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Updated: Jan 7, 2026

A Calcium Phosphate-Induced Mouse Abdominal Aortic Aneurysm Model
Published on: November 18, 2022
Calcium channel blockers increase the risk of aortic aneurysm and dissection
Tianfeng Ma1, Zeyu Cai2, Xinming Xu3
1Department of Vascular and Endovascular Surgery, Chinese PLA General Hospital, Beijing, China.
Insights
Calcium channel blockers (CCBs) may increase the risk of aortic aneurysm and dissection (AAD). CCBs also worsened AAD outcomes in mouse models and patients, suggesting caution in prescribing them for hypertension.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Vascular Biology
Background:
- Aortic aneurysm and dissection (AAD) are critical vascular conditions lacking effective pharmacological treatments.
- Impaired vascular smooth muscle cell (VSMC) contractility is implicated in AAD pathogenesis.
- The precise role of calcium channel blockers (CCBs) in AAD development and progression is not well understood.
Purpose of the Study:
- To investigate the association between calcium channel blocker (CCB) use and the risk of aortic aneurysm and dissection (AAD).
- To evaluate the impact of CCBs on AAD progression and outcomes in preclinical models and human patients.
Main Methods:
- Analysis of data from 501,878 participants in the UK Biobank, with a median follow-up of 13.5 years.
- Assessment of CCB effects on aortic stiffness and AAD development in mouse models.
- Evaluation of CCB impact on AAD regression in patients with type B aortic dissection post-endovascular repair.
Main Results:
- CCB users exhibited a significantly higher risk of AAD (Hazard Ratio = 1.31) compared to untreated hypertensive individuals.
- In mouse models, CCBs exacerbated aortic stiffness and promoted AAD development.
- CCB use was associated with limited AAD regression in patients undergoing endovascular repair for type B aortic dissection.
- Silencing of protein kinase cGMP-dependent 1 (PRKG1) attenuated CCB-induced AAD progression.
Conclusions:
- Calcium channel blockers (CCBs) may be associated with an increased risk of aortic aneurysm and dissection (AAD).
- CCBs might negatively impact AAD prognosis and post-surgical outcomes.
- Caution is advised when prescribing CCBs to hypertensive patients at risk for AAD.
Abstract:
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.
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