Antihypertensive therapy increases cerebral blood flow and carotid distensibility in hypertensive elderly subjects.
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.
Lipsitz
Lewis A
LA
Hebrew Rehabilitation Center for Aged, Boston, MA 02131, USA. lipsitz@mail.hrca.harvard.edu
Gagnon
Margaret
M
Vyas
Mitul
M
Iloputaife
Ikechukwu
I
Kiely
Dan K
DK
Sorond
Farzaneh
F
Serrador
Jorge
J
Cheng
Debbie M
DM
Babikian
Viken
V
Cupples
L Adrienne
LA
D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D003187:Compliance / Q000187:drug effects; D005260:Female; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D017706:Lisinopril / Q000627:therapeutic use; D008297:Male; D020768:Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D009543:Nifedipine / Q000627:therapeutic use; D017156:Photoplethysmography; D011446:Prospective Studies; D017585:Ultrasonography, Doppler, Transcranial; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000627:therapeutic use
D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D014665:Vasodilator Agents; D006852:Hydrochlorothiazide; D017706:Lisinopril; D009543:Nifedipine