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Cholesterol lowering therapy inhibits the low‐flow mediated vasoconstriction of the brachial artery in hypercholesterolaemic subjects
Author(s) -
MEGNIEN JEAN LOUIS,
SIMON ALAIN,
ANDRIANI ANTONIA,
SEGOND PATRICK,
JEANNIN SOPHIE,
LEVENSON JAIME
Publication year - 1996
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.1996.04047.x
Subject(s) - pravastatin , medicine , vasoconstriction , placebo , brachial artery , vasospasm , cardiology , reactive hyperemia , blood flow , endocrinology , hemodynamics , anesthesia , cholesterol , blood pressure , pathology , alternative medicine , subarachnoid hemorrhage
1 We tested whether lipid lowering treatment with HMG CoA reductase inhibitor modified the flow mediated large artery reactivity in primary pure hypercholesterolaemia. 2 Abnormalities in arterial reactivity have been described in the presence of high blood cholesterol, in particular an enhanced constriction of the brachial artery in response to acute induction of a low flow state. 3 Using pulsed‐Doppler, we measured brachial artery diameter and flow velocity at rest and their changes induced by wrist occlusion before and after 3 months of double‐blind treatment by pravastatin (40 mg orally) in 13 subjects and placebo in 15 others. 4 The significant decrease ( P <0.01) in diameter induced by wrist occlusion before (0.34±0.08 mm) placebo and pravastatin (0.39±0.10 mm) persisted after placebo (0.26±0.07 mm) but was abolished after pravastatin (0.07±0.05 mm). The absolute change in diameter induced by wrist occlusion was lower after than before pravastatin ( P <0.01) and lower after pravastin than after placebo ( P <0.05). Diameter during wrist occlusion was higher after pravastatin than after placebo (4.35±0.16 vs 3.89±0.09 mm); P <0.01). 5 These findings indicate that the lipid changes induced by pravastatin and/or some unknown but direct mechanism of the drug itself inhibit low‐flow‐mediated vasoconstriction associated with hypercholesterolaemia. Such effects may have important implications for the treatment of vasospasm often seen in the presence of high blood cholesterol.