The objective was to examine whether previous coronary artery disease (CAD) influences
the add-on effects of the angiotensin II receptor blocker (ARB) valsartan on cardio-cerebrovascular
morbidity and mortality in high-risk hypertensive patients who participated in the
Kyoto Heart Study. The primary end point was the same as in the main study: a composite
of new-onset and/or worsening of cardiovascular and cerebrovascular events. Median
follow-up was 3.27 years. According to the presence of previous CAD at baseline, the
study population was divided into 2 groups (with CAD, n = 707; without CAD, n = 2,324)
in which primary end-point events occurred more frequently in patients with CAD than
in patients without CAD (15.1% vs 5.6%, hazard ratio [HR] 2.68, 95% confidence interval
[CI] 2.11 to 3.42). Add-on valsartan significantly decreased the occurrence of the
primary end-point events in patients with CAD (11.3% vs 19.0%, HR 0.59, 95% CI 0.41
to 0.85) and without CAD (3.7% vs 7.6%, HR 0.49, 95% CI 0.34 to 0.70) compared to
non-ARB treatment. In the presence of previous CAD, patients with valsartan add-on
treatment had a significantly lower prevalence of angina pectoris and stroke than
those with non-ARB treatment, whereas the valsartan add-on effects on angina and stroke
were not significant in the absence of CAD. Changes in blood pressure during the follow-up
period did not differ significantly between study subgroups. In conclusion, in the
presence or absence of previous CAD, valsartan add-on treatment prevented more cardio-cerebrovascular
events than conventional non-ARB treatment in high-risk hypertensive patients. In
addition, valsartan add-on treatment conferred not only an antianginal effect but
also stroke prevention exclusively in hypertensive patients with CAD compared to those
without CAD.
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Article info
Publication history
Published online: February 13, 2012
Accepted:
December 19,
2011
Received in revised form:
December 19,
2011
Received:
October 16,
2011
Identification
Copyright
© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.