Lipsitz Lewis A, Gagnon Margaret, Vyas Mitul, Iloputaife Ikechukwu, Kiely Dan K, Sorond Farzaneh, Serrador Jorge, Cheng Debbie M, Babikian Viken, Cupples L Adrienne
Hebrew Rehabilitation Center for Aged, Boston, MA 02131, USA.
Hypertension. 2005 Feb;45(2):216-21. doi: 10.1161/01.HYP.0000153094.09615.11. Epub 2005 Jan 17.
Many physicians are reluctant to lower blood pressure to recommended levels in elderly hypertensive patients because of concern about producing cerebral hypoperfusion. Because hypertension is associated with potentially reversible structural and functional alterations in the cerebral circulation that may improve with treatment, we investigated whether long-term pharmacological reduction of systolic blood pressure will improve, rather than worsen, cerebral blood flow and its regulation. Three groups of elderly subjects 65 years of age or older were studied prospectively: normotensive subjects (N=19), treated hypertensive subjects with systolic pressure <140 mm Hg (N=18), and uncontrolled hypertensive subjects with systolic pressure >160 mm Hg at entry into the study (N=14). We measured beat-to-beat blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasonography), finger arterial pressure (photoplethysmography), and pulsatile distensibility of the carotid artery (duplex Doppler ultrasonography) at baseline and after 6 months of observation or antihypertensive therapy. After baseline hemodynamic measurements, uncontrolled hypertensive subjects underwent aggressive treatment with lisinopril with or without hydroclorothiazide or, if not tolerated, nifedipine or an angiotensin receptor blocker to bring their systolic pressure <140 mm Hg for 6 months. The other 2 groups were observed for 6 months. After 6 months of successful treatment, uncontrolled hypertensive subjects had significant increases in cerebral blood flow velocity and carotid distensibility that was not seen in the other groups. Treatment reduced cerebrovascular resistance and did not impair cerebral autoregulation. Therefore, judicious long-term treatment of systolic hypertension in otherwise healthy elderly subjects does not cause cerebral hypoperfusion.
许多医生不愿将老年高血压患者的血压降至推荐水平，因为担心会导致脑灌注不足。由于高血压与脑循环中潜在可逆的结构和功能改变有关，而这些改变可能会随着治疗而改善，因此我们研究了长期药物降低收缩压是否会改善而非恶化脑血流量及其调节。前瞻性地研究了三组65岁及以上的老年受试者：血压正常的受试者（N = 19）、收缩压<140 mmHg的已治疗高血压受试者（N = 18），以及研究开始时收缩压>160 mmHg的未控制高血压受试者（N = 14）。我们在基线时以及观察或抗高血压治疗6个月后，测量了大脑中动脉的逐搏血流速度（经颅多普勒超声检查）、手指动脉压（光电容积描记法）和颈动脉的搏动扩张性（双功多普勒超声检查）。在进行基线血流动力学测量后，未控制的高血压受试者接受了赖诺普利联合或不联合氢氯噻嗪的积极治疗，或者如果不耐受，则使用硝苯地平或血管紧张素受体阻滞剂，以使他们的收缩压<140 mmHg持续6个月。另外两组观察6个月。经过6个月的成功治疗后，未控制的高血压受试者的脑血流速度和颈动脉扩张性显著增加，而其他组未观察到这种情况。治疗降低了脑血管阻力，且未损害脑自动调节功能。因此，对其他方面健康的老年受试者进行明智的收缩期高血压长期治疗不会导致脑灌注不足。
