Every third person with Parkinson's disease (PD) may suffer from orthostatic hypotension (OH).¹ Besides classic OH (cOH), transient orthostatic blood pressure (BP) drops may occur within the first minute upon standing, qualifying for transient OH (tOH).² It is unclear whether morphometric factors, such as height and body mass index (BMI),³ promote OH in people with PD.

For this reason, we analyzed a previously published cohort of 173 European patients with PD for differences in height and BMI across individuals with laboratory-confirmed cOH, tOH, or no OH.²

After comparing the morphometric and other clinicodemographic characteristics across patients with and without OH, we tested the association between BMI, height, and cOH or tOH, by calculating the area under the receiver operating characteristic (ROC) curve in males and females separately. The Youden index applied to the coordinates of the ROC curves determined the most accurate BMI and height cut-offs distinguishing patients with either cOH or tOH from those without. Whenever significant cut-offs were found, we compared the derived subgroups for differences in clinicodemographic features and autonomic function indices by means of univariate, binary logistic regression analysis and age-adjusted ANOVA for repeated measurements.

The clinicodemographic features of the study population are reported elsewhere.² In our cohort, cOH occurred in 19% (n = 32) of patients and tOH in 24% (n = 41).

BMI did not differ between patients with either cOH (P = 0.270) or tOH (P = 0.798) compared with those without OH (Fig. 1).

The ROC curve analysis excluded any differences in height among female patients with or without OH, but pinpointed a positive association between cOH and taller stature in male patients (Fig. 1). Male patients with cOH did not otherwise differ for any other clinicodemographic characteristic from those with tOH or no OH. The Youden index identified a height cutoff of ≥172.5 cm for predicting cOH in male patients with PD (Fig. 1). Both univariate and age-adjusted logistic regression analysis confirmed a negative association between cOH and shorter stature in males (odds ratio = 0.14 [95% confidence interval, 0.03–0.66]; P = 0.013), despite higher, yet not significant after Benjamini–Hochberg correction, frequencies of cardiovascular comorbidities and use of antihypertensive medications (Supporting Information Table S1).

At hemodynamic monitoring, shorter patients showed an average systolic BP increase after 3 minutes on standing, while patients ≥172.5 cm tall had a decrease (P = 0.030; Supporting Information Fig. S1). The remaining cardiovascular autonomic function indices did not differ across the height groups (Supporting Information Fig. S1).

Pilot studies in Asian PD populations suggested an association between lower BMI and cOH.^4-6 Here we did not observe any difference in BMI across male or female patients with PD with either cOH, tOH or no OH. This inconsistency possibly reflects ethnic and morphometric differences between European and Asian natives.

Elderly, otherwise healthy, shorter subjects show higher BP values compared with taller subjects, potentially reflecting underlying hydrostatic mechanisms.⁷ The fact that cardiovascular autonomic function indices other than cOH were equally impaired in shorter and taller patients suggests that analogous, non-neurogenic mechanisms may prevent shorter individuals with PD from developing clinically relevant BP declines on standing.

Identifying individual OH risk factors may optimize screening measures for this frequently overlooked condition.

每三分之一患有帕金森病 (PD) 的人都可能患有直立性低血压 (OH)。¹除了经典的 OH (cOH)，站立后的第一分钟内可能会出现短暂的直立性血压 (BP) 下降，符合暂时性 OH (tOH) 的条件。²尚不清楚诸如身高和体重指数 (BMI) 等形态测量因素³是否会促进 PD 患者的 OH。

出于这个原因，我们分析了先前发表的 173 名欧洲 PD 患者的队列，以了解实验室确认的 cOH、tOH 或无 OH 个体的身高和 BMI 差异。²

在比较了有和没有 OH 患者的形态学和其他临床人口统计学特征后，我们通过分别计算男性和女性的接受者操作特征 (ROC) 曲线下面积来测试 BMI、身高和 cOH 或 tOH 之间的关联。应用于 ROC 曲线坐标的约登指数确定了区分患有 cOH 或 tOH 的患者与未患有 cOH 或 tOH 的患者的最准确的 BMI 和身高截止值。每当发现显着临界值时，我们通过单变量、二元逻辑回归分析和重复测量的年龄调整方差分析来比较衍生亚组的临床人口统计学特征和自主神经功能指数的差异。

研究人群的临床人口统计学特征在别处报告。²在我们的队列中，19% (n = 32) 的患者发生 cOH，24% (n = 41) 发生 tOH。

与没有 OH 的患者相比，患有 cOH ( P  = 0.270) 或 tOH ( P = 0.798) 的患者的 BMI 没有差异 （图 1）。

ROC 曲线分析排除了有或没有 OH 的女性患者的身高差异，但确定了男性患者的 cOH 与更高的身材之间存在正相关（图 1）。患有 cOH 的男性患者在任何其他临床人口统计学特征上与患有 tOH 或没有 OH 的患者没有其他差异。Youden 指数确定了 ≥172.5 cm 的身高临界值，用于预测男性 PD 患者的 cOH（图 1）。单变量和年龄调整逻辑回归分析均证实了 cOH 与男性身材矮小呈负相关（优势比 = 0.14 [95% 置信区间，0.03-0.66]；P = 0.013），尽管在 Benjamini-Hochberg 校正后，心血管合并症的频率和抗高血压药物的使用率更高，但并不显着（支持信息表 S1）。

在血流动力学监测中，身高较矮的患者在站立 3 分钟后平均收缩压升高，而身高 ≥172.5 厘米的患者收缩压降低（P  = 0.030；支持信息图 S1）。其余心血管自主功能指数在不同身高组之间没有差异（支持信息图 S1）。

亚洲 PD 人群的初步研究表明，较低的 BMI 和 cOH 之间存在关联。^4-6在这里，我们没有观察到男性或女性 PD 患者的 BMI 有任何差异，无论是 cOH、tOH 还是无 OH。这种不一致可能反映了欧洲和亚洲原住民之间的种族和形态差异。

与较高的受试者相比，老年人、其他方面健康、较矮的受试者显示出更高的 BP 值，这可能反映了潜在的流体静力学机制。⁷除了 cOH 以外的心血管自主神经功能指标在矮个子和高个子患者中同样受损这一事实表明，类似的非神经源性机制可能会阻止矮个子 PD 患者在站立时出现临床相关的血压下降。

识别个体 OH 风险因素可以优化针对这种经常被忽视的情况的筛查措施。