PMID- 19081397
OWN - NLM
STAT- MEDLINE
DCOM- 20090122
LR  - 20181201
IS  - 1097-6744 (Electronic)
IS  - 0002-8703 (Linking)
VI  - 157
IP  - 1
DP  - 2009 Jan
TI  - Randomized trial comparing 600- with 300-mg loading dose of clopidogrel in 
      patients with non-ST elevation acute coronary syndrome undergoing percutaneous 
      coronary intervention: results of the Platelet Responsiveness to Aspirin and 
      Clopidogrel and Troponin Increment after Coronary intervention in Acute coronary 
      Lesions (PRACTICAL) Trial.
PG  - 60.e1-9
LID - 10.1016/j.ahj.2008.09.024 [doi]
AB  - BACKGROUND: There is uncertainty about the benefit of a higher loading dose (LD) 
      of clopidogrel in patients with non-ST elevation acute coronary syndrome 
      (NSTEACS) undergoing early percutaneous coronary intervention (PCI). METHODS: We 
      compared the effects of a 600- versus a 300-mg LD of clopidogrel on inhibition of 
      platelet aggregation, myonecrosis, and clinical outcomes in patients with NSTEACS 
      undergoing an early invasive management strategy. Patients with NSTEACS (n = 256, 
      mean age 63 years, 81.6% elevated troponin) without thienopyridine for at least 7 
      days were randomized to receive 600- or 300-mg LD of clopidogrel. Percutaneous 
      coronary intervention was performed in 140 patients, with glycoprotein IIb/IIIa 
      inhibitor use in 68.6%. Adenosine diphosphate (ADP)-induced platelet aggregation 
      was measured by optical platelet aggregometry immediately before coronary 
      angiography. RESULTS: Post-PCI myonecrosis was defined as a next-day troponin I 
      greater than 5 times the upper limit of reference range and greater than baseline 
      levels. Clopidogrel 600-mg LD compared with 300-mg LD was associated with 
      significantly reduced ADP-induced platelet aggregation (49.7% vs 55.7% with ADP 
      20 micromol/L) but did not reduce post-PCI myonecrosis or adverse clinical 
      outcomes to 6 months. There was no association between preprocedural platelet 
      aggregation and outcome. CONCLUSIONS: These data confirm a modest incremental 
      antiplatelet effect of a 600-mg clopidogrel LD compared with 300-mg LD but 
      provide no support for a clinical benefit in patients with NSTEACS managed with 
      an early invasive strategy including a high rate (69%) of glycoprotein IIb/IIIa 
      inhibitor use during PCI.
FAU - Yong, Gerald
AU  - Yong G
AD  - Royal Perth Hospital, Perth, Western Australia, Australia.
FAU - Rankin, Jamie
AU  - Rankin J
FAU - Ferguson, Louise
AU  - Ferguson L
FAU - Thom, Jim
AU  - Thom J
FAU - French, John
AU  - French J
FAU - Brieger, David
AU  - Brieger D
FAU - Chew, Derek P
AU  - Chew DP
FAU - Dick, Ron
AU  - Dick R
FAU - Eccleston, David
AU  - Eccleston D
FAU - Hockings, Bernard
AU  - Hockings B
FAU - Walters, Darren
AU  - Walters D
FAU - Whelan, Alan
AU  - Whelan A
FAU - Eikelboom, John W
AU  - Eikelboom JW
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 0 (Troponin)
RN  - A74586SNO7 (Clopidogrel)
RN  - OM90ZUW7M1 (Ticlopidine)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Acute Coronary Syndrome/blood/*therapy
MH  - *Angioplasty, Balloon, Coronary
MH  - Aspirin/therapeutic use
MH  - Blood Platelets/drug effects/physiology
MH  - Clopidogrel
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardium/pathology
MH  - Necrosis
MH  - Platelet Aggregation Inhibitors/*administration & dosage
MH  - Ticlopidine/administration & dosage/*analogs & derivatives
MH  - Troponin/blood
EDAT- 2008/12/17 09:00
MHDA- 2009/01/23 09:00
CRDT- 2008/12/17 09:00
PHST- 2008/06/06 00:00 [received]
PHST- 2008/09/29 00:00 [accepted]
PHST- 2008/12/17 09:00 [entrez]
PHST- 2008/12/17 09:00 [pubmed]
PHST- 2009/01/23 09:00 [medline]
AID - S0002-8703(08)00831-4 [pii]
AID - 10.1016/j.ahj.2008.09.024 [doi]
PST - ppublish
SO  - Am Heart J. 2009 Jan;157(1):60.e1-9. doi: 10.1016/j.ahj.2008.09.024.