Clopidogrel Pretreatment Associated with Improved Outcomes for Patients Undergoing Primary PCI for STEMI

NEW ORLEANS, La—At ACC.11, the American College of Cardiology’s 60th Annual Scientific Sessions, study investigators reported that clopidogrel pretreatment was associated with a significant reduction in platelet ADP induced aggregation in primary percutaneous intervention (PPCI) for STEMI, which was associated with improved myocardial reperfusion. Small retrospective studies have suggested clinical benefit for clopidogrel pretreatment in the setting of PPCI in patients with STEMI. However, the antiplatelet effect of pretreatment with clopidogrel prior to PPCI, during the narrow “door to balloon” timeframe, in patients presenting with STEMI had yet to be evaluated.

Roy Beigel, MD from Sheba Medical Center, Tel Hashomer, Israel, and colleagues prospectively assessed platelet function tests (using light transmitted aggregometry) in 31 patients presenting with STEMI. All patients were treated with a clopidogrel loading dose of 600mg upon admission. Blood was drawn for ADP-induced aggregation prior to clopidogrel loading, at PPCI, and at 72 hours later. In addition, an ECG (recorded at presentation and after PPCI evaluating ST segment resolution) was assessed as a marker for myocardial reperfusion.

Baseline ADP-induced aggregation was 81 ± 7%. The mean clopidogrel to balloon time was 50 ± 18 minutes, during which ADP-induced aggregation was reduced to 76 ± 10% (P=0.0096). A positive response to clopidogrel was defined as >10% reduction in ADP-induced aggregation or <70% ADP-induced aggregation with 19% and 26% of the patients meeting these definitions, respectively. ADP-induced aggregation was further reduced 72 hours later to 50 ± 18% (P<0.001 to baseline). Early ST segment resolution of >50% upon ECG was associated with achieving lower ADP induced aggregation at PPCI (82 ± 6.1 vs. 74 ± 10; P=0.029). In patients undergoing PPCI for STEMI, clopidogrel pretreatment was associated with a significant but modest reduction in platelet ADP induced aggregation. See Table.

Approximately one-third of patients achieved adequate early platelet inhibition (ADP induced PA ≤70%) at PPCI. This reduction may account for the previously shown clinical benefit of clopidogrel pretreatment in patients undergoing PPCI. Early responders had both lower baseline ADP and a greater actual response to clopidogrel at PCI. Early responders were more likely to show early ST-resolution immediately post-PPCI, which suggested improved myocardial perfusion. Investigators stated that the use of newer ADP blockers with a more rapid onset of action and potent effect may prove even greater benefit in patients undergoing PPCI.