Antiplatelet therapies: An overview
The role of blood components including platelets, in initiating inflammation, endothelial dysfunction, atherosclerosis, thrombus formation, thrombus growth, and acute vascular ischemic events, is well established. Given this recognized role played by platelets, there is a considerable interest in un...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2016-01-01
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| Series: | Journal of Clinical and Preventive Cardiology |
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| Online Access: | http://www.jcpconline.org/article.asp?issn=2250-3528;year=2016;volume=5;issue=4;spage=130;epage=137;aulast=Rao |
| _version_ | 1818298926841724928 |
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| author | Gundu H R Rao |
| author_facet | Gundu H R Rao |
| author_sort | Gundu H R Rao |
| collection | DOAJ |
| description | The role of blood components including platelets, in initiating inflammation, endothelial dysfunction, atherosclerosis, thrombus formation, thrombus growth, and acute vascular ischemic events, is well established. Given this recognized role played by platelets, there is a considerable interest in understanding the physiology and function of platelets, as well as in the development of novel platelet function-inhibitory drugs. The generation of the second messengers, calcium mobilization, shape change, adhesion, aggregation, contraction, release of granule contents, thrombus development, thrombus growth, and formation of hemostatic plug at the injured vessel surfaces, in brief, constitute platelet activation. Some of the known compounds that inhibit platelet activation include inhibitors of arachidonic metabolism (cyclooxygenase-1 inhibitors; aspirin, ibuprofen, etc.), adenosine diphosphate receptor antagonists (P2Y 12 inhibitors), adenylyl and guanylyl cyclase stimulators, calcium antagonists, and GP11b/111a receptor antagonists. Since platelets have multiple mechanisms of achieving in vivo activation, it is difficult to design a novel drug that offers total protection for developing acute ischemic vascular events, without compromising coagulation mechanisms. Given this complexity, any aggressive antiplatelet therapy results in increased bleeding episodes. Having said that, we feel that there is a great window of opportunity for developing novel antiplatelet therapies. There is also scope for the development of fixed-dose combinations for the primary and secondary management of chronic diseases such as hypertension, heart disease, and type-2 diabetes. |
| first_indexed | 2024-12-13T04:43:06Z |
| format | Article |
| id | doaj.art-a116b88b1c5b498e9df747983c074ec6 |
| institution | Directory Open Access Journal |
| issn | 2250-3528 |
| language | English |
| last_indexed | 2024-12-13T04:43:06Z |
| publishDate | 2016-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Journal of Clinical and Preventive Cardiology |
| spelling | doaj.art-a116b88b1c5b498e9df747983c074ec62022-12-21T23:59:15ZengWolters Kluwer Medknow PublicationsJournal of Clinical and Preventive Cardiology2250-35282016-01-015413013710.4103/2250-3528.192696Antiplatelet therapies: An overviewGundu H R RaoThe role of blood components including platelets, in initiating inflammation, endothelial dysfunction, atherosclerosis, thrombus formation, thrombus growth, and acute vascular ischemic events, is well established. Given this recognized role played by platelets, there is a considerable interest in understanding the physiology and function of platelets, as well as in the development of novel platelet function-inhibitory drugs. The generation of the second messengers, calcium mobilization, shape change, adhesion, aggregation, contraction, release of granule contents, thrombus development, thrombus growth, and formation of hemostatic plug at the injured vessel surfaces, in brief, constitute platelet activation. Some of the known compounds that inhibit platelet activation include inhibitors of arachidonic metabolism (cyclooxygenase-1 inhibitors; aspirin, ibuprofen, etc.), adenosine diphosphate receptor antagonists (P2Y 12 inhibitors), adenylyl and guanylyl cyclase stimulators, calcium antagonists, and GP11b/111a receptor antagonists. Since platelets have multiple mechanisms of achieving in vivo activation, it is difficult to design a novel drug that offers total protection for developing acute ischemic vascular events, without compromising coagulation mechanisms. Given this complexity, any aggressive antiplatelet therapy results in increased bleeding episodes. Having said that, we feel that there is a great window of opportunity for developing novel antiplatelet therapies. There is also scope for the development of fixed-dose combinations for the primary and secondary management of chronic diseases such as hypertension, heart disease, and type-2 diabetes.http://www.jcpconline.org/article.asp?issn=2250-3528;year=2016;volume=5;issue=4;spage=130;epage=137;aulast=RaoAntiplatelet therapiesaspirinclopidogrelfixed-dose combinationsP2Y 12 inhibitorsplatelet activationplatelet pharmacologyReoPro |
| spellingShingle | Gundu H R Rao Antiplatelet therapies: An overview Journal of Clinical and Preventive Cardiology Antiplatelet therapies aspirin clopidogrel fixed-dose combinations P2Y 12 inhibitors platelet activation platelet pharmacology ReoPro |
| title | Antiplatelet therapies: An overview |
| title_full | Antiplatelet therapies: An overview |
| title_fullStr | Antiplatelet therapies: An overview |
| title_full_unstemmed | Antiplatelet therapies: An overview |
| title_short | Antiplatelet therapies: An overview |
| title_sort | antiplatelet therapies an overview |
| topic | Antiplatelet therapies aspirin clopidogrel fixed-dose combinations P2Y 12 inhibitors platelet activation platelet pharmacology ReoPro |
| url | http://www.jcpconline.org/article.asp?issn=2250-3528;year=2016;volume=5;issue=4;spage=130;epage=137;aulast=Rao |
| work_keys_str_mv | AT gunduhrrao antiplatelettherapiesanoverview |