Author + information
- Received March 6, 1995
- Revision received June 22, 1995
- Accepted August 10, 1995
- Published online January 1, 1996.
- Tatsuya Komaru, MDa,
- Shogen Isoyama, MDa,**,
- Nobuyo Sekiguchi, MDa,
- Kenjiro Akai, MDa,
- Nobuyuki Shiba, MDa,
- Satoshi Yasuda, MDa,
- Masayuki Funakoshi, MDa,
- Kunio Shirato, MDa,
- Masayuki Zuguchi, MDa,
- Eiji Nozaki, MD*,
- Osamu Nishioka, MD* and
- Kenji Tamaki, MD*
- ↵**Address for correspondence: Dr. Shogen Isoyama, The First Department of Internal Medicine, Tohoku University School of Medicine. 1-1, Seiryo-machi, Aoba-ku, Sendai, 980 Japan.
Objectives. This study sought to investigate the effect of coronary angioplasty on chronic hypoperfusion-induced endothelial dysfunction in patients with coronary heart disease.
Background. The endothelium is an important component for organ flow regulation. Ischemia with or without reperfusion is known to cause endothelial dysfunction. We tested the hypothesis that chronic hypoperfusion impairs endothelial function in the angiographically normal coronary artery segment distal to stenosis and that the impairment by chronic hypoperfusion is reduced by coronary angioplasty.
Methods. In 13 patients with stable angina pectoris, substance P (10, 30 and 100 pmol) and nitroglycerin (200 μg) were sequentially infused into the coronary artery in a cumulative manner on the day after coronary angioplasty. In 10 of these patients, vascular responses to these agents were again investigated 3 months after angioplasty. Changes in vascular diameter were evaluated in vessels located proximal and distal to the target lesion, both of which were angiographically normal, by performing computer-assisted quantitative coronary angiography. In five patients, the transstenotic pressure gradient was also measured with a pressure sensor-mounted guide wire before angioplasty.
Results. On the day after angioplasty, the magnitude of dilation by substance P in distal segments was significantly less than that in proximal segments and inversely correlated with the transstenotic pressure gradient (p < 0.05) and lesion stenosis (p < 0.05). There was no difference in nitroglycerin-induced vasodilation between the two vessel segment groups. Three months later, the impaired response to substance P in the distal segment was restored to normal.
Conclusions. We conclude that chronic hypoperfusion impairs endothelium-dependent dilation of coronary artery distal to critical stenosis in patients with ischemic heart disease and that coronary angioplasty ameliorates the endothelial dysfunction within 3 months.
This study was supported in part by Grants 06670688 and 07670745 from the Scientific Research Fund of the Ministry of Education, Science and Culture, Tokyo, Japan.
- Received March 6, 1995.
- Revision received June 22, 1995.
- Accepted August 10, 1995.
- American College of Cardiology