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(Circulation. 1997;95:1169-1175.)
© 1997 American Heart Association, Inc.

Articles

Electron Microscopic Studies of Phenotypic Modulation of Smooth Muscle Cells in Coronary Arteries of Patients With Unstable Angina Pectoris and Postangioplasty Restenosis

Ying-Hwa Chen, MD; Yuh-Lien Chen, PhD; Shing-Jong Lin, MD, PhD; Chia-Yu Chou, MD; Guang-Yuan Mar, MD; Mau-Song Chang, MD; Shih-Pu Wang, MD

the Division of Cardiology, Department of Medicine, Veterans General Hospital-Taipei (Y.-H.C., S.-J.L., C.-Y.C., G.-Y.M., M.-S.C., S.-P.W.), and the Institute of Anatomy (Y.-L.C.), School of Life Science, and the Institute of Clinical Medicine (S.-J.L.), School of Medicine, National Yang-Ming University, Taipei, Taiwan.

Correspondence to Shing-Jong Lin, MD, PhD, Division of Cardiology, Department of Medicine, Veterans General Hospital-Taipei, 201 Shih-Pai Rd, Section 2, Taipei, Taiwan 112.

Background Proliferation and matrix protein secretion of coronary smooth muscle cells (SMCs) have been suggested as one of the mechanisms responsible for the development of postangioplasty restenosis and an alternative cause of unstable angina. Phenotypic modulation of SMCs may produce a pool of cells potentially responsive to growth stimulation that can synthesize abundant extracellular matrix. This study tested the hypothesis that phenotypic modulation of SMCs occurred during the evolution of postangioplasty restenosis and unstable angina.

Methods and Results The SMCs of coronary atherectomy specimens from 24 patients were identified under electron microscope. Volume fractions of synthetic organelles (VFSOs) and other features related to phenotypic modulation of SMCs were measured. The results showed that the VFSO in SMCs from 5 patients with unstable angina (group 2) resembled those from 9 patients with postangioplasty restenosis (group 3; 0.42±0.13 versus 0.36±0.10; P=NS), and both were significantly higher than those from 6 patients with stable angina (group 1; 0.21±0.11). Four patients with restenosis lesions who underwent angioplasty >6 months ago (group 4) also had a low VFSO in SMCs (0.19±0.05). This value was significantly less than those in groups 2 and 3 (P<.05) but similar to that in group 1.

Conclusions The coronary lesions from patients with unstable angina resembled those from patients with postangioplasty restenosis in terms of the phenotypic modulation and VFSO in SMCs. Our findings therefore suggest that after phenotypic modulation, the SMCs may become responsive to growth stimulation, with an ability to massively proliferate and synthesize abundant extracellular matrix. These processes may lead to plaque expansion and eventually to the development of unstable angina and restenosis.

Key Words: smooth muscle • angina • angioplasty • restenosis

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