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

Secretory type-II phospholipase A(2) (sPLA(2)-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 sPLA(2)-II in the atherosclerotic plaque facilitates an inflammatory response to induce plaque instability or rupture. We have studied the presence of sPLA(2)-II in culprit lesions in the coronary arteries of patients with acute myocardial infarction (AMI) or angina pectoris.

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 sPLA(2)-II, macrophages and smooth muscle cells. Immunopositive areas were calculated as a percentage of the total tissue area using image analysis software.

Intracellular sPLA(2)-II was found in atherosclerotic lesions in the macrophages of the intima as well as in vascular smooth muscle cells. Next to this, extracellular sPLA(2)-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).

Extracellular sPLA(2)-II is more abundantly present in atherosclerotic culprit lesions that have led to myocardial infarction. This suggests a role for extracellular sPLA(2)-II in the development of complications of atherosclerotic lesions in coronary arteries.