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<p>Aortic aneurysm and dissection (AAD) are life-threatening conditions without effective medications. Impaired contractility of vascular smooth muscle cells (VSMCs) is strongly linked to AAD, but the role of calcium channel blockers (CCBs), which directly inhibits VSMC contractility, in AAD remains unclear. Here we showed data from 501,878 initially AAD-free participants in UK Biobank. Over a median follow-up of 13.5 years, CCB users had higher AAD risk (HR = 1.31) than hypertensive patients not receiving antihypertensive treatment. In mouse models of AAD, CCBs significantly aggravated aortic stiffness and AAD development. For patients with type B aortic dissection who underwent endovascular repair, CCBs limited AAD regression compared with other antihypertensives. Moreover, silencing of protein kinase cGMP-dependent 1 (PRKG1) significantly mitigated CCB-aggravated AAD progression. These findings suggest that CCBs may increase AAD risk and post-stent surgery prognosis, highlighting the need for caution when prescribing CCBs to hypertensive patients at risk for AAD.</p>

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Calcium channel blockers increase the risk of aortic aneurysm and dissection

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月25日

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  • Tianfeng Ma,
  • Zeyu Cai,
  • Xinming Xu,
  • Long Cao,
  • Ao Wang,
  • Zhongshuang Zhang,
  • Siting Zhang,
  • Zhenkun Huang,
  • Jingjing Luo,
  • Sen Lin,
  • Jiashu Ge,
  • Xinhao Wang,
  • Yi Fu,
  • Fang Yu,
  • Jing Zhou,
  • Lixin Wang,
  • Hongpeng Zhang,
  • Xiang Gao,
  • Wei Guo,
  • Wei Kong

摘要

Aortic aneurysm and dissection (AAD) are life-threatening conditions without effective medications. Impaired contractility of vascular smooth muscle cells (VSMCs) is strongly linked to AAD, but the role of calcium channel blockers (CCBs), which directly inhibits VSMC contractility, in AAD remains unclear. Here we showed data from 501,878 initially AAD-free participants in UK Biobank. Over a median follow-up of 13.5 years, CCB users had higher AAD risk (HR = 1.31) than hypertensive patients not receiving antihypertensive treatment. In mouse models of AAD, CCBs significantly aggravated aortic stiffness and AAD development. For patients with type B aortic dissection who underwent endovascular repair, CCBs limited AAD regression compared with other antihypertensives. Moreover, silencing of protein kinase cGMP-dependent 1 (PRKG1) significantly mitigated CCB-aggravated AAD progression. These findings suggest that CCBs may increase AAD risk and post-stent surgery prognosis, highlighting the need for caution when prescribing CCBs to hypertensive patients at risk for AAD.