cause of the majority of cardiovascular events. The infestation of vascular calcification in the Plaques creates a mechanically complex tissue composite. Local stress concentrations and Plaque tissue strength properties are the governing parameters required to predict Plaque ruptures. Advanced imaging techniques have permitted insight into fundamental mechanisms driving the initiating inflammatory-driven vascular calcification of the diseased intima at the (sub-) micron scale and up to the macroscale. Clinical studies have potentiated the biomechanical relevance of calcification through the derivation of links between local Plaque rupture and specific macrocalcification geometrical features. The clinical implications of the data presented in this review indicate that the combination of imaging, experimental testing, and computational modelling efforts are crucial to predict the rupture risk for atherosclerotic Plaques. Specialised experimental tests and modelling efforts have further enhanced the knowledge base for calcified Plaque tissue mechanical properties. However, capturing the temporal instability and rupture causality in the Plaque fibrous caps remains elusive. Is it necessary to move our experimental efforts down in scale towards the fundamental (sub-) micron scales in order to interpret the true mechanical behaviour of calcified Plaque tissue interactions that is presented on a macroscale in the clinic and to further optimally assess calcified Plaques in the context of biomechanical modelling.
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Abstract 126: Are Carotid Plaques With IntraPlaque Hemorrhage Different in Plaque Size, Distribution and Shear Stress?
Arteriosclerosis Thrombosis and Vascular Biology, 2014Co-Authors: Zaid A. M. Kassar, Frank J. H. Gijsen, Mariana Selwaness, Lambert Speelman, Merih Cibis, Anouk C. Van Dijk, Anton F. W. Van Der Steen, Aad Van Der Lugt, Jolanda J WentzelAbstract:Introduction: IntraPlaque hemorrhage (IPH) is associated with risk at ischemic stroke. In addition, Plaques that contain IPH show accelerated Plaque growth, which might affect the local shear stress (SS) distribution over the Plaque. Blood flow induced SS is known to be involved in the development and destabilization of atherosclerotic Plaques. It is unknown whether the SS distribution over Plaques with IPH differs from Plaques without IPH and whether SS is involved in Plaque progression/destabilization of Plaques with IPH. We compared the Plaque size, distribution and SS over Plaques with and without IPH in symptomatic patients. Methods: 38 patients with a recent (
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Shear stress and advanced atherosclerosis in human coronary arteries
Journal of Biomechanics, 2012Co-Authors: Frank J. H. Gijsen, Alina Van Der Giessen, Anton F. W. Van Der Steen, Jolanda J WentzelAbstract:Abstract The role of low and oscillating shear stress as a key factor for localizing early atherosclerotic Plaques is generally accepted. Once more advanced Plaques protrude into the lumen, the shear stress they are exposed to changes. The influence of shear stress on Plaque composition in advanced atherosclerosis is not fully understood. In this review, we discuss our recent studies on the relationship between shear stress and Plaque composition and the location of Plaque rupture in human coronary arteries. We have shown that elevated shear stress levels can be found over Plaques inducing only mild luminal narrowing and are not subjected to treatment. Regional exposure of certain Plaque regions to high shear stress is therefore a condition that will pertain for a prolonged period of time. We have also shown that in more advanced atherosclerosis the necrotic core experiences higher shear stress. Low shear stress Plaque regions can be found downstream of the Plaque and are stiffer. High shear stress Plaque regions can be found either at the upstream, shoulder or cap region of the Plaque and are softer. The Plaque regions with the highest strain levels are the regions that are exposed to the highest shear stress. The high shear stress Plaque regions are the only Plaque regions that get softer over time. Finally, high shear stress is also associated with the location of Plaque rupture in non-culprit lesion in human coronary arteries. Combining our findings with data from literature, we can conclude that advanced coronary Plaques grow in the distal regions. The distal Plaque regions are exposed to low shear stress, are stiffer and have a stable Plaque phenotype. The regions exposed to high shear stress are softer, and are associated with vulnerable Plaque features.
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current diagnostic modalities for vulnerable Plaque detection
Current Pharmaceutical Design, 2007Co-Authors: Johannes A Schaar, Patrick W Serruys, Evelyn Regar, Frits Mastik, Jolanda J Wentzel, Frank J. H. Gijsen, A F W Van Der StehenAbstract:Rupture of vulnerable Plaques is the main cause of acute coronary syndrome and myocardial infarction. Identification of vulnerable Plaques is therefore essential to enable the development of treatment modalities to stabilize such Plaques. Several diagnostic methods are currently tested to detect vulnerable Plaques. Angiography has a low discriminatory power to identify the vulnerable Plaque, but does provide information about the entire coronary tree and serves as guide for invasive imaging techniques and therapy. Angioscopy offers a direct visualization of the Plaque surface and intra- luminal structures like thrombi and tears. However, angioscopy is difficult to perform, invasive and only the proximal part of the vessels can be investigated. IVUS (intravascular ultrasound) provides some insight into the composition of Plaques. The detection of vulnerable Plaques is mainly based on series of case reports with a lack of prospectivity and follow- up. Palpography, an IVUS derived technique, reveals information, which is not recognizable in IVUS. It can differentiate between deformable and non-deformable tissue, which enables the technique to detect vulnerable Plaques with a positive predictive value. The clinical value of palpography is currently under investigation. Thermography assesses the temperature heterogeneity as an indicator of the metabolic state of the Plaque. A coincidence of temperature rise and localization of vulnerable Plaque was suggested. OCT (optical coherence tomography) can provide images with ultrahigh resolution utililizing the back-reflection of near-infrared light from optical interfaces in tissue. Drawbacks are the low penetration depth into tissue and the absorbance of light by blood. Raman spectroscopy can provide quantification about the molecular composition of the Plaque. Long acquisition time, the low penetration depth and light absorbance by blood limit the performance of the technique. Another light emitting technique is NIR (near infrared spectroscopy), which identifies lipid loaded Plaques and is tested currently in clinical trials. Non-invasive MRI (magnetic resonance imaging) and multislice spiral computed tomography (MSCT), with their excellent ability to identify lipid-rich tissue, have been utilized to characterize potentially vulnerable Plaques foremost in non-moving structures like the carotid arteries. Due to the resolution of the techniques small Plaque structure cannot be assessed. The role of non-invasive imaging in vulnerable Plaque detection is currently under investigation. Several invasive and non-invasive techniques are currently under development to assess the vulnerable Plaque. Most of the techniques show exiting features, but none have proven their value in an extensive in vivo validation and all have a lack of prospective data.
Johannes A Schaar - One of the best experts on this subject based on the ideXlab platform.
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current diagnostic modalities for vulnerable Plaque detection
Current Pharmaceutical Design, 2007Co-Authors: Johannes A Schaar, Patrick W Serruys, Evelyn Regar, Frits Mastik, Jolanda J Wentzel, Frank J. H. Gijsen, A F W Van Der StehenAbstract:Rupture of vulnerable Plaques is the main cause of acute coronary syndrome and myocardial infarction. Identification of vulnerable Plaques is therefore essential to enable the development of treatment modalities to stabilize such Plaques. Several diagnostic methods are currently tested to detect vulnerable Plaques. Angiography has a low discriminatory power to identify the vulnerable Plaque, but does provide information about the entire coronary tree and serves as guide for invasive imaging techniques and therapy. Angioscopy offers a direct visualization of the Plaque surface and intra- luminal structures like thrombi and tears. However, angioscopy is difficult to perform, invasive and only the proximal part of the vessels can be investigated. IVUS (intravascular ultrasound) provides some insight into the composition of Plaques. The detection of vulnerable Plaques is mainly based on series of case reports with a lack of prospectivity and follow- up. Palpography, an IVUS derived technique, reveals information, which is not recognizable in IVUS. It can differentiate between deformable and non-deformable tissue, which enables the technique to detect vulnerable Plaques with a positive predictive value. The clinical value of palpography is currently under investigation. Thermography assesses the temperature heterogeneity as an indicator of the metabolic state of the Plaque. A coincidence of temperature rise and localization of vulnerable Plaque was suggested. OCT (optical coherence tomography) can provide images with ultrahigh resolution utililizing the back-reflection of near-infrared light from optical interfaces in tissue. Drawbacks are the low penetration depth into tissue and the absorbance of light by blood. Raman spectroscopy can provide quantification about the molecular composition of the Plaque. Long acquisition time, the low penetration depth and light absorbance by blood limit the performance of the technique. Another light emitting technique is NIR (near infrared spectroscopy), which identifies lipid loaded Plaques and is tested currently in clinical trials. Non-invasive MRI (magnetic resonance imaging) and multislice spiral computed tomography (MSCT), with their excellent ability to identify lipid-rich tissue, have been utilized to characterize potentially vulnerable Plaques foremost in non-moving structures like the carotid arteries. Due to the resolution of the techniques small Plaque structure cannot be assessed. The role of non-invasive imaging in vulnerable Plaque detection is currently under investigation. Several invasive and non-invasive techniques are currently under development to assess the vulnerable Plaque. Most of the techniques show exiting features, but none have proven their value in an extensive in vivo validation and all have a lack of prospective data.
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characterizing vulnerable Plaque features with intravascular elastography
Circulation, 2003Co-Authors: Johannes A Schaar, Patrick W Serruys, Gerard Pasterkamp, Frits Mastik, Chaylendra Strijder, Chris L De Korte, Eric Boersma, Anton F. W. Van Der SteenAbstract:BACKGROUND: In vivo detection of vulnerable Plaques is presently limited by a lack of diagnostic tools. Intravascular ultrasound elastography is a new technique based on intravascular ultrasound and has the potential to differentiate between different Plaques phenotypes. However, the predictive value of intravascular elastography to detect vulnerable Plaques had not been studied. METHODS AND RESULTS: Postmortem coronary arteries were investigated with intravascular elastography and subsequently processed for histology. In histology, a vulnerable Plaque was defined as a Plaque consisting of a thin cap (<250 microm) with moderate to heavy macrophage infiltration and at least 40% of atheroma. In elastography, a vulnerable Plaque was defined as a Plaque with a high strain region at the surface with adjacent low strain regions. In 24 diseased coronary arteries, we studied 54 cross sections. In histology, 26 vulnerable Plaques and 28 nonvulnerable Plaques were found. Receiver operator characteristic analysis revealed a maximum predictive power for a strain value threshold of 1.26%. The area under the receiver operator characteristic curve was 0.85. The sensitivity was 88%, and the specificity was 89% to detect vulnerable Plaques. Linear regression showed high correlation between the strain in caps and the amount of macrophages (P<0.006) and an inverse relation between the amount of smooth muscle cells and strain (P<0.0001). Plaques, which are declared vulnerable in elastography, have a thinner cap than nonvulnerable Plaques (P<0.0001). CONCLUSIONS: Intravascular elastography has a high sensitivity and specificity to detect vulnerable Plaques in vitro.
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Characterizing Vulnerable Plaque Features With Intravascular Elastography
Circulation, 2003Co-Authors: Johannes A Schaar, Patrick W Serruys, Gerard Pasterkamp, Frits Mastik, Chaylendra Strijder, Chris L De Korte, Eric Boersma, Anton F. W. Van Der SteenAbstract:BACKGROUND: In vivo detection of vulnerable Plaques is presently limited by a lack of diagnostic tools. Intravascular ultrasound elastography is a new technique based on intravascular ultrasound and has the potential to differentiate between different Plaques phenotypes. However, the predictive value of intravascular elastography to detect vulnerable Plaques had not been studied. METHODS AND RESULTS: Postmortem coronary arteries were investigated with intravascular elastography and subsequently processed for histology. In histology, a vulnerable Plaque was defined as a Plaque consisting of a thin cap (
Anton F. W. Van Der Steen - One of the best experts on this subject based on the ideXlab platform.
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Shear stress and advanced atherosclerosis in human coronary arteries
Journal of Biomechanics, 2012Co-Authors: Frank J. H. Gijsen, Alina Van Der Giessen, Anton F. W. Van Der Steen, Jolanda J WentzelAbstract:Abstract The role of low and oscillating shear stress as a key factor for localizing early atherosclerotic Plaques is generally accepted. Once more advanced Plaques protrude into the lumen, the shear stress they are exposed to changes. The influence of shear stress on Plaque composition in advanced atherosclerosis is not fully understood. In this review, we discuss our recent studies on the relationship between shear stress and Plaque composition and the location of Plaque rupture in human coronary arteries. We have shown that elevated shear stress levels can be found over Plaques inducing only mild luminal narrowing and are not subjected to treatment. Regional exposure of certain Plaque regions to high shear stress is therefore a condition that will pertain for a prolonged period of time. We have also shown that in more advanced atherosclerosis the necrotic core experiences higher shear stress. Low shear stress Plaque regions can be found downstream of the Plaque and are stiffer. High shear stress Plaque regions can be found either at the upstream, shoulder or cap region of the Plaque and are softer. The Plaque regions with the highest strain levels are the regions that are exposed to the highest shear stress. The high shear stress Plaque regions are the only Plaque regions that get softer over time. Finally, high shear stress is also associated with the location of Plaque rupture in non-culprit lesion in human coronary arteries. Combining our findings with data from literature, we can conclude that advanced coronary Plaques grow in the distal regions. The distal Plaque regions are exposed to low shear stress, are stiffer and have a stable Plaque phenotype. The regions exposed to high shear stress are softer, and are associated with vulnerable Plaque features.
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characterizing vulnerable Plaque features with intravascular elastography
Circulation, 2003Co-Authors: Johannes A Schaar, Patrick W Serruys, Gerard Pasterkamp, Frits Mastik, Chaylendra Strijder, Chris L De Korte, Eric Boersma, Anton F. W. Van Der SteenAbstract:BACKGROUND: In vivo detection of vulnerable Plaques is presently limited by a lack of diagnostic tools. Intravascular ultrasound elastography is a new technique based on intravascular ultrasound and has the potential to differentiate between different Plaques phenotypes. However, the predictive value of intravascular elastography to detect vulnerable Plaques had not been studied. METHODS AND RESULTS: Postmortem coronary arteries were investigated with intravascular elastography and subsequently processed for histology. In histology, a vulnerable Plaque was defined as a Plaque consisting of a thin cap (<250 microm) with moderate to heavy macrophage infiltration and at least 40% of atheroma. In elastography, a vulnerable Plaque was defined as a Plaque with a high strain region at the surface with adjacent low strain regions. In 24 diseased coronary arteries, we studied 54 cross sections. In histology, 26 vulnerable Plaques and 28 nonvulnerable Plaques were found. Receiver operator characteristic analysis revealed a maximum predictive power for a strain value threshold of 1.26%. The area under the receiver operator characteristic curve was 0.85. The sensitivity was 88%, and the specificity was 89% to detect vulnerable Plaques. Linear regression showed high correlation between the strain in caps and the amount of macrophages (P<0.006) and an inverse relation between the amount of smooth muscle cells and strain (P<0.0001). Plaques, which are declared vulnerable in elastography, have a thinner cap than nonvulnerable Plaques (P<0.0001). CONCLUSIONS: Intravascular elastography has a high sensitivity and specificity to detect vulnerable Plaques in vitro.
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Characterizing Vulnerable Plaque Features With Intravascular Elastography
Circulation, 2003Co-Authors: Johannes A Schaar, Patrick W Serruys, Gerard Pasterkamp, Frits Mastik, Chaylendra Strijder, Chris L De Korte, Eric Boersma, Anton F. W. Van Der SteenAbstract:BACKGROUND: In vivo detection of vulnerable Plaques is presently limited by a lack of diagnostic tools. Intravascular ultrasound elastography is a new technique based on intravascular ultrasound and has the potential to differentiate between different Plaques phenotypes. However, the predictive value of intravascular elastography to detect vulnerable Plaques had not been studied. METHODS AND RESULTS: Postmortem coronary arteries were investigated with intravascular elastography and subsequently processed for histology. In histology, a vulnerable Plaque was defined as a Plaque consisting of a thin cap (
