Author + information
- Received January 19, 1994
- Revision received August 3, 1994
- Accepted August 5, 1994
- Published online January 1, 1995.
- Masakazu Yamagishi, MD, PhDa,
- Steven E Nissen, MD, FACC∗,a,
- David C Booth, MD, FACC†,
- John C Gurley, MD, FACC†,
- Jun Koyama, MDa,
- Shigeo Kawano, MDa and
- Anthony N DeMaria, MD, FACC†
- ↵∗Present address and address for correspondence: Dr. Steven E. Nissen, Department of Cardiology, Desk F-15, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106.
Objectives. This study was designed to assess the extent and timing of vasodilation after intracoronary administration of nitroglycerin using intravascular ultrasound. We also sought to relate the magnitude of nitroglycerin-induced dilation to the distribution of atherosclerotic plaque.
Background. Although previous angiographic studies have shown that nitroglycerin can dilate both normal and stenotic coronary arteries, it remains uncertain whether atherosclerotic vessels can respond to nitroglycerin to the same extent as normal arteries in the clinical setting.
Methods. We analyzed a total of 48 segments from 48 patients by means of a multielement 3.5F to 5.5F 20-MHz intravascular ultrasound system before and after intracoronary administration of nitroglycerin (250 μg). Videotaped images were digitized, and the lumen cross-sectional area was measured with an electronic cursor. In noncircumferential lesions, the perimeters of the normal and diseased portions were measured separately to compare the reactivity to nitroglycerin in each portion.
Results. Of 48 sites examined 14 were normal by ultrasound, and 34 revealed atherosclerotic lesions. In the 14 normal segments nitroglycerin produced a large increase in cross-sectional area (31 ± 16% [mean ± SD]) within 60 s after injection. In the 34 atherosclerotic segments, nitroglycerin-induced dilation was impaired, and the cross-sectional area increased only 12 ± 8% (p < 0.01). In 15 of 34 atherosclerotic segments, a noncircumferential lesion was identified, and the cross-sectional area after nitroglycerin increased an average of 17 ± 6%. In the remaining 19 sites, circumferential disease was present, and the cross-sectional area increased by only 8 ± 7% (p < 0.05 vs. normal or noncircumferential atherosclerotic segments). In noncircumferential lesions, the increase in the perimeter of the normal portion of the wall was significantly greater (14 ± 6%) than the increase in the diseased portion (5 ± 3%, p < 0.05).
Conclusions. These data indicate that vasoreactivity after nitroglycerin administration is reduced in segments with atherosclerosis by ultrasound. We suggest that nitroglycerin-induced vasodilation at the stenotic segments can be produced primarily by expansion of the nondiseased portion of the vessel wall.
☆ This study was supported in part by grants from the Japan Heart Foundation, Tokyo; Takeda Medical Research Foundation, Osaka; and Shimadzu Science Research Foundation, Kyoto, Japan. It was presented in part at the 41st Annual Scientific Session of the American College of Cardiology, Dallas, Texas, April 1992.
- Received January 19, 1994.
- Revision received August 3, 1994.
- Accepted August 5, 1994.