Platelet dysfunction in acute coronary syndromes: diagnostic aspects and relation to angiographic patency

Thrombosis on top of an atheromatus unstable plaque is now accepted as the most common mechanism underlying acute ischemic syndromes (ACS), and in that process platelet dysfunction plays a central pivotal role through interaction with the vessel wall. The present study is an attempt to highlight and re-evaluate the role of platelets in the pathogenesis of ACS via the combined approach of aggregometry and flow cytometry techniques before applying any reperfusion therapy.

Methods

For this purpose we studied 44 individuals who were classified into three groups, group (1): 24 patients (pts) with acute myocardial infarction (AMI) (21 M, 3 F, mean age: 49 ± 11 years), group (2): 10 pts with unstable angina pectoris (UAP) (6 M, 4 F mean age: 49 ± 7 years), and group (3) 10 normal individuals who served as controls (9 M, 1 F, mean age: 27 ± 2 years). All cases were selected in such a way as to be free from gross liver and kidney impairment and were subjected to clinical examination, ECG and echocardiography. Coronary angiography was performed to assess the extent of CAD (the number of lesions in the coronary arteries with more than 50% stenosis as well as the patency of the infarct-related artery according to TIMI flow grading system).

Blood samples were withdrawn from pts on admission to the critical care department of Cairo University before any intervention. Specific lab investigations to assess the platelet activity included measurement of platelet aggregation with ADP, collagen, and ristocetin using the four channels chronolog aggregometer whereas the flow cytometry was employed to assess surface expression of glycoprotein IIb/IIIa receptors.

Results

Compared to healthy control subjects, pts with AMI and UAP had significantly greater aggregatory response to ADP (102%, 105% vs 75%, P < 0.001) to collagen (88%, 91% vs 74%, P < 0.001) and to ristocetin (77%, 90% vs 71%, P < 0.001) and substantially greater number of glycoprotein IIb receptors: (91, 90% vs 73%, P < 0.001) and gp IIIa (94, 96% vs 67%, P < 0.001) respectively. Platelet aggregatory response to ADP, collagen, and ristocetin had no significant correlation with the number of coronary vessels affected (P = 0.4), nor the patency across the culprit vessel (P = 0.33).

Conclusion

Compared to the healthy controls and prior to reperfusion therapy, pts with ACS exhibit a significant platelet aggregatory activity. Contrary to our expectations our data clearly show no correlation between platelet activity neither with the number of coronary vessels affected nor with different grades of TIMI flow.