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Circulation. 2004;110:2241-2245
Published online before print October 4, 2004, doi: 10.1161/01.CIR.0000144472.08647.40
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(Circulation. 2004;110:2241-2245.)
© 2004 American Heart Association, Inc.


Vascular Medicine

Impaired Cerebral Autoregulation in Patients With Malignant Hypertension

Rogier V. Immink, MD; Bert-Jan H. van den Born, MD; Gert A. van Montfrans, MD, PhD; Richard P. Koopmans, MD, PhD; John M. Karemaker, PhD; Johannes J. van Lieshout, MD, PhD

From the Departments of Physiology (R.V.I., J.M.K.), Internal Medicine (B.-J.H.v.d.B., G.A.v.M., J.J.v.L.), and Pharmacology and Pharmacotherapy (R.P.K.), Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

Correspondence to Johannes J. van Lieshout, MD, PhD, Department of Internal Medicine, Room F7-205, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail j.j.vanlieshout{at}amc.uva.nl

Received May 24, 2004; revision received July 29, 2004; accepted August 3, 2004.

Background— In patients with a malignant hypertension, immediate parenteral treatment with blood pressure–lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients.

Methods and Results— In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA Vmean to MAP phase lead and static CA as the MCA Vmean to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA Vmean to MAP phase lead was lower (30±8° versus 58±5°, mean±SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA Vmean decrease was 22±4%, along with a 27±3% reduction in MAP (from 166±4 to 121±6 mm Hg; P<0.05) in a linear fashion (averaged slope, 0.82±0.15% cm · s–1 · % mm Hg–1; r=0.70±0.07).

Conclusions— In patients with malignant hypertension, dynamic CA is impaired. An MCA Vmean plateau was not detected during the whole SNP treatment, indicating loss of static CA as well. This study showed that during the whole rapid reduction in blood pressure with SNP, MCA Vmean decreases almost one on one with MAP.


Key Words: blood flow velocity • cerebrovascular circulation • hypertension • ultrasonics




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