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接受基于替格瑞洛的维持性双联抗血小板治疗的冠心病患者中,ADP诱导的全血血小板聚集与血清低密度脂蛋白胆固醇的关联

Association of ADP-Induced Whole-Blood Platelet Aggregation with Serum Low-Density Lipoprotein Cholesterol in Patients with Coronary Artery Disease When Receiving Maintenance Ticagrelor-Based Dual Antiplatelet Therapy.

作者信息

Chyrchel Bernadeta, Kruszelnicka Olga, Wieczorek-Surdacka Ewa, Surdacki Andrzej

机构信息

Second Department of Cardiology, Institute of Cardiology, Faculty of Medicine, Jagiellonian University Medical College, 2 Jakubowskiego Street, 30-688 Cracow, Poland.

Department of Cardiology and Cardiovascular Interventions, University Hospital, 2 Jakubowskiego Street, 30-688 Cracow, Poland.

出版信息

J Clin Med. 2023 Jul 6;12(13):4530. doi: 10.3390/jcm12134530.

DOI:10.3390/jcm12134530
PMID:37445565
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10342583/
Abstract

The degree of platelet inhibition in patients undergoing dual antiplatelet therapy (DAPT) affects cardiovascular outcomes after acute coronary syndromes (ACS) and/or percutaneous coronary intervention. Our aim was to search for correlates of residual ex vivo platelet reactivity and circulating soluble P-selectin (sP-selectin), an index of in vivo platelet activation, in patients being treated by DAPT with ticagrelor. Adenosine diphosphate (ADP)-induced platelet aggregability (by multiple electrode aggregometry) and plasma sP-selectin were estimated in 62 stable post-ACS subjects (46 men and 16 women; mean age: 64 ± 10 years; 30 with type 2 diabetes (T2DM)) undergoing maintenance DAPT with ticagrelor and aspirin. These patients did not exhibit heart failure or other relevant coexistent diseases except for properly controlled T2DM, mild renal insufficiency, and hypertension. We also assessed this in 64 subjects on clopidogrel-based DAPT matched for age, sex, and T2DM status. ADP-induced platelet aggregation was below the optimal levels (190-460 arbitrary units (AU) * min) in most patients receiving ticagrelor-based DAPT, especially in those with below-median (<1.9 mmol/L) serum concentrations of low-density lipoprotein cholesterol (LDL-c) (128 ± 61 vs. 167 ± 73 AU * min for below-median and above-median LDL-c, respectively, = 0.025). In contrast, platelet reactivity did not differ by LDL-c on clopidogrel-based DAPT (246 ± 101 vs. 268 ± 108 AU * min for below-median and above-median LDL-c, respectively, > 0.4). Plasma sP-selectin was found to be unrelated to serum LDL-c when receiving DAPT with ticagrelor ( > 0.4) or clopidogrel ( > 0.8). In conclusion, our preliminary observational study suggests the association of lower residual ex vivo platelet aggregability with better LDL-c control in patients undergoing ticagrelor-based maintenance DAPT, which does not appear to be reflected by plasma sP-selectin. Whether the serum LDL-c level should be considered among the factors affecting the degree of platelet inhibition for those treated with ticagrelor-based DAPT needs to be investigated in larger studies.

摘要

接受双联抗血小板治疗(DAPT)的患者的血小板抑制程度会影响急性冠状动脉综合征(ACS)和/或经皮冠状动脉介入治疗后的心血管结局。我们的目的是寻找在接受替格瑞洛DAPT治疗的患者中,体外残余血小板反应性与循环可溶性P-选择素(sP-选择素,体内血小板活化指标)之间的相关性。对62例接受替格瑞洛和阿司匹林维持DAPT治疗的ACS稳定期患者(46例男性和16例女性;平均年龄:64±10岁;30例患有2型糖尿病(T2DM))进行了二磷酸腺苷(ADP)诱导的血小板聚集性(通过多电极聚集测定法)和血浆sP-选择素评估。这些患者除了T2DM得到适当控制、轻度肾功能不全和高血压外,未表现出心力衰竭或其他相关并存疾病。我们还对64例年龄、性别和T2DM状态相匹配的接受基于氯吡格雷的DAPT治疗的患者进行了评估。在大多数接受基于替格瑞洛的DAPT治疗的患者中,ADP诱导的血小板聚集低于最佳水平(190 - 460任意单位(AU)*分钟),尤其是在血清低密度脂蛋白胆固醇(LDL-c)浓度低于中位数(<1.9 mmol/L)的患者中(低于中位数和高于中位数LDL-c的患者分别为128±61和167±73 AU*分钟,P = 0.025)。相比之下,在基于氯吡格雷的DAPT治疗中,血小板反应性在LDL-c水平上没有差异(低于中位数和高于中位数LDL-c的患者分别为246±101和268±108 AU*分钟,P>0.4)。发现接受替格瑞洛(P>0.4)或氯吡格雷(P>0.8)DAPT治疗时,血浆sP-选择素与血清LDL-c无关。总之,我们的初步观察性研究表明,在接受基于替格瑞洛的维持DAPT治疗的患者中,较低的体外残余血小板聚集性与更好的LDL-c控制相关,而血浆sP-选择素似乎未反映这一点。对于接受基于替格瑞洛的DAPT治疗的患者,血清LDL-c水平是否应被视为影响血小板抑制程度的因素之一,需要在更大规模的研究中进行调查。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb45/10342583/6e266e67007b/jcm-12-04530-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb45/10342583/6b89fc4fc7ce/jcm-12-04530-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb45/10342583/6e266e67007b/jcm-12-04530-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb45/10342583/6b89fc4fc7ce/jcm-12-04530-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb45/10342583/6e266e67007b/jcm-12-04530-g002.jpg

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