Background Smooth muscle dysfunction in atherosclerotic disease is characterized by increased cytokines, which increase fibrosis and smooth muscle cell proliferation. We sought to evaluate the association between smooth muscle function and the tissue characterization of coronary artery plaque in culprit lesion. Methods Study subjects consisted of 130 consecutive patients (90 males (69.2%), mean 59.7짹11.6 years) who analyzed tissue characterization of culprit lesion by intravascular ultrasound (IVUS) – virtual histology (VH) and vascular smooth muscle function by nitroglyerin mediated brachial artery dilatation (NMD). Results NMD of study subjects was 10.4짹6.3%. Lesion length, plaque volume, fibous volume, fibro-fatty volume, calcium volume and necrotic core volume of culprit lesion were 21.0짹13.0mm, 197.1짹128.6���, 76.6짹61.1���, 18.7짹20.0���, 9.2짹9.6���, 22.2짹21.2���, respectively. Minimal luminal area (MLA) was 4.0짹1.2��� and plaque burden at MLA was 72.4짹9.7%. Tissue characteristics of the lesion at the MLA showed 5.2짹3.0��� of fibrous area, 1.4짹1.6��� of fibro-fatty area, 0.5짹0.4��� of dense calcium area and 1.4짹1.1��� of necrotic core area. NMD was correlated with fibrous volume (r=-0.19, p=0.029), MLA (r=0.27, p=0.002), plaque burden (r=-0.29, p=0.001), fibrous area (r=-0.19, p=0.027) and necrotic core area (r=-0.18, p=0.042). Conclusion: Smooth muscle dysfunction was related with increased fibrous volume of coronary artery plaque in culprit lesion, plaque burden and fibrous area of the lesion at the MLA. This study suggests that smooth muscle cell dysfunction of the brachial artery is correlated with the higher degree of plaque burden, especially fibrous volume, in culprit coronary lesion.