Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Anton Horrevoets
The session approached the role of biomechanical factors as the driving force for atherosclerosis from different angles, spanning from molecular mechanisms to clinical outcome trials.Dr Brenda Kwak started the session by introducing the close link between blood flow patterns and the cellular aspects of inflammatory vessel wall pathology. Atheroma develops at bends and bifurcations of the arterial tree where, due to turbulence, the shear stress is low, progressing from early fatty lesions to thin cap fibrous atheroma and plaque rupture. Several biomechanically sensitive factors of the endothelium were introduced, including the atheroprotective transcription factor KLF2. KLF2 drives expression of atheroprotective genes while suppressing NFkB-dependent proinflammatory gene expression.Next, she zoomed in on the connexins, which, via formation of gap junctions, connect all endothelial cells in a monolayer, and are responsible for the exchange of small signalling molecules between the individual cells. Based on her recent data using cell and animal models, she convincingly showed that Cx37 is specifically associated with healthy endothelial cells but is lacking in lesions, and is a novel specific target of KLF2.This lack of Cx37 is associated with an inhibition of cell-cell communication leading to desynchronization of the endothelial cells.Dr Peter Stone expanded on the role of shear stress during atheroma development by introducing the concept of excessive expansive remodelling, which leads to continued low shear stress despite growth of the plaque. This creates a vicious circle of low shear stress, inflammatory cell influx producing expression of matrix degrading enzymes like MMP (metalloproteinases) and cathepsins which further weaken the vessel wall, leading to further expansive remodelling and weakening of the fibrous cap.Next, results from the PREDICTION trial were presented, designed to follow the natural history of plaque development in 506 ACS patients as assessed by IVUS (Intra vascular ultrasound) from time of intervention to 12 months follow-up. Results show that baseline low shear stress regions in coronary vessels indeed show progressive atherosclerosis and excessive expansive remodelling over the 12 months after the acute treatment, and that these baseline levels of shear stress reliably predict the adverse clinical outcome of the patients.
Dr Frank Gijsen introduced the different stages of atheroma development in relation to wall shear stress. Whereas stage 1 is dominated by low shear stress leading to lipid influx, inflammation and outward remodelling, during stage 2 the plaque becomes too big and starts the occlude the lumen via inward remodelling leading to an increase in shear stress. Results were presented on in vivo modelling of a shear stress and wall strain map of the coronary artery wall and its bifurcations after combined measurements using IVUS and multislice CT to establish wall thickness and computational fluid dynamics. Unexpectedly, the majority of patient lesions were associated with high shear regions that exhibited high strain. As high strain indicates soft tissue with inflammation and matrix degradation, it serves as a surrogate marker for plaque composition and indicates potentially vulnerable plaque.Next, shear and strain were related to sites of plaque rupture in relation to the topography of the plaque and its shear gradients. Sites of rupture were shown to correlate to the high shear regions. Based on these data, he concluded that whereas low shear stress might be the driving force for plaque initiation and initial progression, in stage 2 the clinical outcome is actually predicted by the high shear regions.
Dr Rob Krams introduced new technology to establish the molecular mechanisms underlying mechanosensing using in vitro models, pharmacological and genetic interventions and his mouse carotid artery model, which allows to specifically and spatially determine shear profiles through micro-CT and to link these to molecular events in the vessel wall. Using a systems biology approach, he hopes to unravel this multicomponent system to come to a unifying theory on the relation of biomechanics and atherosclerosis.
Overall, this session proved very fruitful as the complementary approaches of the 4 speakers start to unravel the multiple aspects of the relation between biomechanics and atheroma development from molecules to cells to vessel wall to patient outcome.
Blood flow patterns control atherosclerotic plaque development