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Photodynamic therapy (PDT) is the result of an interaction between light and a photoactive drug. The interaction produces cytotoxic oxygen radicals and radicals and microvascular collapse, resulting in tissue death. A number of photoactive drugs have been shown to accumulate in greater concentration in atherosclerotic plaque than in normal arterial wall and are potentially useful for PDT. The newer generation agents are safe and have brief skin phototoxicity as the only significant side effect. PDT in several animal models of atherosclerosis has shown plaque removal without damage to the artery wall if appropriate light energy is used, with no perforation, and no distal embolization or obstruction. In one such study we found that PDT using Photofrin and 630 nm laser light reduced the mean percent stenosis of 12 stenoses in 8 pigs from 63% to 40%, and in 7/12 of the segments from 63% to 16%, whereas in 2 untreated control lesions the mean stenosis progressed from 60% to 85%. PDT requires several days for tissue destruction, and immediate luminal enlargement by an adjunct angioplasty intervention may be appropriate. Animal studies suggest that PDT also inhibits the intimal hyperplasia process which follows vascular injury, and PDT may inhibit restenosis following clinical coronary angioplasty. The enthusiasm for PDT of atherosclerosis, therefore, stems from three important potential advantages of the technique: the apparent selectivity and safety of the process, the potential for effective debulking of plaque and the possibility of reduction or inhibition or restenosis.
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