{"title":"与同型半胱氨酸相关的心血管缺血对ASA的次优反应","authors":"F. Cacciapuoti","doi":"10.17554/J.ISSN.2309-6861.2015.02.103","DOIUrl":null,"url":null,"abstract":"Some epidemiological reports showed a significant association between the increased homocysteine serum levels (H-Hcy) and risk of ischemic cardiovascular disease (CVD). Acetyl-Salicylic Acid (ASA) is the drug commonly used to antagonize pro-thrombotic effect of Hcy. But, human and animal studies evidenced that ASA, given at habitual anti-ischemic dosage, may induce an incomplete inhibition of platelet (aspirin-resistance) in patients with CVD Hcy-related by several mechanisms. In these patients, doses higher than normal are requested to obtain an optimal ASA-response (aspirin-sensitivity). That happens because Hcy “per se” is a pro-aggregatory agent and acts as specific sensitizer of blood platelets with several mechanisms. On the contrary, its acetylated form (N-acetyl-homocysteine) obtained using high ASA doses, is able to reverse this effect restoring the platelets’ sensitivity. That happens with a still unknown mechanism.","PeriodicalId":92802,"journal":{"name":"Journal of clinical cardiology and cardiovascular therapy","volume":"7 1","pages":"456-458"},"PeriodicalIF":0.0000,"publicationDate":"2015-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Sub-Optimal Response to ASA in Cardiovascular Ischemia Homocysteine-Related\",\"authors\":\"F. Cacciapuoti\",\"doi\":\"10.17554/J.ISSN.2309-6861.2015.02.103\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Some epidemiological reports showed a significant association between the increased homocysteine serum levels (H-Hcy) and risk of ischemic cardiovascular disease (CVD). Acetyl-Salicylic Acid (ASA) is the drug commonly used to antagonize pro-thrombotic effect of Hcy. But, human and animal studies evidenced that ASA, given at habitual anti-ischemic dosage, may induce an incomplete inhibition of platelet (aspirin-resistance) in patients with CVD Hcy-related by several mechanisms. In these patients, doses higher than normal are requested to obtain an optimal ASA-response (aspirin-sensitivity). That happens because Hcy “per se” is a pro-aggregatory agent and acts as specific sensitizer of blood platelets with several mechanisms. On the contrary, its acetylated form (N-acetyl-homocysteine) obtained using high ASA doses, is able to reverse this effect restoring the platelets’ sensitivity. That happens with a still unknown mechanism.\",\"PeriodicalId\":92802,\"journal\":{\"name\":\"Journal of clinical cardiology and cardiovascular therapy\",\"volume\":\"7 1\",\"pages\":\"456-458\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-12-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of clinical cardiology and cardiovascular therapy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.17554/J.ISSN.2309-6861.2015.02.103\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of clinical cardiology and cardiovascular therapy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17554/J.ISSN.2309-6861.2015.02.103","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Sub-Optimal Response to ASA in Cardiovascular Ischemia Homocysteine-Related
Some epidemiological reports showed a significant association between the increased homocysteine serum levels (H-Hcy) and risk of ischemic cardiovascular disease (CVD). Acetyl-Salicylic Acid (ASA) is the drug commonly used to antagonize pro-thrombotic effect of Hcy. But, human and animal studies evidenced that ASA, given at habitual anti-ischemic dosage, may induce an incomplete inhibition of platelet (aspirin-resistance) in patients with CVD Hcy-related by several mechanisms. In these patients, doses higher than normal are requested to obtain an optimal ASA-response (aspirin-sensitivity). That happens because Hcy “per se” is a pro-aggregatory agent and acts as specific sensitizer of blood platelets with several mechanisms. On the contrary, its acetylated form (N-acetyl-homocysteine) obtained using high ASA doses, is able to reverse this effect restoring the platelets’ sensitivity. That happens with a still unknown mechanism.