阿司匹林抵抗

阿司匹林对心脑血管病缺血事件的预防作用已得到广泛认可,但服用治疗剂量的阿司匹林并不能对所有个体产生有效的预防作用,因此有学者提出了阿司匹林抵抗的概念,但目前还存在许多不同观点。     

阿司匹林抵抗

研究表明在接受阿司匹林治疗的心血管疾病患者中有5%～45%存在阿司匹林抵抗,由于全球有大量的患者依赖阿司匹林的抗血小板治疗,所以关于阿司匹林抵抗的研究已经引起广泛关注.本文综述阿司匹林抵抗的可能机制.     

阿司匹林抵抗的研究进展

近年研究发现,一些个体规律服用适当剂量的阿司匹林,仍不能免除缺血性事件的发生,其机制可能与环氧化酶-2、单核苷酸多态性或变异等有关。     

阿司匹林抵抗

阿司匹林抵抗是指阿司匹林不能:(1)保护服用者不发生血栓性并发症;(2)延长出血时间;(3)抑制血栓素的生物合成或(4)在体外试验中对血小板功能发挥预期影响。阿司匹林抵抗的可能机制包括:(1)5%～40%的缺血性血管病并非动脉粥样硬化所致;(2)依从性差或剂量不足。阿司匹林抵抗尚无特异性治疗方法。对于不能耐受阿司匹林或出现阿司匹林抵抗的患者,应选择ADP受体拮抗剂氯吡格雷或其他抗血小板药治疗。     

阿司匹林抗血小板作用的抗药性--阿司匹林抵抗

近年研究发现 ,常规剂量的阿司匹林 ,甚至加大剂量的阿司匹林在一些个体不能阻断血栓素的合成。从而保护机体免受血栓性疾病的损害。其机制可能与单核巨噬细胞合成前列腺素H2 ,以及环氧化酶 1的基因多态性或变异有关     

阿司匹林抵抗现象

阿司匹林是心血管病中应用最为广泛的一种抗血小板药物 ,但对有些患者却并未达到足够的抗血小板效果 ,这一现象被称为“阿司匹林抵抗”。本文就阿司匹林抵抗的提出、可能机制、临床意义及防治对策作一综述。     

阿司匹林抵抗的研究进展

阿司匹林通过不可逆地乙酰化环氧化酶-1,在心血管疾病的防治中发挥着重要作用.但部分患者存在阿司匹林抵抗现象,其发生机制尚未明确,可能与药物剂量、依从性、基因多态性等有关.实验室检测阿司匹林抵抗的方法有光学聚集法、全血电阻抗法、血栓素的测定等.研究证实阿司匹林抵抗与临床事件的发生具有相关性.因此,将来有待进一步研究阿司匹林抵抗的相关机制、检测方法及防治策略,旨在相关临床事件发生之前筛选出抵抗患者,从而优化抗血小板药物治疗.     

阿司匹林抵抗的临床特征分析

阿司匹林是目前应用最广的心脑血管疾病一二级预防用药.已证实阿司匹林的使用可降低致死性和/或非致死性血管事件的发生率.然而最近关注到,在长期服用阿司匹林的人群中,部分人群仍有血栓形成事件的发生,由此提出阿司匹林抵抗概念.已有多个大型多中心临床试验对阿司匹林抵抗患者的临床特征进行分析,以利于早期对该类患者进行识别.文章对阿司匹林抵抗患者的临床特征及其出现的可能原因进行综述.     

阿司匹林抵抗现象的研究

阿司匹林是一种有着百年历史的临床药物,在心血管系统疾病,尤其是缺血性心脏病治疗中被广泛应用,但近年来发现有部分患者存在阿司匹林抵抗(AR)现象,本文就对这一现象作一综述。1 AR的定义阿司匹林在血栓性心血管疾病的1、2级预防中具有重要作用〔1〕。然而有部分患者虽然应用阿     

阿司匹林抵抗研究进展

阿司匹林为最常用的抗血小板药物,在心脑血管疾病的一级预防和二级预防中有重要作用.临床上将应用阿司匹林治疗不能充分抑制血小板聚集功能而导致临床血栓事件发生的现象称之为阿司匹林抵抗(aspirin resistance,AR)[1].现将AR的研究进展综述如下.     

阿司匹林抵抗

阿司匹林能有效预防缺血性脑血管病,但由于"阿司匹林抵抗"现象的存在,仍有部分患者在阿司匹林治疗期间发生缺血事件.文章主要对阿司匹林抵抗的机制、筛查方法 和处理措施进行了综述.     

Aspirin resistance

Aspirin resistance is the inability of aspirin to reduce platelet production of thromboxane A2 and thereby platelet activation and aggregation. Increasing degrees of aspirin resistance may correlate independently with increasing risk of cardiovascular events. Aspirin resistance can be detected by laboratory tests of platelet thromboxane A2 production or platelet function that depend on platelet thromboxane production. Potential causes of aspirin resistance include inadequate dose, drug interactions, genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet sources of thromboxane biosynthesis, and increased platelet turnover. Aspirin resistance can be overcome by treating the cause or causes, and reduced by minimising thromboxane production and activity, and blocking other pathways of platelet activation. Future research is aimed at defining aspirin resistance, developing reliable tests for it, and establishing the risk of associated cardiovascular events. Potential mechanisms of aspirin resistance can then be explored and treatments assessed.     

Aspirin "resistance"

A variable responsiveness to antiplatelet drugs is a clinical phenomenon that does not principally differ from other drug treatments in other therapeutic fields. The pharmacological part is to clarify whether a "true" resistance exists in pharmacological terms, i.e., a reduced potency of the compound to work as suggested and to find out the underlying cellular mechanism(s). Two principally different methods of laboratory control for platelet sensitivity to aspirin (ASA) are available: measurement of platelet function (ex vivo) or measurement of inhibition of thromboxane formation. Both methods have limitations and did not yet result in a generally accepted definition of a pharmacological ASA "resistance". The new typological approach of Weber et al. [A.A. Weber, B. Przytulski, A. Schanz, et al., Towards a definition of aspirin resistance: a typological approach. Platelets 13 (2002) 37.] helps to identify different subtypes of ASA resistance in pharmacological terms by combining in vitro aggregometry with thromboxane measurement. Using this method, a "true" pharmacological resistance, associated with a reduced antiplatelet response to ASA and reduced inhibition of thromboxane formation, was found in patients undergoing coronary artery bypass surgery. Platelets of these patients expressed a hitherto unknown isoform of COX-2-COX-2a which might generate a different gene product. In this context, it is interesting that CABG patients express transiently an immunoreactive COX-2 protein with lower molecular weight. Studies on the significance of this finding for ASA resistance are in progress.     

Aspirin resistance in atherosclerosis

Clinically, aspirin resistance is defined as the failure of aspirin therapy to prevent an acute vascular thrombotic event despite regular intake of appropriate doses. In the laboratory, aspirin resistance encompasses the drug’s failure to attain a particular level of platelet inhibition. From a clinical standpoint, the inability of aspirin to prevent a thrombotic event, despite appropriate cyclooxygenase-1 inhibition, implies the involvement of other factors. Evidence is emerging that aspirin resistance, as defined by residual platelet activity, merely reflects an individual’s enhanced basal platelet function and suggests a hereditary component. Due to the multifactorial nature of cardiovascular disease, it is likely that a single therapy like aspirin cannot fully treat and prevent all thrombotic complications in the setting of atherosclerosis.     

阿司匹林和氯吡格雷抵抗

阿司匹林通过不可逆抑制环氧合酶（COX）-1,阻止花生四烯酸代谢产物血栓素A2（TXA2）形成,从而发挥其抑制血小板聚集作用.汇总分析表明,接受阿司匹林治疗的高危患者血管性事件（包括心肌梗死、卒中或死亡）发生率降低25%～30%,但是仍有10%～20%的患者5年内再发血管性事件.     

Aspirin resistance in hypertensive patients

J Clin Hypertens (Greenwich). 2010;12:714–720. ^©2010 Wiley Periodicals, Inc. Aspirin resistance is associated with poor clinical prognosis. The authors investigated aspirin resistance in 200 hypertensive patients (111 men, age: 68.3±11.4 years) by the Ultegra Rapid Platelet Function Assay-ASA (Accumetrics Inc., San Diego, CA). Aspirin resistance was defined as an aspirin reaction unit ≥550. Aspirin resistance was detected in 42 patients. Aspirin resistance was present in 25.6% of the patients with poor blood pressure control, while in 17.8% of the patients with controlled blood pressure (P=.182). Female gender and creatinine levels were significantly higher (P=.028 and P=.030, respectively), while platelet count was significantly lower (P=.007) in aspirin-resistant patients. Multivariate analysis revealed that female gender (odds ratio [OR], 2.445; P=.045), creatinine levels (OR, 1.297; P=.015) and platelet count (OR, 0.993; P=.005) were independent predictors of aspirin resistance. The frequency of aspirin resistance is not low in hypertensive patients. Female hypertensive patients, especially, with higher creatinine levels and lower platelet count are at higher risk for aspirin resistance.     

Aspirin resistance: An update

Aspirin resistance (AR) still lacks a universally accepted definition, but it may be discussed as either a laboratory phenomenon or a clinical presentation. Laboratory resistance is mainly defined as abnormal platelet response to aspirin, whereas the clinical manifestation is the failure of aspirin to prevent cardiovascular events. Although there is evidence of an association, it appears that a laboratory abnormality in platelet function is not the only risk factor for the clinical manifestation of AR. Therapies for primary and secondary prevention of AR still need to be elucidated, but there are some data to suggest that in an acute episode of aspirin failure because of AR, different therapeutic interventions need to be considered.