2020
DOI: 10.1016/j.numecd.2019.09.018
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Homocysteine levels and platelet reactivity in coronary artery disease patients treated with ticagrelor

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Cited by 16 publications
(18 citation statements)
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“…In fact, homocysteine concentrations above the 90th percentile are associated with increased risk of degenerative and atherosclerotic processes [9] in the coronary, cerebral and peripheral circulatory system. In this regard, determining homocysteine together with other cardiovascular risk markers (Apo B, Lp(a), LDL, fibrinogen, PAI-1) now belongs to the clinical practice [10]; moreover, recent evidence suggests the role of homocysteine as a risk factor for thromboembolism, given its influence on platelet reactivity [11][12][13].…”
mentioning
confidence: 99%
“…In fact, homocysteine concentrations above the 90th percentile are associated with increased risk of degenerative and atherosclerotic processes [9] in the coronary, cerebral and peripheral circulatory system. In this regard, determining homocysteine together with other cardiovascular risk markers (Apo B, Lp(a), LDL, fibrinogen, PAI-1) now belongs to the clinical practice [10]; moreover, recent evidence suggests the role of homocysteine as a risk factor for thromboembolism, given its influence on platelet reactivity [11][12][13].…”
mentioning
confidence: 99%
“…These con icting results may be due to differences in the test methods of platelet reactivity or the inclusion criteria. The underlying mechanism of platelet hyperactivity in patients with impaired renal function might be related to chronic low-grade in ammation, vascular injury [20] and the accumulation of uremic toxins, such as indoxyl sulfate [21] and homocysteine [22]. Furthermore, preactivation of platelets and platelet turnover [23] also play roles in the pathogenesis of insu cient platelet inhibition by aspirin in patients with impaired renal function.…”
Section: Discussionmentioning
confidence: 99%
“…eGFR was an independent factor of HTPR. The further mechanism of platelet hyperactivity in patients with impaired renal function might be relevant to the accumulation of uremic toxins, such as indoxyl sulfate [25] and homocysteine [26]. Furthermore, pre-activation of platelets in CKD [27] may play a role in the pathogenesis of insu cient platelet inhibition by aspirin in patients with impaired kidney function.…”
Section: Discussionmentioning
confidence: 99%
“…These con icting results may be due to differences in the test methods of platelet reactivity or the inclusion criteria. The underlying mechanism of platelet hyperactivity in patients with impaired renal function might be related to chronic low-grade in ammation, vascular injury [20] and the accumulation of uremic toxins, such as indoxyl sulfate [21] and homocysteine [22]. Furthermore, preactivation of platelets and platelet turnover [19,23] also play roles in the pathogenesis of insu cient platelet inhibition by aspirin in patients with impaired renal function.…”
Section: Discussionmentioning
confidence: 99%