title: Complex plaques in the proximal descending aorta: an underestimated embolic source of stroke.
abstract: OBJECTIVE
  To investigate the incidence of retrograde flow from complex plaques (> or =4-mm-thick, ulcerated, or superimposed thrombi) of the descending aorta (DAo) and its potential role in embolic stroke.
  
  
  METHODS
  Ninety-four consecutive acute stroke patients with aortic plaques > or =3-mm-thick in transesophageal echocardiography were prospectively included. MRI was performed to localize complex plaques and to measure time-resolved 3-dimensional blood flow within the aorta. Three-dimensional visualization was used to evaluate if diastolic retrograde flow connected plaque location with the outlet of the left subclavian artery, left common carotid artery, or brachiocephalic trunk. Complex DAo plaques were considered an embolic source if retrograde flow reached a supra-aortic vessel that supplied the territory of visible acute and embolic retinal or cerebral infarction.
  
  
  RESULTS
  Only decreasing heart rate was correlated (P<0.02) with increasing flow reversal to the aortic arch. Retrograde flow from complex DAo plaques reached the left subclavian artery in 55 (58.5%), the left common carotid artery in 23 (24.5%), and the brachiocephalic trunk in 13 patients (13.8%). Based on routine diagnostics and MRI of the ascending aorta/aortic arch, stroke etiology was determined in 57 and cryptogenic in 37 patients. Potential embolization from DAo plaques was then identified in 19 of 57 patients (33.3%) with determined and in 9 of 37 patients (24.3%) with cryptogenic stroke.
  
  
  CONCLUSIONS
  Retrograde flow from complex DAo plaques was frequent in both determined and cryptogenic stroke and could explain embolism to all brain territories. These findings suggest that complex DAo plaques should be considered a new source of stroke.
authors.affiliation: University Hospital Freiburg, Department of Neurology, Breisacher Strasse 64, 79106 Freiburg, Germany. andreas.harloff@uniklinik-freiburg.de
authors.forename: Andreas
authors.initials: A
authors.lastname: Harloff
authors.forename: Jan
authors.initials: J
authors.lastname: Simon
authors.forename: Stefanie
authors.initials: S
authors.lastname: Brendecke
authors.forename: Dawit
authors.initials: D
authors.lastname: Assefa
authors.forename: Thomas
authors.initials: T
authors.lastname: Helbing
authors.forename: Alex
authors.initials: A
authors.lastname: Frydrychowicz
authors.forename: Johannes
authors.initials: J
authors.lastname: Weber
authors.forename: Manfred
authors.initials: M
authors.lastname: Olschewski
authors.forename: Christoph
authors.initials: C
authors.lastname: Strecker
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hennig
authors.forename: Cornelius
authors.initials: C
authors.lastname: Weiller
authors.forename: Michael
authors.initials: M
authors.lastname: Markl
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001013:Aorta, Thoracic / Q000473:pathology / Q000503:physiopathology; D050197:Atherosclerosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D002339:Carotid Arteries / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006339:Heart Rate; D006801:Humans; D020766:Intracranial Embolism / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D020521:Stroke / Q000209:etiology / Q000473:pathology / Q000503:physiopathology