Lisinopril improves arterial function in hyperlipidaemia

Alison F. C. Lee, John B. C. Dick, Clare E. Bonnar, Allan D. Struthers

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    Endothelial function is defective in hypercholesterolaemia, and animal models have suggested that angiotensin-converting enzyme inhibitors may prevent arterial damage. We studied the effect of 6 months treatment with lisinopril on endothelial function in a group of patients with hypercholesterolaemia. Forty patients were studied. Forearm blood flow responses to acetylcholine and sodium nitroprusside were assessed by venous occlusion plethysmography. Subjects were then randomized in a double-blind fashion to receive either lisinopril, 20 mg/day (n=20), or placebo (n=20) for 6 months. Plethysmography was then repeated. Baseline variables between groups were comparable. In the lisinopril group blood pressure fell significantly [systolic: 145±4 to 128±4 mmHg (P < 0.001); diastolic: 84±2 to 74±2 mmHg (P < 0.001)]. An improvement was found in the vasodilatory response (expressed as a ratio of the infused/control arm) to acetylcholine, e.g. 3.33±0.3 (pre) versus 4.45±0.48 (post) at 30 µg/ml (P < 0.03), and also to nitroprusside, e.g. 3.0±0.2 (pre) versus 3.86±0.3 (post) at 3.2 µg/ml (P < 0.01). In the placebo group vasodilatation did not change significantly in response to acetylcholine, and nitroprusside responses were unchanged. The data presented suggest that 6 months of lisinopril therapy have a beneficial effect on arterial function in subjects with hyperlipidaemia. Further work should now investigate whether angiotensin-converting enzyme inhibitors are beneficial in reducing mortality and morbidity in hypercholesterolaemia.

    Original languageEnglish
    Pages (from-to)441-8
    Number of pages8
    JournalClinical Science
    Issue number5
    Publication statusPublished - May 1999


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