title: Mechanisms of myocardial hypoperfusion during rotational atherectomy of de novo coronary artery lesions and stenosed coronary stents: insights from serial myocardial scintigraphy.
abstract: BACKGROUND
  Rotational atherectomy (rotablation) frequently results in transient myocardial hypoperfusion due to peripheral vessel obstruction. This study compares the incidence, extent, and severity of perfusion defects induced by rotablation of de novo coronary lesions with rotablation of in-stent restenosis.
  
  
  RESULTS
  Twenty-five patients undergoing rotablation for restenosed stents (group A) were studied by technetium 99m sestamibi single photon emission computed scintigraphy at rest before rotablation, during rotablation, and 2 days after the procedure. For semiquantitative analysis, perfusion in 24 left ventricular regions was expressed as percentage of maximal sestamibi uptake. The results were compared with those of 25 patients treated for de novo coronary lesions (group B). Transient perfusion defects were observed in 22 (88%) of 25 patients in group A and, similarly, in 23 (92%) of 25 in group B. Perfusion was significantly reduced during rotablation in 3.1 +/- 2.6 (mean +/- SD) regions in group A and in 3.3 +/- 2.5 regions in group B. Perfusion in the region with maximal reduction during rotablation in groups A and B was 77% +/- 13% and 76% +/- 15% at baseline. Technetium uptake decreased to 59% +/- 19% and 54% +/- 14% during rotablation (P <.001 vs baseline, P = not significant for A vs B) and returned to 76% +/- 16% and 76% +/- 15% after rotablation. Intravascular ultrasonography indicated no correlation between the volume of ablated plaque and the extent and severity of perfusion defects in in-stent restenosis.
  
  
  CONCLUSIONS
  Incidence, extent, and severity of rotablation-related transient hypoperfusion are influenced by neither the type nor the quantity of ablated plaque material. Thus embolization of ablated plaque may be less important compared with other factors such as microcavitation or platelet aggregation.
authors.affiliation: Department of Cardiology (Medizinische Klinik I), University Hospital, RWTH Aachen, Pauwelstrasse 30, D-52057 Aachen, Germany.
authors.forename: Karl-Christian
authors.initials: KC
authors.lastname: Koch
authors.forename: Peter W
authors.initials: PW
authors.lastname: Radke
authors.forename: Eduard
authors.initials: E
authors.lastname: Kleinhans
authors.forename: Susanne
authors.initials: S
authors.lastname: Ninnemann
authors.forename: Uwe
authors.initials: U
authors.lastname: Janssens
authors.forename: Heinrich G
authors.initials: HG
authors.lastname: Klues
authors.forename: Udalrich
authors.initials: U
authors.lastname: Buell
authors.forename: Peter
authors.initials: P
authors.lastname: Hanrath
authors.forename: Juergen
authors.initials: J
authors.lastname: vom Dahl
mesh_terms: D017225:Atherectomy, Coronary; D016022:Case-Control Studies; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology / Q000601:surgery* / Q000628:therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology; D019275:Radiopharmaceuticals; D015607:Stents; D017256:Technetium Tc 99m Sestamibi; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D019275:Radiopharmaceuticals; D017256:Technetium Tc 99m Sestamibi