title: PhotoPoint photodynamic therapy promotes stabilization of atherosclerotic plaques and inhibits plaque progression.
abstract: OBJECTIVE
  The purpose of this study was to determine how photodynamic therapy (PDT) promotes stabilization and reduction of regional atherosclerosis.
  
  
  BACKGROUND
  Photodynamic therapy, a combination of photosensitizer and targeted light to promote cell apoptosis, has been shown to reduce atherosclerotic plaque inflammation.
  
  
  METHODS
  Forty New Zealand White rabbits were fed with cholesterol. The iliac arteries were balloon denuded and randomized to receive either PhotoPoint PDT treatment (photosensitizer and light) (Miravant Medical Technologies, Santa Barbara, California), photosensitizer (MV0611) alone, or light alone and were then compared at 7 and 28 days. Arteries were examined for evidence of plaque volume, cell number, macrophage and smooth muscle cell (SMC) content, and plaque cell proliferation.
  
  
  RESULTS
  Compared with contralateral iliac artery controls at 7 days, plaque progression was reduced by approximately 35% (p < 0.01); plaque progression was further reduced to approximately 53% (p < 0.01) by 28 days, leading to an increase in lumen patency (p < 0.05). At 7 days after PDT, percent plaque area occupied by macrophages decreased by approximately 98% (p < 0.001) and SMCs by approximately 72% (p < 0.05). At 28 days after PDT, removal of macrophages was sustained (approximately 92% decrease, p < 0.001) and plaques were repopulated with non-proliferating SMCs (approximately 220% increase, p < 0.001). There was no evidence of negative or expansive arterial remodeling, thrombosis, or aneurysm formation.
  
  
  CONCLUSIONS
  Photodynamic therapy simultaneously reduces plaque inflammation and promotes repopulation of plaques with a SMC-rich stable plaque cell phenotype while reducing disease progression. These early healing responses suggest that PDT is a promising therapy for the treatment of acute coronary syndromes.
authors.affiliation: Cardiovascular Research Institute, Washington Hospital Center, Washington, DC 20010, USA. ron.waksman@medstar.net
authors.forename: Ron
authors.initials: R
authors.lastname: Waksman
authors.forename: Pauline E
authors.initials: PE
authors.lastname: McEwan
authors.forename: Travis I
authors.initials: TI
authors.lastname: Moore
authors.forename: Rajbabu
authors.initials: R
authors.lastname: Pakala
authors.forename: Frank D
authors.initials: FD
authors.lastname: Kolodgie
authors.forename: David G
authors.initials: DG
authors.lastname: Hellinga
authors.forename: Rufus C
authors.initials: RC
authors.lastname: Seabron
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Rychnovsky
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Vasek
authors.forename: Robert W
authors.initials: RW
authors.lastname: Scott
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D007083:Iliac Artery / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D008652:Mesoporphyrins / Q000494:pharmacology / Q000627:therapeutic use*; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D010778:Photochemotherapy / Q000009:adverse effects; D017319:Photosensitizing Agents / Q000494:pharmacology / Q000627:therapeutic use*; D010865:Pilot Projects; D011817:Rabbits; D014945:Wound Healing / Q000187:drug effects
chemical_list: C532479:MV0611 compound; D008652:Mesoporphyrins; D017319:Photosensitizing Agents; D002784:Cholesterol