Author + information
- Received December 26, 1991
- Revision received February 14, 1992
- Accepted March 13, 1992
- Published online October 1, 1992.
- Sammy Y. Chan, MDa,b,
- Richard C. Brunken, MD, FACCa,b,1,
- Johannes Czernin, MDa,b,
- Gerold Porenta, MDa,b,
- William Kuhle, MDa,b,2,
- Janine Krivokapich, MD, FACCa,b,
- Michael E. Phelps, PhDa,b and
- Heinrich R. Schelbert, MD, FACC∗,a,b
- ↵∗Address for correspondence: Heinrich R, Schelbert, MD, Division of Nuclear Medicine and Biophysics, University of California, Los Angeles School of Medicine. Los Angeles, California 90024-1721.
Objective. This study compared quantitatively the efficacy of intravenous adenosine and dipyridamole for pharmacologic induction of myocardial hyperemia.
Background. Pharmacologic vasodilation is used increasingly for induction of myocardial hyperemia in conjunction with radionuclide imaging of myocardial blood flow. Although both intravenous dipyridamole and adenosine have been used, the magnitude of hyperemia induced by these agents and the hyperemia to baseline blood flow ratios have not been quantified and compared.
Methods. Twenty normal volunteers were studied with dynamic positron emission tomography (PET) and intravenous nitrogen-13 ammonia. Myocardial blood flow was quantified with a two-compartment tracer kinetic model.
Results. Myocardial blood flow at rest averaged 1.1 ± 0.2 ml/min per g and increased significantly to 4.4 ± 0.9 ml/min per g during adenosine and 43 ± 1.3 ml/min per g after dipyridamole administration. Hyperemia to baseline flow ratios averaged 4.3 ± 1.6 for adenosine and 4.0 ± 1.3 for dipyridamole. The average flow ratios and the maximal flows achieved were similar for both agents, but there was considerable variation in the individual response to these agents, as indicated by the range of hyperemia to baseline flow ratios (from 2.0 to 8.4 for adenosine and from 1.5 to 5.8 for dipyridamole). in addition, the hyperemic responses to dipyridamole and to adenosine differed by > 1 ml/min per g in nine subjects.
Conclusions. Despite these inter- and istraindividual differences, we conclude that both agents are equally effective in producing myocardial hyperemia.
↵1 Dr. Brunken is the recipient of a Clinical Investigator Award (HL 02022-02) from the National Institutes of Health.
↵2 Dr. Kuhle the recipient of a Medical Student Research Fellowship from the American Heart Association, Greater Los Angeles Affiliate, Los Angeles, California.
☆ The Laboratory of Biomedical and Environmental Sciences is operated for the United States Department of Energy by the University of California under contract DE-FC03-87ER60615. This work was supported in part by the Director of the Office of Energy Research, Office of Health and Environmentel Research, Washington, D.C., by Research Grants HL 29845, HL 33177 and HL 36232 from the National Institutes of Health, Bethesda, Maryland, and by an Investigative Group Award, Greater Los Angeles Affiliate, American Heart Association, Los Angeles, California.
☆☆ The study drugs were supplied by Medco Research, Inc., Los Angeles, California and Boehringer Ingelheim, Ingelheim, Germany.
- Received December 26, 1991.
- Revision received February 14, 1992.
- Accepted March 13, 1992.