Title of article :
Effects of Prolonging Peak Dobutamine Dose During Stress Echocardiography
Author/Authors :
Neil J. Weissman MD، نويسنده , , FACC، نويسنده , , Geoffrey A. Rose MD، نويسنده , , Gary P. Foster MD، نويسنده , , Michael H. Picard MD، نويسنده , , FACC، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1997
Abstract :
Objectives. This study sought to test whether the physiologic advantage of prolonged dobutamine stage during stress echocardiography can be effectively combined with clinically practical infusion protocol.
Background. Dobutamine has half-life of 2 min and requires up to 10 min to achieve steady state. Despite these known pharmacodynamics, dobutamine stress echocardiography is routinely performed by advancing doses at 3-min intervals. Canine studies have shown that dobutamine stress echocardiography end points will occur at lower dose if each stage is prolonged, but these findings have yet to be used in the clinical setting.
Methods. The standard 3-min dobutamine dose stage during stress echocardiography was modified by extending the peak dose (40 μg/kg body weight per min) for an additional 2 min. Consecutive patients underwent this modified protocol to test whether the requirement for atropine could be reduced. According to this modified protocol, if dobutamine stress echocardiographic end point (85% of maximal predicted heart rate, new wall motion abnormalities, hypotension, arrhythmi or intolerable symptoms) was not reached at 3 min of the peak dose, this dose was prolonged for an additional 2 min. If dobutamine stress echocardiographic end point was still not attained, atropine (up to 1.0 mg intravenously) was administered.
Results. The study included 84 patients, 22 of whom (26.2%) achieved dobutamine stress echocardiographic end point using the standard 3-min stage. Of the 62 patients who did not reach an end point in the initial 3 min of peak dobutamine dose, the additional 2 min of dobutamine increased heart rate (from 99.6 ± 23.8 to 107.2 ± 23.2 beats/min, p < 0.01) and allowed 20 patients (32.3%, p < 0.01) to attain an end point. Of the remaining 42 patients, 23 never achieved stress echocardiographic end point, despite 1.0 mg of atropine. One patient developed supraventricular tachycardi during the additional 2 min of dobutamine, and one developed nonsustained ventricular tachycardi after receiving atropine.
Conclusions. These dat demonstrate that significant number of patients (32%) who do not reach dobutamine stress echocardiographic end point with the standard protocol can safely attain an end point solely by extending the duration of the peak dose. Adoption of this strategy may reduce the need for supplemental atropine and its potential adverse effects.
Journal title :
JACC (Journal of the American College of Cardiology)
Journal title :
JACC (Journal of the American College of Cardiology)