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J Hypertens. 2019 Jul 1. doi: 10.1097/HJH.0000000000002189. [Epub ahead of print]

Allopurinol treatment adversely impacts left ventricular mass regression in patients with well-controlled hypertension.

Author information

1
Division of Molecular and Clinical Medicine, University of Dundee.
2
Department of Clinical Radiology.
3
MEMO and Hypertension Research Centre, University of Dundee, Dundee, UK.
4
Population Health Sciences Division.

Abstract

OBJECTIVES:

Previous studies have demonstrated that high-dose allopurinol is able to regress left ventricular (LV) mass in cohorts with established cardiovascular disease. The aim of this study was to assess whether treatment with high-dose allopurinol would regress LV mass in a cohort with essential hypertension, LV hypertrophy and well-controlled blood pressure but without established cardiovascular disease.

METHODS:

We conducted a mechanistic proof-of-concept randomized, placebo-controlled, double-blind trial of allopurinol (600 mg/day) versus placebo on LV mass regression. Duration of treatment was 12 months. LV mass regression was assessed by Cardiac Magnetic Resonance. Secondary outcomes were changes in endothelial function (flow-mediated dilatation), arterial stiffness (pulse wave velocity) and biomarkers of oxidative stress.

RESULTS:

Seventy-two patients were randomized into the trial. Mean baseline urate was 362.2 ± 96.7 μmol/l. Despite good blood pressure control, LV mass regression was significantly reduced in the allopurinol cohort compared with placebo (LV mass -0.37 ± 6.08 versus -3.75 ± 3.89 g; P = 0.012). Oxidative stress markers (thiobarbituric acid reactive substances) were significantly higher in the allopurinol group versus placebo (0.26 ± 0.85 versus -0.34 ± 0.83 μmol/l; P = 0.007). Other markers of vascular function were not significantly different between the two groups.

CONCLUSION:

Treatment with high-dose allopurinol in normouricemic controlled hypertensive patients and LV hypertrophy is detrimental. It results in reduced LV mass regression and increased oxidative stress over a 12-month period. This may be because of an adverse impact on redox balance. Cohort selection for future cardiovascular trials with allopurinol is crucial.

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