Secretory type II phospholipase A2 in culprit coronary lesions is associated with myocardial infarction.

Background Secretory type-II phospholipase A₂ (sPLA₂-II) is a cardiovascular risk marker since higher levels of this acute phase protein imply an increased risk for coronary artery disease. Moreover, it is hypothesized that local activity of sPLA₂-II in the atherosclerotic plaque facilitates an inflammatory response to induce plaque instability or rupture. We have studied the presence of sPLA₂-II in culprit lesions in the coronary arteries of patients with acute myocardial infarction (AMI) or angina pectoris. Materials and methods We performed a histological examination of culprit lesions in 41 patients with stable (SAP) or unstable angina pectoris (UAP), or AMI using directed coronary atherectomy (DCA). Frozen slides were analysed immuno-histochemically for the presence of sPLA₂-II, macrophages and smooth muscle cells. Immunopositive areas were calculated as a percentage of the total tissue area using image analysis software. Results Intracellular sPLA₂-II was found in atherosclerotic lesions in the macrophages of the intima as well as in vascular smooth muscle cells. Next to this, extracellular sPLA₂-II depositions were also found. These depositions were significantly more extensive in patients with AMI, i.e. 26%^median[6%^{25th(percentile)}–44%^{75th(percentile)}] of the intima area, than in patients with SAP 0%^median (0%^25th–10%^75th; P = 0·013) or UAP 0%^median (0%^25th–0%^75th; P = 0·04). Conclusions Extracellular sPLA₂-II is more abundantly present in atherosclerotic culprit lesions that have led to myocardial infarction. This suggests a role for extracellular sPLA₂-II in the development of complications of atherosclerotic lesions in coronary arteries. [ABSTRACT FROM AUTHOR]