TY - JOUR
T1 - Stabilisation of atherosclerotic plaques position paper of the european society of cardiology (ESC) working group on atherosclerosis and vascular biology
AU - Ylä-Herttuala, Seppo
AU - Bentzon, Jacob Fog
AU - Daemen, Mat
AU - Falk, Erling
AU - Garcia-Garcia, Hector M.
AU - Herrmann, Joerg
AU - Hoefer, Imo
AU - Wouter Jukema, J.
AU - Krams, Rob
AU - Kwak, Brenda R.
AU - Marx, Nikolaus
AU - Naruszewicz, Marek
AU - Newby, Andrew
AU - Pasterkamp, Gerard
AU - Serruys, Patrick W.J.C.
AU - Waltenberger, Johannes
AU - Weber, Christian
AU - Tokgözoglu, Lale
PY - 2011/7
Y1 - 2011/7
N2 - Plaque rupture and subsequent thrombotic occlusion of the coronary arteryaccount for as many as three quarters of myocardial infarctions. Theconcept of plaque stabilisation emerged about 20 years ago to explainthe discrepancy between the reduction of cardiovascular events in patientsreceiving lipid lowering therapy and the small decrease seen in angiographicevaluation of atherosclerosis. Since then, the concept of a vulnerableplaque has received a lot of attention in basic and clinical researchleading to a better understanding of the pathophysiology of thevulnerable plaque and acute coronary syndromes. From pathological andclinical observations, plaques that have recently ruptured have thin fibrouscaps, large lipid cores, exhibit outward remodelling and invasion byvasa vasorum. Ruptured plaques are also focally inflamed and this maybe a common denominator of the other pathological features. Plaqueswith similar characteristics, but which have not yet ruptured, are believ ed to be vulnerable to rupture. Experimental studies strongly support thevalidity of anti-inflammatory approaches to promote plaque stability. Unfortunately,reliable non-invasive methods for imaging and detection ofsuch plaques are not yet readily available. There is a strong biologicalbasis and supportive clinical evidence that low-density lipoprotein loweringwith statins is useful for the stabilisation of vulnerable plaques. Thereis also some clinical evidence for the usefulness of antiplatelet agents,beta blockers and renin-angiotensin-aldosterone system inhibitors forplaque stabilisation. Determining the causes of plaque rupture and designingdiagnostics and interventions to prevent them are urgent prioritiesfor current basic and clinical research in cardiovascular area.
AB - Plaque rupture and subsequent thrombotic occlusion of the coronary arteryaccount for as many as three quarters of myocardial infarctions. Theconcept of plaque stabilisation emerged about 20 years ago to explainthe discrepancy between the reduction of cardiovascular events in patientsreceiving lipid lowering therapy and the small decrease seen in angiographicevaluation of atherosclerosis. Since then, the concept of a vulnerableplaque has received a lot of attention in basic and clinical researchleading to a better understanding of the pathophysiology of thevulnerable plaque and acute coronary syndromes. From pathological andclinical observations, plaques that have recently ruptured have thin fibrouscaps, large lipid cores, exhibit outward remodelling and invasion byvasa vasorum. Ruptured plaques are also focally inflamed and this maybe a common denominator of the other pathological features. Plaqueswith similar characteristics, but which have not yet ruptured, are believ ed to be vulnerable to rupture. Experimental studies strongly support thevalidity of anti-inflammatory approaches to promote plaque stability. Unfortunately,reliable non-invasive methods for imaging and detection ofsuch plaques are not yet readily available. There is a strong biologicalbasis and supportive clinical evidence that low-density lipoprotein loweringwith statins is useful for the stabilisation of vulnerable plaques. Thereis also some clinical evidence for the usefulness of antiplatelet agents,beta blockers and renin-angiotensin-aldosterone system inhibitors forplaque stabilisation. Determining the causes of plaque rupture and designingdiagnostics and interventions to prevent them are urgent prioritiesfor current basic and clinical research in cardiovascular area.
KW - Atherosclerosis
KW - Imaging
KW - Plaque stabilisation
KW - Treatment
KW - Vulnerable plaques
UR - http://www.scopus.com/inward/record.url?scp=79960048075&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79960048075&partnerID=8YFLogxK
U2 - 10.1160/TH10-12-0784
DO - 10.1160/TH10-12-0784
M3 - Article
C2 - 21670845
AN - SCOPUS:79960048075
VL - 106
SP - 1
EP - 19
JO - Thrombosis and Haemostasis
JF - Thrombosis and Haemostasis
SN - 0340-6245
IS - 1
ER -