Association between supine hypertension and orthostatic hypotension in autonomic failure
Association between supine hypertension and orthostatic hypotension in autonomic failure
复制标题
DOI：
10.1161/01.hyp.0000081216.11623.c3
复制
发表时间：
2003-08-01
期刊：
影响因子：
8.3
通讯作者：
Sharabi, Y
中科院分区：
文献类型：
--
作者：
Goldstein, DS;Pechnik, S;Sharabi, Y
仰卧高血压常见于原发性慢性自主神经衰竭。本研究探讨了这种情况下仰卧位高血压是否与直立性低血压（OH）相关，如果是，这种关联的机制可能是什么。在纯自主神经衰竭（PAF）、多系统萎缩（MSA）伴或不伴OH、帕金森病（PD）伴或不伴OH时，测量仰卧和直立血压、对Valsalva动作的血流动力学反应、压力反射-心血管增益和血浆去甲肾上腺素（NE）水平。对照组包括年龄匹配的健康志愿者和原发性高血压患者或因自主神经异常转诊的患者。根据Valsalva动作期间搏动间隔与收缩压之间的关系计算barrefrefal - cardiovascular gain。PAF、MSA合并OH、PD合并OH均表现为仰卧位高血压，且无论氟可的松治疗与否，其严重程度与原发性高血压相当。在PD或MSA患者中，有OH的患者仰卧休息时平均动脉压（109 +/- 3 mm Hg）高于无OH的患者（96 +/- 3 mm Hg, P = 0.002）。在所有3组OH中，barreflex - cardiovascular gain和直立性血浆NE水平的增量均显著降低。在PD或MSA患者中，有OH的患者比没有OH的患者（3.13 +/- 0.72 ms/mm Hg, P = 0.0002）有更低的平均压力反射-心血管增益（0.74 +/- 0.10 ms/mm Hg）。在PAF中，仰卧位高血压与OH和低压力反射-心血管增益有关。仰卧位高血压患者血浆NE水平低于非仰卧位高血压患者，提示与交感神经系统无关的升压机制有关。
Supine hypertension occurs commonly in primary chronic autonomic failure. This study explored whether supine hypertension in this setting is associated with orthostatic hypotension ( OH), and if so, what mechanisms might underlie this association. Supine and upright blood pressures, hemodynamic responses to the Valsalva maneuver, baroreflex-cardiovagal gain, and plasma norepinephrine ( NE) levels were measured in pure autonomic failure (PAF), multiple- system atrophy (MSA) with or without OH, and Parkinson's disease (PD) with or without OH. Controls included age-matched, healthy volunteers and patients with essential hypertension or those referred for dysautonomia. Baroreflex-cardiovagal gain was calculated from the relation between the interbeat interval and systolic pressure during the Valsalva maneuver. PAF, MSA with OH, and PD with OH all featured supine hypertension, which was equivalent in severity to that in essential hypertension, regardless of fludrocortisone treatment. Among patients with PD or MSA, those with OH had higher mean arterial pressure during supine rest ( 109 +/- 3 mm Hg) than did those lacking OH ( 96 +/- 3 mm Hg, P = 0.002). Baroreflex-cardiovagal gain and orthostatic increments in plasma NE levels were markedly decreased in all 3 groups with OH. Among patients with PD or MSA, those with OH had much lower mean baroreflex-cardiovagal gain (0.74 +/- 0.10 ms/mm Hg) than did those lacking OH ( 3.13 +/- 0.72 ms/mm Hg, P = 0.0002). In PAF, supine hypertension is linked to both OH and low baroreflex-cardiovagal gain. The finding of lower plasma NE levels in patients with than without supine hypertension suggests involvement of pressor mechanisms independent of the sympathetic nervous system.