Rath P C, Chidambaram Sundar, Rath Pallavi, Dikshit Byomakesh, Naik Sudhir, Sahoo Prashant K, Das Brajraj, Mahalingam Mohanshankar, Khandrika Lakshmipathi, Jain Jugnu
Director of Cardiology & Cath Lab, Apollo Hospital, Jubilee Hills, Hyderabad, India.
Apollo Hospital, Jubilee Hills, Hyderabad, India.
Indian Heart J. 2015 Mar-Apr;67(2):114-21. doi: 10.1016/j.ihj.2015.03.017. Epub 2015 Apr 27.
A thorough understanding of the patient's genotype and their functional response to a medication is necessary for improving event free survival. Several outcome studies support this view particularly if the patient is to be started on clopidogrel due to the prevalence of clopidogrel resistance. Such guided therapy has reduced the incidence of Major Adverse Cardiac Events (MACE) after stent implantation.
Between August 2013 and August 2014, 200 patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) were prescribed any one of the anti-platelet medications such as clopidogrel, prasugrel or ticagrelor and offered testing to detect CYP2C19 gene mutations along with a platelet reactivity assay (PRA). Intended outcome was modification of anti-platelet therapy defined as either dose escalation of clopidogrel or replacement of clopidogrel with prasugrel or ticagrelor for the patients in clopidogrel arm, and replacement of ticagrelor or prasugrel with clopidogrel if those patients were non-carrier of mutant genes and also if they demonstrated bleeding tendencies in the ticagrelor and prasugrel arms.
Clopidogrel resistance was observed to be 16.5% in our study population. PRA was useful in monitoring the efficacy of thienopyridines. By having this test, one can be safely maintained on clopidogrel in non-carriers, or with increased dose of clopidogrel in intermediate metabolizers or with newer drugs such as ticagrelor or prasugrel in poor metabolizers. Patients on ticagrelor and prasugrel identified as non-carriers of gene mutations for clopidogrel metabolism could be offered clopidogrel resulting in economic benefits to the patients. Patients at high risk of bleeding were also identified by the PRA.
全面了解患者的基因型及其对药物的功能反应对于提高无事件生存率至关重要。多项结果研究支持这一观点，特别是当患者因氯吡格雷抵抗的普遍性而开始使用氯吡格雷时。这种有指导的治疗降低了支架植入后主要不良心脏事件（MACE）的发生率。
在2013年8月至2014年8月期间，200例接受经皮冠状动脉介入治疗（PCI）的冠心病患者被处方使用氯吡格雷、普拉格雷或替卡格雷等抗血小板药物之一，并接受检测以检测CYP2C19基因突变以及血小板反应性测定（PRA）。预期结果是调整抗血小板治疗，对于氯吡格雷组的患者，定义为氯吡格雷剂量增加或用普拉格雷或替卡格雷替代氯吡格雷；对于替卡格雷或普拉格雷组中那些非突变基因携带者且有出血倾向的患者，用氯吡格雷替代替卡格雷或普拉格雷。
在我们的研究人群中观察到氯吡格雷抵抗率为16.5%。PRA有助于监测噻吩并吡啶类药物的疗效。通过这项检测，非携带者可安全地继续使用氯吡格雷，中间代谢者可增加氯吡格雷剂量，慢代谢者可使用替卡格雷或普拉格雷等新药。替卡格雷和普拉格雷组中被确定为氯吡格雷代谢基因突变非携带者的患者可以改用氯吡格雷，从而为患者带来经济效益。PRA还能识别出血高危患者。
