UNASSIGNED:与ASA单药治疗相比,联合使用乙酰水杨酸(ASA)和低剂量利伐沙班的双路抑制(DPI)可减少外周动脉疾病(PAD)患者的心血管事件。一个潜在的解释是因子Xa的抑制通过凝血和炎症途径之间的串扰改善内皮功能,随后减轻心血管事件的发生。我们假设PAD患者在ASA中加用利伐沙班可改善内皮功能。
未经批准:一名调查员发起,研究DPI对内皮功能影响的多中心试验。
未经证实:患者,诊断为PAD,纳入两个队列:队列A(卢瑟福I-III)和队列B(卢瑟福IV-VI)。参与者接受ASA单药治疗,为期4周,随后是12周的DPI。通过测量交感神经刺激后的颈动脉反应性和测量血浆内皮素-1浓度来研究大血管和微血管内皮功能障碍。分别。所有测量均在使用ASA(基线)期间和DPI12周后进行。
未经批准:159名PAD患者(111组A,纳入48个队列B)。20名患者早期停用研究药物。在基线(ASA)和12周DPI后,交感神经刺激后的颈动脉收缩在全组相似,22.0vs.22.7%(p=1.000),和亚组(队列A22.6vs.23.7%,p=1.000;队列B20.5vs.20.5%,p=1.000),分别。基线时和DPI12周后血浆内皮素-1的平均浓度没有差异,1.70±0.5vs.总组1.66±0.64pmol/L(p=0.440),1.69±0.59vs.队列A中1.62±0.55pmol/L(p=0.202),和1.73±0.53vs.队列B中1.77±0.82pmol/L(p=0.682),分别。
未经批准:大血管和微血管内皮功能障碍,如颈动脉反应性和血浆内皮素-1浓度所反映,在PAD患者中,通过在ASA单药治疗中添加低剂量利伐沙班12周不受影响。
UNASSIGNED:https://clinicaltrials.gov/ct2/show/NCT04218656。
UNASSIGNED: Dual pathway inhibition (DPI) by combining acetylsalicylic acid (ASA) with low-dose rivaroxaban has been shown to reduce cardiovascular events in patients with peripheral arterial disease (PAD) when compared to ASA monotherapy. A potential explanation is that inhibition of factor Xa improves endothelial function through crosstalk between coagulation and inflammatory pathways, subsequently attenuating the occurrence of cardiovascular events. We hypothesize that the addition of rivaroxaban to ASA in PAD patients leads to improved endothelial function.
UNASSIGNED: An investigator-initiated, multicentre
trial investigating the effect of DPI on endothelial function.
UNASSIGNED: Patients, diagnosed with PAD, were enrolled in two cohorts: cohort A (Rutherford I-III) and cohort B (Rutherford IV-VI). Participants received ASA monotherapy for a 4-weeks run-in period, followed by 12 weeks of DPI. Macro- and microvascular endothelial dysfunction were studied by measuring carotid artery reactivity upon sympathetic stimulus and by measuring plasma endothelin-1 concentrations, respectively. All measurements were performed during the use of ASA (baseline) and after 12 weeks of DPI.
UNASSIGNED: 159 PAD patients (111 cohort A, 48 cohort B) were enrolled. Twenty patients discontinued
study drugs early. Carotid artery constriction upon sympathetic stimulation at baseline (ASA) and after 12 weeks of DPI was similar in the total group, 22.0 vs. 22.7% (p = 1.000), and in the subgroups (Cohort A 22.6 vs. 23.7%, p = 1.000; cohort B 20.5 vs. 20.5%, p = 1.000), respectively. The mean concentration of plasma endothelin-1 at baseline and after 12 weeks of DPI did not differ, 1.70 ± 0.5 vs. 1.66 ± 0.64 pmol/L (p = 0.440) in the total group, 1.69 ± 0.59 vs. 1.62 ± 0.55 pmol/L in cohort A (p = 0.202), and 1.73 ± 0.53 vs. 1.77 ± 0.82 pmol/L in cohort B (p = 0.682), respectively.
UNASSIGNED: Macro- and microvascular endothelial dysfunction, as reflected by carotid artery reactivity and plasma endothelin-1 concentrations, are not influenced in PAD patients by addition of low-dose rivaroxaban to ASA monotherapy for 12 weeks.
UNASSIGNED: https://clinicaltrials.gov/ct2/show/NCT04218656.