Author + information
- Received April 26, 1993
- Revision received August 9, 1993
- Accepted September 15, 1993
- Published online February 1, 1994.
- Masakazu Yamagishi, MD1,∗,
- Kunio Miyatake, MD1,
- Jun Tamai, MD1,
- Satoshi Nakatani, MD1,
- Jun Koyama, MD1 and
- Steven E. Nissen, MD, FACC1,∗
- ↵∗Address for correspondence: Dr. Masakazu Yamagishi, the Cardiology Division of Medicine, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565, Japan.
Objectives. The purpose of this study was to use intravascular ultrasound imaging to examine the presence of occult atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed segments, testing the role of atherosclerosis in the development of vasospasm.
Background. Previous clinical and experimental studies have suggested that early atherosclerosis is present at the site of focal vasospasm. However, no clinical data exist demonstrating occult disease at the site of vasospasm at angiographically insignificant stenoses.
Methods. Twenty-two patients with chest pain at rest or during exertion, or both, were studied. Vasospasm was provoked by intracoronary administration of ergonovine maleate (0.01 to 0.04 mg). After relief of vasospasm by nitroglycerin administration, intravascular ultrasound imaging was performed with a 32- or 64-element, 20-MHz, synthetic aperture array ultrasound device.
Results. Focal vasospasm (arterial diameter reduction ≥90%) with ST-T segment elevation was provoked in 15 patients: in the left anterior descending coronary artery in 8 patients and in the right coronary artery in 7. The remaining seven patients (control group) showed diffuse narrowing, 22 ± 12% (mean ± SD) in diameter from the baseline angiograms after ergonovine administration. Atherosclerosis, defined as a significantly thickened intimal leading edge (0.42 ± 0.07 mm) associated with an increased sonolucent zone (0.57 ± 0.30 mm), was detected by ultrasound at all 15 sites with focal vasospasm, although these sites were normal or minimally narrowed by angiography. In contrast, seven segments from the control group exhibited a thin intimal leading edge (0.14 ± 0.04 mm, p < 0.01) and sonolucent zone (0.10 ± 0.07 mm, p < 0.01), indicating the absence of localized atherosclerotic lesions.
Conclusions. These results indicate that atherosclerosis is present at the site of focal vasospasm, even in the absence of angiographically significant coronary disease. We suggest that the existence of such atherosclerotic lesions is related to the occurrence of focal vasospasm in the clinical settings.
☆ This work was supported in part by grants from the Japan Heart Foundation, `Tokyo (Dr. Yamagishi) and the Takeda Medical Research Foundation, Osaka (Dr. Yamagishi) and a research grant (3A-7) from the Ministry of Health and Welfare of Japan, Tokyo (Dr. Miyatake). This work was presented in part at the 42nd Annual Scientific Session of the American College of Cardiology, Anaheim, California, March 1993.
- Received April 26, 1993.
- Revision received August 9, 1993.
- Accepted September 15, 1993.