PMID- 17917621
OWN - NLM
STAT- MEDLINE
DCOM- 20071025
LR  - 20201209
IS  - 1530-6550 (Print)
IS  - 1530-6550 (Linking)
VI  - 8 Suppl 3
DP  - 2007
TI  - Anticoagulation for acute coronary syndromes: from heparin to direct thrombin 
      inhibitors.
PG  - S9-17
AB  - The anticoagulant properties of heparin were discovered in 1916, and by the 1930s 
      researchers were evaluating its therapeutic use in clinical trials. Treatment of 
      unstable angina with unfractionated heparin (UFH), in addition to aspirin, was 
      introduced into clinical practice in the early 1980s. UFH was combined with 
      aspirin to suppress thrombin propagation and fibrin formation in patients 
      presenting with acute coronary syndromes (ACS) or patients undergoing 
      percutaneous coronary intervention (PCI). However, UFH stimulates platelets, 
      leading to both activation and aggregation, which may further promote clot 
      formation. Clinical trials have demonstrated that newer agents, such as the 
      low-molecular-weight heparins (LMWHs), are superior to UFH for medical management 
      of unstable angina or non-ST-segment elevation myocardial infarction. 
      Increasingly, the LMWHs have been used as the anticoagulant of choice for 
      patients presenting with ACS. For patients undergoing PCI, LMWH provides no 
      sub-stantial benefit over UFH for anticoagulation; however, direct thrombin 
      inhibitors (DTIs) have demonstrated safety and efficacy in this setting. UFH is 
      likely to be replaced by more effective and safer antithrombin agents, such as 
      DTIs. DTIs have antiplatelet effects, anticoagulant action, and most do not bind 
      to plasma proteins, thereby providing a more consistent dose-response effect than 
      UFH. The FDA has approved 4 parenteral DTIs for various indications: lepirudin, 
      argatroban, bivalirudin, and desirudin. The antiplatelet, anticoagulant, and 
      pharmacokinetic properties of bivalirudin support its use as the anticoagulant of 
      choice for both lower- and higher-risk patients, including those undergoing PCI.
FAU - Lepor, Norman E
AU  - Lepor NE
AD  - David Geffen School of Medicine at the University of California at Los Angeles, 
      Cedars-Sinai Medical Center, Los Angeles, California, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Singapore
TA  - Rev Cardiovasc Med
JT  - Reviews in cardiovascular medicine
JID - 100960007
RN  - 0 (Anticoagulants)
RN  - 0 (Heparin, Low-Molecular-Weight)
RN  - 0 (Hirudins)
RN  - 0 (Peptide Fragments)
RN  - 0 (Pipecolic Acids)
RN  - 0 (Polysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Sulfonamides)
RN  - 9005-49-6 (Heparin)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 3.4.21.5 (Thrombin)
RN  - IY90U61Z3S (argatroban)
RN  - J177FOW5JL (Fondaparinux)
RN  - TN9BEX005G (bivalirudin)
RN  - U0JZ726775 (desirudin)
RN  - Y43GF64R34 (lepirudin)
SB  - IM
MH  - Acute Disease
MH  - Angina Pectoris/blood/drug therapy/*etiology
MH  - Angina, Unstable/blood/complications/diagnosis/*drug therapy
MH  - Angioplasty, Balloon, Coronary/adverse effects
MH  - Anticoagulants/adverse effects/chemistry/*therapeutic use
MH  - Arginine/analogs & derivatives
MH  - Fondaparinux
MH  - Hemorrhage/chemically induced
MH  - Heparin/adverse effects/chemistry/*therapeutic use
MH  - Heparin, Low-Molecular-Weight/therapeutic use
MH  - Hirudins
MH  - Humans
MH  - Models, Molecular
MH  - Molecular Structure
MH  - Myocardial Ischemia/blood/complications/diagnosis/*drug therapy
MH  - Peptide Fragments/therapeutic use
MH  - Pipecolic Acids/therapeutic use
MH  - Platelet Activation/drug effects
MH  - Polysaccharides/therapeutic use
MH  - Recombinant Proteins/therapeutic use
MH  - Sulfonamides
MH  - Syndrome
MH  - Thrombin/*antagonists & inhibitors
MH  - Thrombosis/etiology/prevention & control
RF  - 24
EDAT- 2007/10/17 09:00
MHDA- 2007/10/27 09:00
CRDT- 2007/10/17 09:00
PHST- 2007/10/17 09:00 [pubmed]
PHST- 2007/10/27 09:00 [medline]
PHST- 2007/10/17 09:00 [entrez]
PST - ppublish
SO  - Rev Cardiovasc Med. 2007;8 Suppl 3:S9-17.