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Stroke Notes
reduction with ARB, beyond blood pressure control. In the fol-
lowing deliberations, we would like to put forward what we think
is an attractive hypothesis for such a mechanism.
The trend towards stroke reduction may be attributed to the
ability of ARBs to mildly inhibit platelet activity. In fact, platelets
contain angiotensin II receptors within their surface membranes
[2] and, therefore, ARBs may affect platelet activity directly tar-
geting these specific receptors. Indeed, in vitro data strongly sug-
gest antiplatelet properties of not only the prodrugs from the ARB
class, but their principal metabolites as well [3]. Moreover, these
results have been confirmed in a small randomized study suggest-
ing ex vivo platelet inhibition by ARBs in patients with mild to
moderate hypertension [4]. Treatment with valsartan (80–360
mg/day) over 9 weeks resulted in a consistent inhibition of ade-
nosine diphosphate-induced conventional platelet aggregation,
and prolonged closure time by the PFA-100 Platelet Analyzer. In
addition, therapy with ARB has been associated with a downreg-
ulation of the expression of numerous platelet surface receptors
such as glycoprotein Ib, glycoprotein IIb/IIIa activity, vitronectin
receptor, p-selectin, LAMP-1, and CD40-ligand.
It will be critical to know whether the minuscule, yet poten-
tially appealing stroke reduction signal observed in ONTARGET
will translate into significant stroke prevention in such a mega-
trial as PRoFESS [5]. These data are expected soon, and will be
critical for the comprehension of better ways to prevent recidivat-
ing strokes. The focus is on maintaining the optimal balance be-
tween the utilization of blood pressure-lowering medications and
platelet inhibitors to protect such high-risk patients from repeat-
ed vascular events.
The recently published ONgoing Telmisartan Alone and in
combination with Ramipril Global Endpoint Trial (ONTARGET)
was a phase IV randomized study which enrolled 25,620 high-risk
patients with coronary heart disease or diabetes plus additional
risk factors, who were over the age of 55 years of age but did not
have evidence of heart failure [1]. Patients were randomized to
receive either the ACE-inhibitor ramipril (10 mg/day), the angio-
tensin receptor blocker (ARB) telmisartan (80 mg/day), or their
combination. The mean duration of follow-up of the study was 55
months. The primary composite outcome was the time to the first
event of cardiovascular death, myocardial infarction (MI), stroke,
or hospitalization for heart failure. It occurred in 16.5% of pa-
tients treated with ramipril, in 16.7% of those treated with telmis-
artan, and in 16.3% of patients randomized to combination ther-
apy ( table 1). The ONTARGET investigators conclude that telmis-
artan was equivalent to ramipril in high-risk patients with
vascular disease or diabetes. The combination of the two drugs
was associated with more adverse events without an increase in
clinical outcomes benefit.
Even though the evidence presented in table 1 reveals a level
of nonsignificance for the difference of the various outcome mea-
sures among the three treatment arms, the incidence of strokes
may deserve further scrutiny. In absolute numbers, there were 405
strokes (4.7%) in the ramipril arm, compared with 369 strokes
(4.3%) in the telmisartan arm. In the combination group, there
were 373 strokes (4.4%). In fact, this finding represents an 8.5%
stroke reduction with ARB when compared with the ACE inhibi-
tor. Considering the straight-forward and robust study design of
ONTARGET and its long follow-up over 4 years, we suspect that
this mild trend towards a decrease in strokes does not represent a
random play of chance. Furthermore, when those antihyperten-
sive agents were used in combination, the trend towards fewer
strokes remains consistent, representing a 6.4% risk reduction as
compared to monotherapy with the ACE inhibitor, despite the
more potent antihypertensive effect. Since there is a lack of asso-
ciation between the degree of blood pressure lowering and the
incidence of strokes, the ONTARGET data may point to other
distinct underlying mechanism(s) responsible for the mild stroke
Published online: October 21, 2008
© 2008 S. Karger AG, Basel
1015–9770/08/0265–0563$24.50/0
Accessible online at:
www.karger.com/ced
Cerebrovasc Dis 2008;26:563–564
DOI: 10.1159/000164555
Telmisartan and Stroke Reduction in the
ONTARGET Trial: Benefit beyond Blood Pressure
Lowering?
Victor L. Serebruany
a
, Dan Atar
b
, Dan F. Hanley
a
a
HeartDrug
TM
Research Laboratories, Johns Hopkins University,
Towson, Md., USA;
b
Aker University Hospital and Faculty of
Medicine, University of Oslo, Oslo, Norway
Table 1. ONTARGET key outcomes
Outcome Ramipril
(n = 8,576)
%
Telmisartan
(n = 8,542)
%
Combination
(n = 8,502)
%
CV death/MI/stroke/
CHF hospitalization 16.5* 16.7 16.3
CV death/MI/stroke 14.1 13.9 14.1
MI 4.8 5.2 5.2
Stroke 4.7 4.3 4.4
CHF hospitalization 4.1 4.6 3.9
CV death 7.0 7.0 7.3
Any death 11.8 11.6 12.5
Renal impairment 10.2 10.6 13.5
* All nonsignificant among groups. CV = Cardiovascular;
CHF = congestive heart failure.