NEW YORK (Reuters Health) – In high-risk hypertensive patients with or without prior coronary artery disease, adding the angiotensin receptor II blocker valsartan to conventional non-ARB treatment reduces rates of cardio-cerebrovascular morbidity and mortality, according to results of a Japanese study reported in the American Journal of Cardiology online February 13.

The findings come from a post-hoc analysis of data from the Kyoto Heart Study, which demonstrated that valsartan reduced the overall rate cardiovascular and cerebrovascular events in high-risk hypertensive patients. The current study aimed at examining whether existing CAD affected the benefit of ARB treatment.

Accordingly, Dr. Jun Shiraishi, with the Kyoto First Red Cross Hospital, and colleagues divided the study population into 707 with CAD at baseline and 2324 without CAD.

The primary endpoint was a composite of new-onset or recurrent cardiovascular and cerebrovascular events. These included stroke, transient ischemic attack, acute myocardial infarction, angina pectoris, heart failure, dissecting aortic aneurysm, lower limb arterial obstruction, emergency thrombosis, transition to dialysis, and doubling of plasma creatine levels.

As might be expected, these events occurred more often in CAD patients (15.1%) than non-CAD patients (5.6%). The investigators found that add-on valsartan compared to non-ARB treatment significantly decreased the endpoint rate in patients with CAD (11.3% vs 19.0%) and without CAD (3.7% vs 7.6%).

Dr. Shiraishi and colleagues also noted that valsartan was associated with a significant reduction in angina and stroke only in patients with preexisting CAD.

They caution however, that the study has several limitations, given its post-hoc nature. “The difference in patient characteristics among groups cannot be completely excluded and the present study might contain undetected bias,” they point out.


Cardio-Cerebrovascular Protective Effects of Valsartan in High-Risk Hypertensive Patients With Coronary Artery Disease (from the Kyoto Heart Study)

Am J Cardiol 2012.