Effects of blood pressure lowering on cerebral white matter hyperintensities in patients with stroke – The PROGRESS (Perindopril Protection Against Recurrent Stroke Study) Magnetic Resonance Imaging Substudy

1. Circulation. 2005 Sep 13;112(11):1644-50. Epub 2005 Sep 6.

Effects of blood pressure lowering on cerebral white matter hyperintensities in
patients with stroke: the PROGRESS (Perindopril Protection Against Recurrent
Stroke Study) Magnetic Resonance Imaging Substudy.

Dufouil C(1), Chalmers J, Coskun O, Besançon V, Bousser MG, Guillon P, MacMahon
S, Mazoyer B, Neal B, Woodward M, Tzourio-Mazoyer N, Tzourio C; PROGRESS MRI
Substudy Investigators.

Author information:
(1)INSERM U708, Paris, France.

Comment in
Circulation. 2005 Sep 13;112(11):1525-6.

BACKGROUND: The prevalence of white matter hyperintensities (WMHs) detected on
cerebral MRI is associated with hypertension, but it is not known whether blood
pressure lowering can arrest their progression. We report here the results of an
MRI substudy of PROGRESS (Perindopril Protection Against Recurrent Stroke Study),
a randomized trial of blood pressure lowering in subjects with cerebrovascular
disease.
METHODS AND RESULTS: The substudy comprised 192 participants who had a cerebral
MRI both at baseline and after a mean follow-up time of 36 months (SD=6.0
months). At the first MRI, WMHs were graded with a visual rating scale from A (no
WMH) to D (severe WMH). Participants were assigned to a combination of
perindopril plus indapamide (or their placebos; 58%) or to single therapy with
perindopril (or placebo). At the time of the second MRI, the blood pressure
reduction in the active arm compared with the placebo arm was 11.2 mm Hg for
systolic blood pressure and 4.3 mm Hg for diastolic blood pressure. Twenty-four
subjects (12.5%) developed new WMHs at follow-up. The risk of new WMH was reduced
by 43% (95% CI -7% to 89%) in the active treatment group compared with the
placebo group (P=0.17). The mean total volume of new WMHs was significantly
reduced in the active treatment group (0.4 mm3 [SE=0.8]) compared with the
placebo group (2.0 mm3 [SE=0.7]; P=0.012). This difference was greatest for
patients with severe WMH at entry, 0.0 mm3 (SE=0) in the active treatment group
versus 7.6 mm3 (SE=1.0) in the placebo group (P

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