Author + information
- Received January 5, 1987
- Revision received May 5, 1987
- Accepted May 15, 1987
- Published online October 1, 1987.
- Mitsuhiro Yokota, MD*,1,
- Masafumi Koide, MD1,
- Takashi Miyahara, MD1,
- Susumu Kamihara, MD1,
- Atsushi Tsunekawa, MD1,
- Shoji Noda, MD1 and
- Iwao Sotobata, MD1
- ↵*Address for reprints: Mitsuhiro Yokota, MD, Cardiology Section, First Department of Internal Medicine, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan.
The mechanism of the antianginal actions of nilvadipine was investigated in 11 patients with effort angina pectoris. Hemodynamic data were obtained by angina-limited supine multistage bicycle ergometer exercise testing before and after a single 6 mg dose of nilvadipine.
Compared with chest pain during control exercise testing, pain at peak exercise disappeared or abated and the ST segment at peak exercise also showed less significant depression after administration of nilvadipine. At rest and at peak exercise, mean blood pressure, pulmonary artery wedge pressure and systemic vascular resistance decreased significantly, whereas heart rate and cardiac index increased significantly after nilvadipine. Rate-pressure product and stroke volume index did not change significantly. Coronary sinus flow at peak exercise increased significantly and total coronary vascular resistance at rest and at peak exercise decreased significantly after nilvadipine. The plasma concentrations of nilvadipine 1.5 hours after administration ranged from 1.15 to 8.23 ng/ml.
These data suggest that the principal factors in the antianginal actions of nilvadipine are an increase in myocardial oxygen supply due to increased coronary blood flow and a reduction in myocardial oxygen demand mainly by a decrease in afterload and additionally by a decrease in preload.
- Received January 5, 1987.
- Revision received May 5, 1987.
- Accepted May 15, 1987.
- American College of Cardiology Foundation