ELECTRON-MICROSCOPIC STUDIES OF PHENOTYPIC MODULATION OF SMOOTH-MUSCLE CELLS IN CORONARY-ARTERIES OF PATIENTS WITH UNSTABLE ANGINA-PECTORISAND POSTANGIOPLASTY RESTENOSIS

Background Proliferation and matrix protein secretion of coronary smoo th muscle cells (SMCs) have been suggested as one of the mechanisms re sponsible for the development of postangioplasty restenosis and an alt ernative cause of unstable angina. Phenotypic modulation of SMCs may p roduce a pool of cells potentially responsive to growth stimulation th at can synthesize abundant extracellular matrix. This study tested the hypothesis that phenotypic modulation of SMCs occurred during the evo lution of postangioplasty restenosis and unstable angina. Methods and Results The SMCs of coronary atherectomy specimens from 24 patients we re identified under electron microscope. Volume fractions of synthetic organelles (VFSOs) and other features related to phenotypic modulatio n of SMCs were measured. The results showed that the VFSO in SMCs from 5 patients with unstable angina (group 2) resembled those from 9 pati ents 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 p atients with stable angina (group 1; 0.21+/-0.11). Four patients with restenosis lesions who underwent angioplasty 6 months ago (group 4) al so 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 angin a resembled those from patients with postangioplasty restenosis in ter ms of the phenotypic modulation and VFSO in SMCs. Our findings therefo re suggest that after phenotypic modulation, the SMCs may become respo nsive 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 ang ina and restenosis.