Abstract 11630: Platelet Monocyte Aggregates Correlate with Indices of Microvascular Dysfunction (Coronary Wedge Pressure and Index of Microvascular Resistance) During PCI for Stable Angina and Non-ST Segment Elevation Acute Coronary Syndrome
Background: Microvascular dysfunction is associated with adverse outcome in acute coronary syndrome (ACS). The role of inflammation in ACS is pivotal. Although platelet monocyte interaction and platelet monocyte aggregates (PMA) formation is a physiological process, in the presence of activated platelets, p-selectin positive (CD62+) PMA may be directly involved in the pathophysiology of intracoronary inflammation and microvascular dysfunction in ACS. Aim: Investigate the relationship between microvascular dysfunction and PMA expression in stable angina and non-ST elevation ACS.
Methods: Microvascular dysfunction was assessed by measuring the coronary wedge pressure (CwP) and the index of microvascular resistance (IMR) in 7 patients with stable angina undergoing elective PCI and 7 patients with ACS undergoing non-elective PCI. Blood samples were taken from the coronary artery (distal to the culprit lesion), aorta and the right atrium for PMA estimation using flow cytometry. Total PMA were expressed as percentage of the total monocyte count. CD62+ PMA were expressed as percentage of total PMA.
Results: CwP was higher in patients with ACS [Mean(SD) 47(17.2)] compared with stable angina patients [Mean(SD) 22.7(9.4) p= 0.007]. IMR was also higher in patients with ACS [Mean(SD) 24(12.9)] compared with patients with stable angina [Mean(SD) 19.7(5.3) p=0.4]. Total PMA were non-significantly higher in patients with ACS [Mean(SD) 13.5(4.7)] compared with stable angina [Mean(SD) 10.9(4.3) p=0.09]. CD62+ PMA were significantly higher in patients with ACS [Mean(SD) 23.3(13.7)] compared with stable angina [Mean(SD) 13.7(5.1) p=0.01]. CwP correlated positively with total PMA (r²=0.3; p=0.01) and with CD62+ PMA (r²=0.5; p=0.007) in ACS but not stable angina. However, IMR correlated positively with total PMA in both stable angina (r²=0.2; p=0.02) and ACS (r²=0.2; p=0.07).
Conclusions: PMA are elevated in both stable coronary disease and ACS but elevated CD62+ PMA is a hallmark of ACS. PMA correlate with measured microvascular dysfunction during PCI in stable angina and ACS patients. This study supports the hypothesis that PMA formation may be important determinants of platelet activation, inflammation and microvascular dysfunction in coronary disease
- © 2011 by American Heart Association, Inc.