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Neurogenic Regulation of Basal Tone of Coronary Artery with Mild Atherosclerosis in Humans: Observation Using Two-Dimensional Intravascular Ultrasound

Katsufumi Mizushige, MD

Koji Ohmori, MD

Kazufumi Watanabe, MD

Yuichiro Takagi, MD

Yuzuru Takano, MD

Hirohide Matsuo, MD

Katsufumi Mizushige, MD

Second Department of Internal Medicine Kagawa Medical University 1750-1, Ikenobe, Miki, Kita Kagawa Japan 761-0793

The purpose of this study was to assess the role of the autonomic nervous system in the regulation of basal coronary artery tone in normal and atherosclerotic plaque segments by using intravascular ultrasound in humans. In each of 21 patients, a short-axis image at one site of coronary artery was imaged by means of a 3.2F, 30-MHz intravascular ultrasound before and after intracoronary administration of 2 mg isosorbide dinitrate (ISDN). The authors identified the perimeters of the vessel wall segments with normal or atherosclerotic plaque on ultrasound images and evaluated the basal tone in each segment as a percent increase in each perimeter produced by ISDN. Using heart rate variability analysis for 512 seconds recorded immediately before ISDN administration, they evaluated cardiac sympathetic and vagal activities at rest as the integrated power of fast Fourier transform (FFT) spectrum for the low-frequency (LF: 0.04 to 0.15 Hz), and high-frequency (HF: 0.15 to 0.4 Hz) components, respectively. Of 29 segments examined by ultrasound, 16 were normal and 13 were atherosclerotic plaque. In all 29 segments, ISDN produced an increase in the perimeter of the vessel wall. At the normal 16 segments, the increase in perimeter by ISDN exhibited a significant correlation to the power of HF (r = 0.749, p = 0.0008) but no significant correlation to LF. At 13 plaque segments, however, no significant correlation between the response to ISDN and autonomic nerve activity was observed. In conclusion, the basal tone of normal coronary arterial wall segment is closely related to parasympathetic nerve, whereas the relation is impaired in mild atherosclerotic segments.

Angiology, Vol. 50, No. 12, 989-996 (1999)
DOI: 10.1177/000331979905001204


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