OBJECTIVE: This study aimed to evaluate whether a high relative ADP induced aggregation (r-ADP-agg) is associated with an increased mortality in patients after coronary stent implantation. BACKGROUND: Several trials were not able to improve clinical outcome by adapting platelet inhibition in patients after coronary stent implantation and high platelet reactivity (HPR). Platelet monitoring is complex and conventional definition of adenosindiphosphate (ADP) induced aggregation alone might not transfer the whole picture of adequate platelet inhibition in vivo. METHODS: In a prospective single-centre observational trial multiple electrode aggregometry was performed in whole blood of patients after stent implantation. r-ADP-agg was defined as the ADP-thrombin receptor activating peptide ratio to reflect an individual degree of P2Y12 dependent platelet inhibition with a cut-off value for HPR of ≥ 50%. The primary end point was mortality. RESULTS: Follow-up was completed in 176 of 184 patients (96%) with a mean follow-up time of 3.7 years. 35 (20 %) patients revealed an r-ADP-agg ≥ 50%. An r-ADP-agg ≥ 50% was associated with an increased mortality [unadjusted hazard ratio (HR) 7.006 (2.561-19.17); p = 0.0001]. In a multivariable Cox regression analysis mortality was independently associated with an r-ADP-agg ≥ 50% [HR 3.324 (1.542-7.165); p = 0.0022], ACS-setting [HR 3.249 (1.322-7.989); p = 0.0102] and severely reduced LV function [HR 5.463 (2.098-14.26); p = 0.0005]. CONCLUSION: An r-ADP-agg ≥ 50% is associated with an increased mortality in patients after coronary stent implantation. Furthermore, r-ADP-agg might represent a better tool to predict clinical outcome than the conventional ADP induced platelet aggregation alone.
RCT Entities:
OBJECTIVE: This study aimed to evaluate whether a high relative ADP induced aggregation (r-ADP-agg) is associated with an increased mortality in patients after coronary stent implantation. BACKGROUND: Several trials were not able to improve clinical outcome by adapting platelet inhibition in patients after coronary stent implantation and high platelet reactivity (HPR). Platelet monitoring is complex and conventional definition of adenosindiphosphate (ADP) induced aggregation alone might not transfer the whole picture of adequate platelet inhibition in vivo. METHODS: In a prospective single-centre observational trial multiple electrode aggregometry was performed in whole blood of patients after stent implantation. r-ADP-agg was defined as the ADP-thrombin receptor activating peptide ratio to reflect an individual degree of P2Y12 dependent platelet inhibition with a cut-off value for HPR of ≥ 50%. The primary end point was mortality. RESULTS: Follow-up was completed in 176 of 184 patients (96%) with a mean follow-up time of 3.7 years. 35 (20 %) patients revealed an r-ADP-agg ≥ 50%. An r-ADP-agg ≥ 50% was associated with an increased mortality [unadjusted hazard ratio (HR) 7.006 (2.561-19.17); p = 0.0001]. In a multivariable Cox regression analysis mortality was independently associated with an r-ADP-agg ≥ 50% [HR 3.324 (1.542-7.165); p = 0.0022], ACS-setting [HR 3.249 (1.322-7.989); p = 0.0102] and severely reduced LV function [HR 5.463 (2.098-14.26); p = 0.0005]. CONCLUSION: An r-ADP-agg ≥ 50% is associated with an increased mortality in patients after coronary stent implantation. Furthermore, r-ADP-agg might represent a better tool to predict clinical outcome than the conventional ADP induced platelet aggregation alone.
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