PMID- 11156725
OWN - NLM
STAT- MEDLINE
DCOM- 20010208
LR  - 20121115
IS  - 1042-3931 (Print)
IS  - 1042-3931 (Linking)
VI  - 12 Suppl E
DP  - 2000 Dec
TI  - The scientific basis for combined platelet and thrombin-directed pharmacotherapy 
      in acute coronary syndromes.
PG  - E19-24;discussion E25-8
AB  - There exists incontrovertible scientific evidence that vascular endothelial cell 
      dysfunction and atheromatous plaque disruption are causative pathobiologic events 
      governing the clinical expression of disease in humans with coronary 
      arteriosclerosis. A comprehensive understanding of vascular biology, platelet 
      behavior, and coagulation protein bioamplification sequences forms the scientific 
      basis for pharmacotherapy in acute coronary syndromes (ACS), and identifies the 
      platelet as an attractive target. The three Food and Drug Administration-approved 
      glycoprotein (GP) IIb/IIIa antagonists effectively prevent platelet aggregation. 
      In vitro experiments also showed a dose-dependent decrease in prothrombinase 
      activity and thrombin generation revealing that the GP IIb/IIIa antagonists 
      possess anticoagulant properties as well. Combination pharmacotherapy in ACS is 
      supported by the contribution of platelets and coagulation proteins to coronary 
      artery thrombosis. While unfractionated heparin (UFH) is commonly used 
      conjunctively with GP IIb/IIIa antagonists, several inherent limitations exist, 
      including unpredictable pharmacodynamics, no established therapeutic standards, 
      and the fact that the use of UFH has been associated with platelet activation. 
      Low-molecular-weight heparin preparations offer several potential advantages over 
      UFH: a greater degree of Xa inhibition; more predictable pharmacokinetic profile; 
      the absence of significant platelet activation; and the confirmation of clinical 
      superiority in several large-scale clinical trials. Randomized trials will be 
      required to establish the full clinical impact of combined pharmacotherapy in 
      ACS.
FAU - Becker, R C
AU  - Becker RC
AD  - Cardiovascular Thrombosis Research Center, Division of Cardiovascular Medicine, 
      University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 
      01655, USA. becker@ummhc.org
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Invasive Cardiol
JT  - The Journal of invasive cardiology
JID - 8917477
RN  - 0 (Anticoagulants)
RN  - 0 (Heparin, Low-Molecular-Weight)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 0 (Platelet Glycoprotein GPIIb-IIIa Complex)
RN  - EC 3.4.21.5 (Thrombin)
SB  - IM
MH  - Acute Disease
MH  - Anticoagulants/*therapeutic use
MH  - Blood Platelets/drug effects
MH  - Clinical Trials as Topic/methods
MH  - Coronary Disease/blood/*drug therapy
MH  - Drug Therapy, Combination
MH  - Heparin, Low-Molecular-Weight/therapeutic use
MH  - Humans
MH  - Platelet Aggregation/*drug effects
MH  - Platelet Aggregation Inhibitors/*therapeutic use
MH  - Platelet Glycoprotein GPIIb-IIIa Complex/antagonists & inhibitors
MH  - *Research Design
MH  - Thrombin/*antagonists & inhibitors
RF  - 35
EDAT- 2001/01/13 11:00
MHDA- 2001/03/03 10:01
CRDT- 2001/01/13 11:00
PHST- 2001/01/13 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2001/01/13 11:00 [entrez]
PST - ppublish
SO  - J Invasive Cardiol. 2000 Dec;12 Suppl E:E19-24;discussion E25-8.