Background
Systemic levels of myeloperoxidase (MPO) are a marker of inflammation and of plaque vulnerability in patients with acute coronary syndromes (ACS). We assessed the hypothesis that elevations in MPO levels may reflect different culprit lesion morphologies, such as plaque rupture or plaque erosion, with luminal thrombi.
Methods
Consecutive patients with ACS were enrolled. Optical coherence tomography was used to classify the culprit lesion as ruptured or eroded and detect luminal thrombus. Serum levels of MPO and of high-sensitivity C-reactive protein (CRP) were measured in the peripheral circulation on admission before coronary angiography. In addition, ruptured and eroded plaques with overlying thrombi from postmortem coronary specimens of sudden death victims underwent immunohistochemical analysis with primary antibodies against MPO. The density of MPO-positive cells in the plaque area (fibrous cap in ruptures or thrombus/plaque interface in erosions) and in thrombi was measured.
Methods
Consecutive patients with ACS were enrolled. Optical coherence tomography was used to classify the culprit lesion as ruptured or eroded and detect luminal thrombus. Serum levels of MPO and of high-sensitivity C-reactive protein (CRP) were measured in the peripheral circulation on admission before coronary angiography. In addition, ruptured and eroded plaques with overlying thrombi from postmortem coronary specimens of sudden death victims underwent immunohistochemical analysis with primary antibodies against MPO. The density of MPO-positive cells in the plaque area (fibrous cap in ruptures or thrombus/plaque interface in erosions) and in thrombi was measured.