A critical reappraisal of aspirin for secondary prevention in patients with ischemic heart disease.
Aspirin was established more than a quarter century ago as an evidence-based therapy to reduce recurrent cardiovascular events in patients with coronary artery disease based on limited data by contemporary standards. Indeed it is unclear how regulatory agencies would define the optimal dose or duration of aspirin therapy if assessed in the current era. Subsequent clinical investigation has focused on the addition of antithrombotic agents on top of baseline aspirin therapy in the acute and chronic setting to reduce patient's risk of further ischemic events, at the cost of increased bleeding complications. The current armamentarium of potent and predictable antiplatelet and antithrombotic agents has ushered in a new era where clinicians and scientists are contemplating withdrawal of previously established agents to minimize bleeding risk while sustaining efficacy; indeed, subtraction may lead to the next advance in the treatment of acute and chronic ischemic vascular disease.
Mazankowski Alberta Heart Institute and University of Alberta, Edmonton, Alberta, Canada. Electronic address: Robert.Welsh@albertahealthservices.ca.
Robert C
RC
Welsh
Division of Cardiology, Duke Clinical Research Institute, Duke Medicine, Durham, NC.
Matthew T
MT
Roe
Université Paris-Diderot, Sorbonne Paris Cité, FACT, DHU-FIRE, AP-HP and INSERM U-1148, Paris, France; NHLI, Royal Brompton Hospital, Imperial College, London, United Kingdom.
Philippe Gabriel
PG
Steg
Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
Stefan
S
James
Division of Cardiology, Duke Clinical Research Institute, Duke Medicine, Durham, NC.
Thomas J
TJ
Povsic
University of Freiburg, Freiburg, Germany.
Christoph
C
Bode
Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Charles Michael
CM
Gibson
Division of Cardiology, Duke Clinical Research Institute, Duke Medicine, Durham, NC.
Erik Magnus
EM
Ohman
D000241:Adenosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000991:Antithrombins / Q000627:therapeutic use; D001241:Aspirin / Q000266:history / Q000627:therapeutic use*; D000077144:Clopidogrel; D004359:Drug Therapy, Combination; D019317:Evidence-Based Medicine; D065427:Factor Xa Inhibitors / Q000627:therapeutic use*; D006470:Hemorrhage / Q000139:chemically induced; D049673:History, 20th Century; D049674:History, 21st Century; D049690:History, Ancient; D006801:Humans; D017202:Myocardial Ischemia / Q000188:drug therapy*; D010975:Platelet Aggregation Inhibitors / Q000266:history / Q000627:therapeutic use*; D000068799:Prasugrel Hydrochloride / Q000627:therapeutic use; D058921:Purinergic P2Y Receptor Antagonists / Q000627:therapeutic use*; D055502:Secondary Prevention; D000077486:Ticagrelor; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use
D000991:Antithrombins; D065427:Factor Xa Inhibitors; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D000077486:Ticagrelor; D000241:Adenosine; D013988:Ticlopidine; D001241:Aspirin