CHOLESTEROL-LOWERING THERAPY INHIBITS THE LOW-FLOW MEDIATED VASOCONSTRICTION OF THE BRACHIAL-ARTERY IN HYPERCHOLESTEROLEMIC SUBJECTS

1 We tested whether lipid lowering treatment with HMG CoA reductase in hibitor modified the flow mediated large artery reactivity in primary pure hypercholesterolaemia. 2 Abnormalities in arterial reactivity hav e been described in the presence of high blood cholesterol, in particu lar an enhanced constriction of the brachial artery in response to acu te induction of a low flow state. 3 Using pulsed-Doppler, we measured brachial artery diameter and flow velocity at rest and their changes i nduced by wrist occlusion before and after 3 months of double-blind tr eatment 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 (0.3 9 +/- 0.10 mm) persisted after placebo (0.26 +/- 0.07 mm) but was abol ished after pravastatin (0.07 +/- 0.05 mm). The absolute change in dia meter induced by wrist occlusion was lower after than before pravastat in (P < 0/01) and lower after pravastin than after placebo (P < 0.05). Diameter during wrist occlusion was higher after pravastatin than aft er placebo (4.35 +/- 0.16 vs 3.89 +/- 0.09 mm); P < 0.01). 5 These fin dings indicate that the lipid changes induced by pravastatin and/or so me unknown but direct mechanism of the drug itself inhibit low-flow-me diated vasoconstriction associated with hypercholesterolaemia. Such ef fects may have important implications for the treatment of vasospasm o ften seen in the presence of high blood cholesterol.