Scholarlink

Background <p>Patients with coronary artery disease (CAD) are at increased risk of developing ischemic events and contemporary antiplatelet therapy often leads to bleeding events following percutaneous coronary intervention (PCI). Glycoprotein VI (GPVI) is the key receptor of collagen-dependent thrombus formation and crucial for platelet homeostasis. </p> Methods <p>We analysed the influence of GPVI inhibition with revacept in a randomized double-blinded trial enrolling 334 patients with CAD undergoing elective PCI. Ex vivo platelet function analyses were assessed alongside plasma chemokine concentrations. We then elucidate changes of GPVI-dependent chemokine concentrations in patients with bleeding events during the 30-day clinical follow-up.</p> Results <p>Changes in platelet function occur in patients with revacept treatment and are associated with a characteristic alteration of circulating chemokine concentrations. Further, patients with adverse bleeding events share a distinct fingerprint of chemokines that is associated with modulation of in vitro platelet functions. In addition, assessment of GPVI-associated changes in chemokine signalling and platelet functions demonstrated an increased diagnostic value in patients with CAD and might improve early risk discrimination for bleeding events.</p> Conclusion <p>The composition of platelet-derived chemokines correlated with platelet functions following antiplatelet treatment. Thus, assessment of chemokines may offer the perspective to identify patients at increased risk for bleeding events. Likewise, modulation of platelet chemokines in patients with revacept treatment contributes to the efficacy of antiplatelet treatment and might attenuate pathophysiological cascades leading to haemorrhagic diathesis in patients with CAD.</p> Graphical abstract <p>Study design and rationale: patients with coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI) and the impact of treatment with soluble GPVI inhibitor revacept. Changes in ex vivo platelet function and plasma chemokine concentrations were associated with an increased bleeding risk during the clinical follow-up. Further, GPVI-associated changes in chemokine signalling might attenuate pathophysiological cascades leading to haemorrhagic diathesis and improve early risk discrimination for bleeding events</p> <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Plasma chemokines indicate enhanced bleeding in patients with chronic coronary syndrome undergoing percutaneous coronary stenting

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月21日

查看全文
  • Tobias Harm,
  • Shqipdona Lahu,
  • Katharina Mayer,
  • Dominik Rath,
  • Tobias Geisler,
  • Karin Anne Lydia Müller,
  • Marion Janisch,
  • Kristin Adler,
  • Götz Münch,
  • Steffen Massberg,
  • Adnan Kastrati,
  • Meinrad Paul Gawaz

摘要

Background

Patients with coronary artery disease (CAD) are at increased risk of developing ischemic events and contemporary antiplatelet therapy often leads to bleeding events following percutaneous coronary intervention (PCI). Glycoprotein VI (GPVI) is the key receptor of collagen-dependent thrombus formation and crucial for platelet homeostasis.

Methods

We analysed the influence of GPVI inhibition with revacept in a randomized double-blinded trial enrolling 334 patients with CAD undergoing elective PCI. Ex vivo platelet function analyses were assessed alongside plasma chemokine concentrations. We then elucidate changes of GPVI-dependent chemokine concentrations in patients with bleeding events during the 30-day clinical follow-up.

Results

Changes in platelet function occur in patients with revacept treatment and are associated with a characteristic alteration of circulating chemokine concentrations. Further, patients with adverse bleeding events share a distinct fingerprint of chemokines that is associated with modulation of in vitro platelet functions. In addition, assessment of GPVI-associated changes in chemokine signalling and platelet functions demonstrated an increased diagnostic value in patients with CAD and might improve early risk discrimination for bleeding events.

Conclusion

The composition of platelet-derived chemokines correlated with platelet functions following antiplatelet treatment. Thus, assessment of chemokines may offer the perspective to identify patients at increased risk for bleeding events. Likewise, modulation of platelet chemokines in patients with revacept treatment contributes to the efficacy of antiplatelet treatment and might attenuate pathophysiological cascades leading to haemorrhagic diathesis in patients with CAD.

Graphical abstract

Study design and rationale: patients with coronary artery disease (CAD) undergoing elective percutaneous coronary intervention (PCI) and the impact of treatment with soluble GPVI inhibitor revacept. Changes in ex vivo platelet function and plasma chemokine concentrations were associated with an increased bleeding risk during the clinical follow-up. Further, GPVI-associated changes in chemokine signalling might attenuate pathophysiological cascades leading to haemorrhagic diathesis and improve early risk discrimination for bleeding events