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Lipoprotein-associated phospholipase A2, a marker of vascular inflammation and systemic vulnerability

Thomas Münzel, Tommaso Gori
DOI: http://dx.doi.org/10.1093/eurheartj/ehp311 2829-2831 First published online: 30 August 2009

As interventional cardiologists, we are sometimes prone to believe that plaque quantity, more than plaque biology, is a determinant of patients' prognosis. This concept is unfortunately challenged in daily practice, as accelerated progression of atherosclerosis, rupture of a plaque that was not critical at angiography, and/or dynamic phenomena such as spasm contribute to determine the patient's prognosis. That the extent and severity of coronary artery disease at angiography is a strong prognostic index for the risk of subsequent (cardio)vascular events is not under discussion. However, our understanding of plaque progression and instability remains far from complete. In line with this concept, Lavi et al. recently reported that the presence of an abnormal coronary reactivity to an endothelium-dependent stimulus identifies areas occupied by plaques with a larger necrotic core, i.e. at higher risk for rupture.1 In addition, a number of studies and anecdotal evidence have shown that endothelial dysfunction and/or oxidative stress, systemic or local, may predict disease progression/instability and overall patient prognosis.2 Although it needs to be acknowledged that the best therapeutic strategy for plaques that are histologically vulnerable but cause no severe stenosis at angiography remains unexplored, the search for new markers and techniques that help in detecting vulnerable plaques and vulnerable patients should be considered a priority of modern cardiology.

An effort in this direction is presented by Herrmann et al.3 who describe the important role of lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and activity, as measured at the level of carotid plaques, in predicting future cardiovascular events. This concept provides further support for the idea that atherosclerosis is a systemic disease, and that plaque activation in a given vascular district is associated with a global increased cardio- or cerebrovascular risk.

PLA2s belong to a superfamily that contains 15 separate groups and …

*Corresponding author. Tel: +49 6131 17 7250, Fax: +49 6131 17 6615, Email: tmuenzel{at}uni-mainz.de

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