Lisinopril improves arterial function in hyperlipidaemia

• Published in: Clinical science (1979) Vol. 96; no. 5; pp. 441 - 448
• Main Authors: LEE, A. F. C, DICK, J. B. C, BONNAR, C. E, STRUTHERS, A. D
• Format: Journal Article
• Language: English
• Published: London Portland Press 01.05.1999
• Subjects: Acetylcholine; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Antihypertensive agents; Arteries; Biological and medical sciences; Cardiovascular system; Double-Blind Method; Endothelium, Vascular - drug effects; Female; Forearm - blood supply; Humans; Hyperlipidemias - drug therapy; Hyperlipidemias - physiopathology; Lisinopril - therapeutic use; Male; Medical sciences; Middle Aged; Nitroprusside; Pharmacology. Drug treatments; Plethysmography; Vasodilator Agents; Human; Lisinopril; Prognosis; Treatment efficiency; Metabolic diseases; Cardiovascular disease; Lipids; Hyperlipoproteinemia; Artery; Endothelium; Chemotherapy; Hypercholesterolemia; Treatment; Follow up study; Antihypertensive agent; Dyslipemia; ACE inhibitor
• ISSN: 0143-5221; 1470-8736
• DOI: 10.1042/CS19980386

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 microg/ml (P<0.03), and also to nitroprusside, e.g. 3.0+/-0.2 (pre) versus 3.86+/-0.3 (post) at 3.2 microg/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.