A large clinical-genetic study has unravelled novel genotype-to-phenotype correlations in HCM and DCM which warrant future investigation of both the underlying mechanisms and the prognostic use.
Background:
It could be shown in various investigations that a reduced response to clopidogrel (Clo) after PCI and stent placement is associated with a significantly worse cardiovascular outcome. At the moment no generally accepted normal values for clopidogrel-response exist.
Methods:
The clopidogrel-response was investigated in 2847 patients (mean age 63,5 +/− 10 years, 67% male, 33% female) undergoing PCI with stent placement in a prospective clinical study over 34 months (elective PCI by chronic stable angina: n=1907 (67%) and acute PCI by acute coronary syndrome (STEMI, NSTEMI): n=940 (33%). The platelet aggregation was analysed conventionelly using an aggregometer 6 –24 hours after application of 600 mg clopidogrel (loading dose) by adding 20 μmol/L adenosine diphosphate (ADP) to citrate plasma (Aggregometer PAP 4 MOELAB, Hilden, Germany).
Results:
In a follow-up period of 30 days after the intervention a subacute stent thrombosis occured in n=51 pts (1,8%). In n=46 (90%) of these patients the ADP-induced platelet final aggregation after Clo (post-treated) was >30% compared with the baseline of each patient without Clo (pre-treated). This corresponds to a platelet inhibition <70%. Taking this value as “cutoff value” results in a responder rate of 68,7% (n=1958) and a hyporesponder rate of 31,2% (n=889) of the entirety of patients. 5,2% (n=46) of the hyporesponders developed a subacute stent thrombosis.
Conclusions:
Clopidogrel (Clo) hyporesponders have a significantly increased risk of developing a subacute stent thrombosis after coronary stent placement. 90% of these endangered patients are identified with a cutoff value of platelet inhibition <70% respectively final aggregation > 30% showing the importance of periinterventional evaluation of the Clo-response status of each patient. If these patients would profit from an intensified antiplatelet strategy (for example increased doses of Clo) should be investigated in further studies.
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