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Abstract
Antiplatelet therapy has been established as a preventive medicine for ischemic cardiovascular diseases both at acute and chronic phases. This therapy is also crucial for the prevention of thrombotic events after coronary stent implantation. So far, many lines of clinical evidence have demonstrated the beneficial effects of aspirin (an irreversible cyclooxygenase inhibitor) and thienopyridine derivatives (adenosine diphosphate (ADP)‐receptor P2Y12 inhibitors). Recently, it has been reported that the cardiovascular risk is elevated in patients with platelets resistant to these drugs, compared to the good responders. One of the current problems to be solved in antiplatelet therapy is to find out patients resistant to the antiplatelet therapy and improve its preventive effects. In addition to aspirin and thienopyridines, several types of drugs with antiplatelet effects are currently available in clinical practice. Clinical evidence has recently been accumulating for these drugs that can be potential alternatives in patients with aspirin or thienopyridine resistance. In this review, the mechanisms, evidence and approach to the present problems of drugs with antiplatelet effects are discussed.
| Abbreviations | ||
| 5‐HT | = | 5‐hydroxytriptamine |
| ADP | = | adenosine diphosphate |
| ATP | = | adenosine triphosphate |
| cAMP | = | cyclic adenosine monophosphate |
| cGMP | = | cyclic guanosine monophosphate |
| COX | = | cyclooxygenase |
| DHA | = | docosahexaenoic acid |
| EPA | = | eicosapentaenoic acid |
| GP | = | glycoprotein |
| HMG‐CoA | = | 3‐hydroxy‐3‐methylglutaryl coenzyme A |
| NSAID | = | non‐steroidal anti‐inflammatory drug |
| PAD | = | peripheral artery disease |
| PAR | = | protease‐activated receptor |
| PCI | = | percutaneous coronary intervention |
| PDE | = | phosphodiesterase |
| PDGF | = | platelet‐derived growth factor |
| PKA | = | cAMP‐dependent protein kinase |
| PKG | = | cGMP‐dependent protein kinase |
| PRP | = | platelet‐rich plasma |
| RR | = | relative risk |
| SNP | = | single nucleotide polymorphism |
| TF | = | tissue factor |
| VASP | = | vasodilator‐stimulated phosphoprotein |
| vWF | = | von Willebrand factor |
| Abbreviations | ||
| 5‐HT | = | 5‐hydroxytriptamine |
| ADP | = | adenosine diphosphate |
| ATP | = | adenosine triphosphate |
| cAMP | = | cyclic adenosine monophosphate |
| cGMP | = | cyclic guanosine monophosphate |
| COX | = | cyclooxygenase |
| DHA | = | docosahexaenoic acid |
| EPA | = | eicosapentaenoic acid |
| GP | = | glycoprotein |
| HMG‐CoA | = | 3‐hydroxy‐3‐methylglutaryl coenzyme A |
| NSAID | = | non‐steroidal anti‐inflammatory drug |
| PAD | = | peripheral artery disease |
| PAR | = | protease‐activated receptor |
| PCI | = | percutaneous coronary intervention |
| PDE | = | phosphodiesterase |
| PDGF | = | platelet‐derived growth factor |
| PKA | = | cAMP‐dependent protein kinase |
| PKG | = | cGMP‐dependent protein kinase |
| PRP | = | platelet‐rich plasma |
| RR | = | relative risk |
| SNP | = | single nucleotide polymorphism |
| TF | = | tissue factor |
| VASP | = | vasodilator‐stimulated phosphoprotein |
| vWF | = | von Willebrand factor |
Acknowledgements
I am grateful to Dr Susana Prat, Barcelona, a visiting scientist in our Department; Dr Yasuyuki Fujita, London; Dr Arata Tabuchi, Berlin; Dr Hidenori Arai, Kyoto; and members of my laboratory for critical reading and discussion of this manuscript. I also thank Professor Dr Toru Kita for continuous encouragement of my research projects. This work was supported by Ministry of Education, Culture, Sports, Science, and Technology Research Grants No. 16209031, by Health and Labour Sciences Research Grant for Cardiovascular Research H17‐006 from the Ministry of Health Labour and Welfare, Japan and in part by grants from the Takeda Science Foundation, Japan Cardiovascular Research Foundation, and a grant from The Kato Memorial Trust for Nambyo Research.