TY - JOUR
T1 - Laser-tissue interaction during transmyocardial laser revascularization
AU - Jansen, E. Duco
AU - Frenz, Martin
AU - Kadipasaoglu, Kamuran A.
AU - Pfefer, T. Joshua
AU - Altermatt, Hans J.
AU - Motamedi, Massoud
AU - Welch, Ashley J.
N1 - Funding Information:
This work was supported in part by the Albert and Clemmie Caster Foundation and The Office of Naval Research (grant no. N00014-91-J1564). Martin Frenz thanks the German Science Foundation (grant Fr 1147/1-1) for their financial support during his research fellowship at The University of Texas at Austin. We thank Dr John Pearce for use of his birefringence microscope.
PY - 1997/3
Y1 - 1997/3
N2 - Background. The clinical procedure known as transmyocardial revascularization has recently seen its renaissance. Unspite the promising preliminary clinical results, the associated mechanisms are subject to much discussion. This study is an attempt to unravel the basics of the interaction between 800-W CO2 laser radiation and biological tissue. Methods. Time-resolved flash photography was used to visualize the laser-induced channel formation in water and in vitro porcine myocardium. In addition, laser-induced pressures were measured. Light microscopy and birefringence microscopy were used to assess the histologic characteristics of laser-induced thermal damage. Results. The channel depth increased logarithmically with time (ie, with pulse duration) in water and porcine myocardium. Pressure measurements showed the occurrence of numerous small transients during the laser pulse, which corresponded with channel formation, as well as local and partial channel collapse during the laser pulse. Twenty millimeters of myocardium was perforated in 25 ms. Increasing the pulse duration had a small effect on the maximum transversable thickness, but histologic analysis showed that thermal damage around the crater increased with increasing pulse duration. Conclusions. Several basic aspects of the interaction of high-power CO2 laser radiation with myocardial tissue and tissue phantoms were studied in vitro. Although the goal of this study was not to unravel the mechanisms responsible for the beneficial effects of transmyocardial revascularization, it provided important information on the process of channel formation and collapse and tissue damage.
AB - Background. The clinical procedure known as transmyocardial revascularization has recently seen its renaissance. Unspite the promising preliminary clinical results, the associated mechanisms are subject to much discussion. This study is an attempt to unravel the basics of the interaction between 800-W CO2 laser radiation and biological tissue. Methods. Time-resolved flash photography was used to visualize the laser-induced channel formation in water and in vitro porcine myocardium. In addition, laser-induced pressures were measured. Light microscopy and birefringence microscopy were used to assess the histologic characteristics of laser-induced thermal damage. Results. The channel depth increased logarithmically with time (ie, with pulse duration) in water and porcine myocardium. Pressure measurements showed the occurrence of numerous small transients during the laser pulse, which corresponded with channel formation, as well as local and partial channel collapse during the laser pulse. Twenty millimeters of myocardium was perforated in 25 ms. Increasing the pulse duration had a small effect on the maximum transversable thickness, but histologic analysis showed that thermal damage around the crater increased with increasing pulse duration. Conclusions. Several basic aspects of the interaction of high-power CO2 laser radiation with myocardial tissue and tissue phantoms were studied in vitro. Although the goal of this study was not to unravel the mechanisms responsible for the beneficial effects of transmyocardial revascularization, it provided important information on the process of channel formation and collapse and tissue damage.
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U2 - 10.1016/S0003-4975(96)01143-5
DO - 10.1016/S0003-4975(96)01143-5
M3 - Article
C2 - 9066377
AN - SCOPUS:0030940624
SN - 0003-4975
VL - 63
SP - 640
EP - 647
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 3
ER -