Ultrastructural and immunohistochemical analysis of early myocardial changes following transmyocardial laser revascularization

Citation
Sm. Cherian et al., Ultrastructural and immunohistochemical analysis of early myocardial changes following transmyocardial laser revascularization, J CARDIAC S, 15(5), 2000, pp. 341-346
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF CARDIAC SURGERY
ISSN journal
08860440 → ACNP
Volume
15
Issue
5
Year of publication
2000
Pages
341 - 346
Database
ISI
SICI code
0886-0440(200009/10)15:5<341:UAIAOE>2.0.ZU;2-H
Abstract
Background and Aim of the Study: Transmyocardial laser revascularization (T MR) has demonstrated significant relief in patients presenting with refract ory angina. However, the mechanism by which TMR improves clinical symptoms is unclear. This study analyzes the early immunohistochemical and ultrastru ctural features of the human myocardium following TMR. Methods: Specimens o f myocardium that contained laser channels were removed in toto at autopsy from three male patients, ages 41, 57, and 65 (mean age 55.8) who had died 1 to 11 days (mean 6.8) following laser revascularization. Consecutive para llel sections of specimens were stained with cell-type specific antibodies to CD3 (to identify T-lymphocytes), CD68 (macrophages), Factor VIII (endoth elial cells), and myosin (myocytes). Additionally, adjacent areas of myocar dium that contained laser channels were processed and analyzed by transmiss ion electron microscopy. Results: The internal lining surface of laser chan nels was composed of vacuolized and condensed myocardial debris. No obvious connections were noted between laser channels and the ventricular cavity. No endothelialization of channels was observed, whereas the adjacent noninj ured myocardium demonstrated microvessels lined by well-preserved endotheli al cells. The laser channels were surrounded by zones of necrotic cardiomyo cytes. Conclusions: Our observations suggest that laser channels are not li ned by endothelial cells during the early stages following TMR. Mechanisms other than direct myocardial perfusion from the ventricular cavity by paten t endothelialized channels may explain the immediate relief from angina pro vided by TMR.