Local haemodynamic forces have been recognised as an instigator of atherosclerotic disease progression and appear to regulate vessel wall response after percutaneous coronary interventions (PCI). Cumulative data indicates that low endothelial shear stress (ESS) trigger mechanotransduction pathways that promote the formation of high-risk plaques in native and stented segments, while high shear stress appear to lead to plaque destabilisation and rupture. In parallel recent evidence has underscored the implications of plaque structural stress (PSS) on plaque biology showing that it regulates metaloproteinase expression and smooth muscle cell activity, while robust data suggests that PSS is the main instigator of plaque rupture.
Advances in coronary modelling, software design and computer capabilities have recently enabled processing of large imaging data, fast computational modelling and assessment at scale of the role of the local haemodynamic forces on clinical events. ESS and PSS have been recognised as predictors of cardiovascular events in stented and native segments while in silico studies have underscored the potential value of computational modelling in predicting procedural results in complex lesions. These findings have attracted the interest of the scientific community and an effort has been made over the recent years to expedite and simplify the analysis, quantify in real time the local haemodynamic forces distribution and use this information to stratify more accurately cardiovascular risk and improve clinical outcomes.
This Research Topics aims to focus on the advances in computational modelling and on the role of the local haemodynamic forces on atherosclerotic evolution, vulnerable plaque detection, risk stratification and PCI planning.
This issue is to encourage debates about the potential value of the ESS and PSS quantification in the clinical practice and research. We invite clinicians and biomedical engineers to present new methodologies and ex-vivo, animal and human studies that evaluate the implications of the local haemodynamic forces on atherosclerotic evolution and plaque destabilisation and examine their efficacy in predicting high-risk patients and lesions and the vessel wall response to interventional therapies.
Potential topics include but are not limited to the following:
1) Technical developments for fast computational fluid dynamic analyses.
2) Novel methodologies for ESS and PSS quantification.
3) Ex-vivo studies assessing the implications of the local haemodynamic forces on atherosclerotic disease progression.
4) Serial invasive or non-invasive imaging studies in animal and humans examining the interplay between local haemodynamic forces and plaque evolution.
5) Outcome studies evaluating the prognostic efficacy of ESS and PSS.
6) Computational fluid dynamic analyses evaluating the role of the local haemodynamic forces in stent failure.
7) Computational modelling studies that aim to predict vessel wall response during PCI.
Local haemodynamic forces have been recognised as an instigator of atherosclerotic disease progression and appear to regulate vessel wall response after percutaneous coronary interventions (PCI). Cumulative data indicates that low endothelial shear stress (ESS) trigger mechanotransduction pathways that promote the formation of high-risk plaques in native and stented segments, while high shear stress appear to lead to plaque destabilisation and rupture. In parallel recent evidence has underscored the implications of plaque structural stress (PSS) on plaque biology showing that it regulates metaloproteinase expression and smooth muscle cell activity, while robust data suggests that PSS is the main instigator of plaque rupture.
Advances in coronary modelling, software design and computer capabilities have recently enabled processing of large imaging data, fast computational modelling and assessment at scale of the role of the local haemodynamic forces on clinical events. ESS and PSS have been recognised as predictors of cardiovascular events in stented and native segments while in silico studies have underscored the potential value of computational modelling in predicting procedural results in complex lesions. These findings have attracted the interest of the scientific community and an effort has been made over the recent years to expedite and simplify the analysis, quantify in real time the local haemodynamic forces distribution and use this information to stratify more accurately cardiovascular risk and improve clinical outcomes.
This Research Topics aims to focus on the advances in computational modelling and on the role of the local haemodynamic forces on atherosclerotic evolution, vulnerable plaque detection, risk stratification and PCI planning.
This issue is to encourage debates about the potential value of the ESS and PSS quantification in the clinical practice and research. We invite clinicians and biomedical engineers to present new methodologies and ex-vivo, animal and human studies that evaluate the implications of the local haemodynamic forces on atherosclerotic evolution and plaque destabilisation and examine their efficacy in predicting high-risk patients and lesions and the vessel wall response to interventional therapies.
Potential topics include but are not limited to the following:
1) Technical developments for fast computational fluid dynamic analyses.
2) Novel methodologies for ESS and PSS quantification.
3) Ex-vivo studies assessing the implications of the local haemodynamic forces on atherosclerotic disease progression.
4) Serial invasive or non-invasive imaging studies in animal and humans examining the interplay between local haemodynamic forces and plaque evolution.
5) Outcome studies evaluating the prognostic efficacy of ESS and PSS.
6) Computational fluid dynamic analyses evaluating the role of the local haemodynamic forces in stent failure.
7) Computational modelling studies that aim to predict vessel wall response during PCI.
