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Assessment of captopril and nicardipine effects on chronic occlusive arterial disease of the lower extremity using Doppler ultrasound
Authors:D Bernardi  P Bartoli  A Ferreri  A B Geri  A Ieri
Affiliation:Department of Cardiology U.S.L. 17, Ospedale San Pietro Igneo, Fucecchio, Italy.
Abstract:The effects of two potent vasodilating drugs, captopril (C) (25 mg tid), nicardipine (N) (20 mg tid), and placebo (P) were evaluated and compared, in 10 men (mean age of sixty-five years) with intermittent claudication from moderate to severe multilevel chronic occlusive arterial disease (COAD) of the lower extremity, by use of the Doppler ultrasonic method, at rest and after Carter's exercise test. All the examined subjects were normotensive, without diabetes or cardiopathy; all have been smokers. The eight-week total protocol consisted of an initial two-week placebo run-in period followed by two active drug phases and a two-week placebo phase, according to a double-blind, randomized, crossover design. At the end of each two-week period, ankle-arm index (AAI) and, following exercise, onset of lower extremity discomfort time (ODT), duration of exercise (ET), decrease of ankle systolic pressure after test (APD), and recovery time (RT) were determined. Moreover, at rest, just after exercise, and after recovery, simultaneous common femoral artery velocity waves were recorded and analyzed by a quantitative approach to detect the peripheral vasomotor adjustments. None of the patients required the withdrawal of the active treatments. Compared with P, C significantly reduced APD and RT, and N reduced RT and AAI; furthermore N caused a significant decrease in ODT, whereas C showed a trend, although not statistically significant, to increase ODT. Neither active therapy modified ET. These results suggest that C and N have different short-term effects on peripheral circulation in COAD. During exercise, C induces hemodynamic improvement in the ischemic lower extremity probably by inhibition of the sympathetic system and consequent reduction in collateral vessel vasoconstriction.
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