From the Division of Neurocritical Care & Emergency Neurology (J.N.A., C.P.B., A.C.L., V.M.T.-L., A.H., N.H.P., K.N.S., G.J.F.), Department of Neurology, Yale School of Medicine; Frank H. Netter MD School of Medicine (Z.S.D., C.J.C.); Division of Vascular Neurology (N.H.P., L.H.S.), Department of Neurology, Yale School of Medicine; and Department of Internal Medicine (T.M.G.), Yale School of Medicine, New Haven, CT.
Neurology. 2023 Apr 11;100(15):e1587-e1597. doi: 10.1212/WNL.0000000000206763. Epub 2023 Jan 23.
Blood pressure (BP) is often not at goal in stroke survivors, leaving individuals vulnerable to additional vascular events. Given that BP is a highly heritable trait, we hypothesize that a higher polygenic susceptibility to hypertension (PSH) leads to worse BP control in stroke survivors.
We conducted a study within the UK Biobank evaluating persons of European ancestry who survived an ischemic or hemorrhagic stroke. To model the PSH, we created polygenic risk scores (PRSs) for systolic and diastolic BP using 732 genetic variants. We divided the PRSs into quintiles and used linear/logistic regression to test whether higher PSH led to higher observed BP, uncontrolled BP (systolic BP > 140 mm Hg or diastolic BP > 90 mm Hg), and resistant BP (uncontrolled BP despite being on ≥3 antihypertensive drugs). We conducted an independent replication using data from the Vitamin Intervention for Stroke Prevention (VISP) trial.
We analyzed 5,940 stroke survivors. When comparing stroke survivors with very low vs very high PSH, the mean systolic BP was 137 (SD 18) vs 143 (SD 20, < 0.001), the mean diastolic BP was 81 (SD 10) vs 84 (SD 11, < 0.001), the prevalence of uncontrolled BP was 42.8% vs 57.2% ( < 0.001), and the prevalence of resistant hypertension was 3.9% vs 11% ( < 0.001). Results remained significant using multivariable models ( < 0.001) and were replicated in the VISP study (all tests with < 0.05).
A higher PSH is associated with worse BP control in stroke survivors. These findings point to genetic predisposition as an important determinant of poorly controlled BP in this population.
血压（BP）在中风幸存者中往往达不到目标，使个体易发生额外的血管事件。鉴于 BP 是一种高度遗传性特征，我们假设更高的高血压多基因易感性（PSH）导致中风幸存者的 BP 控制更差。
我们在英国生物库中进行了一项研究，评估了患有缺血性或出血性中风后存活的欧洲血统个体。为了对 PSH 进行建模，我们使用 732 个遗传变异创建了收缩压和舒张压的多基因风险评分（PRS）。我们将 PRS 分为五分位数，并使用线性/逻辑回归来检验更高的 PSH 是否导致更高的观察到的 BP、未控制的 BP（收缩压>140mmHg 或舒张压>90mmHg）和耐药性 BP（尽管使用≥3 种降压药物仍未控制的 BP）。我们使用来自维生素干预预防中风（VISP）试验的数据进行了独立的复制。
我们分析了 5940 名中风幸存者。当比较 PSH 非常低与非常高的中风幸存者时，平均收缩压为 137（SD 18）与 143（SD 20，<0.001），平均舒张压为 81（SD 10）与 84（SD 11，<0.001），未控制的 BP 患病率为 42.8%与 57.2%（<0.001），耐药性高血压的患病率为 3.9%与 11%（<0.001）。多变量模型（<0.001）的结果仍然显著，并且在 VISP 研究中得到了复制（所有检验均<0.05）。
更高的 PSH 与中风幸存者的 BP 控制更差相关。这些发现表明遗传易感性是该人群 BP 控制不佳的一个重要决定因素。
