Key result
Dobutamine increased myocardial oxygen consumption while adenosine did not, though both significantly increased great cardiac vein blood flow (p<0.01) and induced myocardial ischemia in patients.
Why the study?
How do coronary hemodynamics differ during dobutamine and adenosine infusions in patients with stable angina and severe LAD stenosis compared to controls?
How do coronary hemodynamics differ during dobutamine and adenosine infusions in patients with stable angina and severe LAD stenosis compared to controls?
Dobutamine induces myocardial ischemia primarily through increased myocardial oxygen consumption, whereas adenosine-induced ischemia may result from regional flow maldistribution without increased oxygen demand.
Dobutamine may raise ischemic risk via increased oxygen consumption; leaves open optimal stress agent selection in coronary disease.
Pharmacologic stress tests are used to evaluate the significance of coronary arterial stenosis, and adenosine and dobutamine are often used for this purpose. The aim of this study was to examine coronary hemodynamics in 16 patients with stable exertional angina who had organic stenosis (> 90%) in the left anterior descending coronary arteries and in 13 control subjects at baseline and during separate intravenous infusions of dobutamine (20 micrograms/kg per min [corrected]) and adenosine (140 micrograms/kg per min [corrected]). Measurements of great cardiac vein blood flow and lactate and oxygen contents in the blood from the aortic root and great cardiac vein were analyzed in patients with ischemic signs of myocardial ischemia (ST-segment depression in the precordial ECG leads and/or myocardial lactate production) during the infusions (in 11 patients during adenosine infusion and in 12 patients during dobutamine infusion) and in control subjects. Myocardial oxygen consumption during adenosine infusion did not change compared with the baseline in both groups, whereas it increased during dobutamine infusion in both groups (p < 0.01 compared with the baseline in each case). However, great cardiac vein blood flow was significantly increased compared with the baseline during both infusions in both groups (p < 0.01 compared with baseline in each case), and the oxygen contents of great cardiac vein blood, which contains effluent from the ischemic region, showed no decrease but increased significantly during both infusions in the patients in comparison with control subjects. Although the global oxygen supply was excessive, myocardial ischemia occurred during dobutamine and adenosine infusions in the patients. As myocardial oxygen consumption remained unchanged during adenosine infusion, regional myocardial flow reduction, possibly as a result of flow maldistribution, may contribute, at least partly, to adenosine-induced myocardial ischemia. An increase in myocardial oxygen consumption may be the principal cause of myocardial ischemia during dobutamine infusion, but an inappropriate flow increase in normal myocardium may occur during dobutamine-induced ischemia.
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Kugiyama et al. (1998) studied Stable exertional angina (n=29). Dobutamine and Adenosine vs. Baseline and control subjects was evaluated on Myocardial oxygen consumption and great cardiac vein blood flow (p=<0.01). Dobutamine increased myocardial oxygen consumption while adenosine did not, though both significantly increased great cardiac vein blood flow (p<0.01) and induced myocardial ischemia in patients.
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