title: Large artery stiffness and carotid flow pulsatility in stroke survivors.
abstract: OBJECTIVE
  Aortic stiffness is increased in lacunar stroke. The precise mechanism linking aortic stiffness to symptomatic lacunar stroke is not well understood. The aim of this study was to compare the effects of aortic stiffness, carotid stiffness, central blood pressure, and cerebrovascular resistance on carotid flow pulsatility according to stroke subtype.
  
  
  METHODS
  Two hundred and one consecutive patients were examined 13 months after hospitalization for their first-ever ischemic stroke. The stroke subtype was classified using the Causative Classification of Stroke System. Carotid-femoral pulse wave velocity (PWV) was used as a measure of aortic stiffness. Common carotid flow pulsatility was expressed as resistive index. Central blood pressure was measured using applanation tonometry.
  
  
  RESULTS
  Complete data were available for 174 patients (mean age… 67 ± 10 years, 64% men). In patients with lacunar stroke, aortic PWV was higher (13.11 ± 2.74 m/s) than in individuals with large artery atherosclerosis (9.98 ± 1.87 m/s, P <0.001), cardioembolic (11.31 ± 3.18 m/s, P = 0.04) or cryptogenic stroke (11.13 ± 3.2 m/s, P = 0.01). Similarly, central SBP and resistive index were higher in patients with lacunar stroke (145 ± 23 mmHg and 0.80 ± 0.04, respectively) than those with large artery atherosclerosis (128 ± 18 mmHg, P <0.01 and 0.74 ± 0.07, P <0.01, respectively) or cryptogenic stroke (132 ± 18 mmHg, P <0.01 and 0.76 ± 0.07, P <0.05, respectively). In multivariate analysis, aortic stiffness and central pulse pressure were the main determinants of resistive index independent of stroke subtype.
  
  
  CONCLUSIONS
  Our results suggest that aortic stiffening, by reducing the buffering function of the aorta and thereby increasing the transmission of pressure and flow pulsatility into the cerebral arterioles, may contribute to the pathogenesis of lacunar stroke.
authors.affiliation: aCenter for Cardiovascular Prevention of the First Faculty of Medicine, Charles University and Thomayer Hospital, Prague bInternational Clinical Research Center, St Ann's University Hospital, Brno cDepartment of Preventive Cardiology, Institute for Clinical and Experimental Medicine, Prague d2nd Department of Internal Medicine, Charles University, Center for Hypertension, Pilsen, Czech Republic eDepartment of Pharmacology, Georges Pompidou European Hospital, INSERM U970 and Paris University Descartes, Paris, France fDepartment of Cardiology and Angiology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
authors.forename: Peter
authors.initials: P
authors.lastname: Wohlfahrt
authors.forename: Alena
authors.initials: A
authors.lastname: Krajcoviechova
authors.forename: Marie
authors.initials: M
authors.lastname: Jozifova
authors.forename: Otto
authors.initials: O
authors.lastname: Mayer
authors.forename: Jiri
authors.initials: J
authors.lastname: Vanek
authors.forename: Jan
authors.initials: J
authors.lastname: Filipovsky
authors.forename: Stephane
authors.initials: S
authors.lastname: Laurent
authors.forename: Renata
authors.initials: R
authors.lastname: Cifkova
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002339:Carotid Arteries / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D063177:Pulse Wave Analysis; D020521:Stroke / Q000503:physiopathology*; D017741:Survivors; D059289:Vascular Stiffness