Origin of arterial wall dissections induced by pulsed excimer and mid-infrared laser ablation in the pig.

To study adjacent tissue damage after delivery of holmium, thulium and excimer laser pulses, porcine thoracic aortas were irradiated in vivo. After 3 days, microscopic analysis of 67 craters produced by all three lasers demonstrated large dissections extending from the craters. The mean diameter of the dissections was smaller for excimer-induced craters (1.38 +/- 0.42 mm; n = 22) than for holmium-induced (2.7 +/- 0.87 mm; n = 22) and thulium-induced (2.37 +/- 0.42 mm; n = 14) craters (p less than 0.01 vs. mid-infrared dissections). In addition, microscopic analysis demonstrated necrosis adjacent to the crater. The lateral necrotic zones of the thulium-induced craters were smaller than the holmium- and excimer-induced necrotic zones (p less than 0.01). To identify the origin of the excessive tissue tearing, laser-saline and laser-tissue interaction were compared in vitro by time-resolved flash photography. In saline solution, the mid-infrared lasers showed bubble formation on a microsecond time scale. The excimer laser produced similar bubbles in the vicinity of tissue. For all three lasers, elevation of the tissue surface was shown during in vitro ablation. Dimension (diameter up to 4 mm) and time course (rise time of 100 to 300 microseconds) of bubble formation and tissue elevation were strikingly similar. Thus, tissue dissections are caused by the expansion of a vapor bubble within the target tissue. Coronary dissections after excimer and mid-infrared laser angioplasty might be related to the forceful bubble expansion.