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Genetic Vascular Risk Factors and Cervical Artery Dissection
Quick Takes
- There is a highly significant association of genetically determined higher systolic BP and diastolic BP with an increased risk of cervical artery dissections (CeADs) (all types, carotid, and vertebral), providing strong evidence for a probable causal relationship.
- BP lowering is often neglected in stroke patients with CeAD, as the latter is perceived to be a transient phenomenon unrelated to vascular risk factors.
- These results may inform expert recommendations for BP monitoring following CeAD and for future trial design for secondary prevention of CeAD, especially with respect to BP-lowering treatment.
Study Questions:
What is the causal relation of vascular risk factors (VRFs) with cervical artery dissection (CeAD) risk and recurrence and its relation with non-CeAD ischemic stroke (IS)?
Methods:
The investigators used two-sample Mendelian randomization analyses to study the association of blood pressure (BP), lipid levels, type 2 diabetes, waist-to-hip ratio, smoking, and body mass index (BMI) with CeAD and non-CeAD IS. To simulate effects of the most frequently used BP-lowering drugs, they constructed genetic proxies and tested their association with CeAD and non-CeAD IS. In analyses among CeAD patients, the authors studied the association between weighted genetic risk scores (wGRS) of VRFs and the risk of multiple or early recurrent dissections. All associations were tested using logistic regression models in R 3.6.1 (glm function) and adjusted for age at admission, sex, type of dissection (carotid or vertebral), and the first four principal components of population stratification, after removing related participants.
Results:
Genetically determined higher systolic BP (SBP) (odds ratio [OR], 1.51; 95% confidence interval [CI], 1.32-1.72) and diastolic BP (DBP) (OR, 2.40; 95% CI, 1.92-3.00) increased the risk of CeAD (p < 0.0001). Genetically determined higher BMI was inconsistently associated with a lower risk of CeAD. Genetic proxies for beta-blocker effects were associated with a lower risk of CeAD (OR, 0.65; 95% CI, 0.50- 0.85), whereas calcium channel blockers were associated with a lower risk of non-CeAD IS (OR, 0.75; 95% CI, 0.63-0.90). A wGRS for SBP and DBP was associated with an increased risk of multiple or early recurrent CeAD.
Conclusions:
The authors report that these results are supportive of a causal association between higher BP and increased CeAD risk and recurrence, and provide genetic evidence for lower CeAD risk under beta-blockers.
Perspective:
This study reports a highly significant association of genetically determined higher SBP and DBP with an increased risk of CeAD (all types, carotid, and vertebral), providing strong evidence for a probable causal relationship. Furthermore, there was a protective association of genetically predicted SBP-lowering effects of beta-blockers on CeAD, but not non-CeAD IS risk. BP lowering is often neglected in stroke patients with CeAD, as the latter is perceived to be a transient phenomenon unrelated to VRFs. These results may inform expert recommendations for BP monitoring following CeAD and for future trial design for secondary prevention of CeAD, especially with respect to BP-lowering treatment.
Clinical Topics: Arrhythmias and Clinical EP, Vascular Medicine, Genetic Arrhythmic Conditions
Keywords: Blood Pressure, Dissection, Genetics, Ischemic Stroke, Risk Factors, Vascular Diseases
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