Dopamine: Its potential for inducing ischemic left ventricular dysfunction

As an agent potentially capable of inducing ischemia in patients with coronary artery disease, dopamine administered intravenously was evaluated as a pharmacologic stress agent by supine radionuclide angiography, and the results were compared with ergometer exercise. In a preliminary group of 11 subjects (4 normal subjects and 7 patients with coronary disease), dopamine alone was administered in increments of 2.5 µg/kg per min to a maximum of 15 µg/kg per min. There were significant differences between exercise and dopamine in maximal stress heart rates, 129.3 ± 30.0 versus 88.0 ± 35.8 beats/min (p < 0.05) in normal subjects and 118.9 ± 21.1 versus 87.6 ± 22.6 beats/min (p < 0.05) in patients with coronary disease, as well as in maximal stress rate-pressure products, 213.3 ± 51.4 versus 155.0 ± 52.5 mm Hg/min x 102 (p < 0.02) in normal subjects and 216.0 ± 45.6 versus 161.0 ± 48.6 mm Hg/min x 102 (p < 0.003) in patients with coronary disease. As a result, in these patients the ejection fraction response was significantly different: −3.3 ± 4.5% with exercise versus +6.3 ± 4.6% with dopamine (p < 0.05). In a second group of 41 subjects (9 normal subjects and 32 patients with coronary disease), atropine (0.6 mg) was administered intravenously before and after every second dopamine dose increment. This produced statistically similar maximal stress heart rates as compared with exercise in all subjects, rate-pressure products in normal subjects and slightly higher values with dopamine in patients with coronary disease: 200.3 ± 47.2 versus 183.1 ± 43.0 (p < 0.05). The ejection fraction response was similar in normal subjects, +1.8 ± 6.6% with exercise versus +4.3 ± 4.5% with dopamine, but dissimilar in patients with coronary artery disease, −3.2 ± 7.0 versus +2.5 ± 8.2% (p < 0.005). The sensitivity for patients with coronary disease was 91 and 56% for exercise and dopamine, respectively, if a criterion of an increase of less than 5% in ejection fraction was used; respective sensitivity was 94 and 66% for an increase of less than 7% and 97 and 78% for an increase of less than 10%. The lack of correlation in ejection fraction response may have been due to slight differences in baseline hemodynamic values and in inotropic or metabolic effects, or both, of dopamine in comparison with exercise. Dopamine, by failing to produce ischemia of the same degree or frequency as that produced by exercise, would not appear suitable as a pharmacologic alternative to exercise stre