Author + information
- Received May 26, 1995
- Revision received February 14, 1996
- Accepted April 24, 1996
- Published online September 1, 1996.
- Janine Krivokapich, M.D., F.A.C.C.∗,
- Johannes Czernin, M.D. and
- Heinrich R. Schelbert, M.D., F.A.C.C.
- ↵∗Address for correspondence: Dr. Janine Krivokopich, University of California Los Angeles School of Medicine, CHS 47-123, Los Angeles, California 90095-1679.
Objectives. This study sought to measure myocardial blood flow at rest and during dobutamine infusion and to correlate flow with cardiac work and severity of coronary artery disease.
Background. Dobutamine is used with cardiac imaging to induced possible ischemia in patients with known or suspected coronary artery disease. Positron emission tomography permits noninvasive quantitation of myocardial blood flow.
Methods. Fifteen patients with quantitative coronary arteriography were studied at rest and during dobutamine infusion using nitrogen-13 ammonia flow imaging with positron emission tomography. Myocardial blood flow was determined in regions corresponding to the three major coronary arteries for myocardium with and without dobutamine flow defects and with and without a >50% diameter stenosis.
Results. Eight patients had at least one dobutamine flow defect; four of whom had a previous myocardial infarction. One patient with >50% diameter stenosis had no flow defects, and one with < 50% diameter stenosis (49%) had one defect. Dobutamine significantly increased myocardial blood flow in regions with and without a dobutamine flow defect or >50% diameter stenosis, with a greater increase when a defect or >05% diameter stenosis was not present. Rest and dobutamine flows in regions without >50% diameter stenosis were 0.93 ± 0.20 (mean ± SD) and 2.16 ± 0.52 ml/min per g (p < 0.01), respectively. The corresponding flows in regions without a defect were 0.94 ± 0.21 and 2.17 ± 0.53 ml/min per g (p < 0.01), respectively. This 2.4-fold increase in flow was significantly correlated (p < 0.001) with a 2.2-fold increase in rate-pressure product induced by dobutamine. The rest and dobutamine flows for regions subtended by a vessel with >50% diameter stenosis were 0.70 ± 0.33 and 1.20 ± 0.54 ml/min per g (p < 0.05), respectively, whereas the corresponding values for regions with a dobutamine flow defect were 0.69 ± 0.33 ml/min per g at rest and 1.23 ± 0.54 ml/min per g during dobutamine (p < 0.05). Dobutamine increased flow inversely proportional to percent diameter stenosis. The rest flow for regions with a dobutamine flow defect were not significantly different from that in regions without defects.
Conclusions. Dobutamine resulted in a significant increase in myocardial blood flow that correlated significantly with both increased cardiac work and degree of stenosis.
☆ This work was supported by Grants HL 36232 and HL33177-06 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland and by Contract DE-AC03-76-SF00012 from the U.S. Department of Energy, Washington, D.C.
- Received May 26, 1995.
- Revision received February 14, 1996.
- Accepted April 24, 1996.