Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Large artery stiffness and carotid flow pulsatility in stroke survivors Peter Wohlfahrt a,b,c , Alena Krajcoviechova a , Marie Jozifova a , Otto Mayer d , Jiri Vanek d , Jan Filipovsky d , Stephane Laurent e , and Renata Cifkova a,b,f 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 ¼ 0.04) or cryptogenic stroke (11.13  3.2 m/s, P ¼ 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. Conclusion: 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. Keywords: aortic stiffness, carotid stiffness, flow pulsatility, ischemic stroke, lacunar stroke, pulsatile index, resistive index Abbreviations: DA, stroke change in lumen area; DP, local pulse pressure; A, diastolic lumen area; BP, blood pressure; CAEM, cardioembolism; CCA, common carotid artery; CCS, Causative Classification of Stroke System; C dist , carotid distensibility; CVR, cerebrovascular resistance; CWS, circumferential wall stress; EDV, end-diastolic velocity; ID, internal diameter of the common carotid artery; IMT, intima–media thickness; LAA, large artery atherosclerosis; MBP, mean blood pressure; MFV, mean flow velocity; PSV, peak systolic velocity; PWV, pulse wave velocity INTRODUCTION T he interchanging heart systole and diastole produces blood pressure (BP) and flow fluctuations. The buffering function of the aorta decreases pressure pulsatility in the arterial system and, through impedance mismatch between the large proximal elastic arteries and distal muscular arteries, prevents the transmission of exces- sive pulsatile energy into the microcirculation [1]. Aortic stiffening caused by aging and cardiovascular risk factors has been shown to be associated with microvascular remodeling [2] that may serve to limit capillary exposure to excessive pulsatility and, also, to impair vascular reac- tivity. These factors may lead to repeated episodes of microvascular ischemia [3]. Lacunar stroke is caused by occlusion of small penetrating arteries. Previously, increased aortic pulse wave velocity (PWV), a measure of arterial stiffness, was found in individuals with asymp- tomatic [4] as well as symptomatic lacunar stroke [5]. Aortic stiffness is an independent predictor of fatal stroke [6], functional outcome after stroke [7,8], and leukoaraiosis [9]. Furthermore, markers of carotid stiffness are associated Journal of Hypertension 2014, 32:000–000 a Center for Cardiovascular Prevention of the First Faculty of Medicine, Charles University and Thomayer Hospital, Prague, b International Clinical Research Center, St Ann’s University Hospital, Brno, c Department of Preventive Cardiology, Institute for Clinical and Experimental Medicine, Prague, d 2nd Department of Internal Medicine, Charles University, Center for Hypertension, Pilsen, Czech Republic, e Department of Pharmacology, Georges Pompidou European Hospital, INSERM U970 and Paris University Descartes, Paris, France and f Department of Cardiology and Angiology, First Faculty of Medicine, Charles University, Prague, Czech Republic Correspondence to Peter Wohlfahrt, MD, Center for Cardiovascular Prevention, Thomayer Hospital, Videnska 800, 140 59 Prague 4, Czech Republic. Tel: +420 261 083 694; fax: +420 261 083 821; e-mail: wohlfp@gmail.com The results were partly presented as an oral presentation at the 23rd European Meeting on Hypertension & Cardiovascular Protection, held in Milan on 14–17 June 2013. Received 10 September 2013 Revised 15 January 2014 Accepted 15 January 2014 J Hypertens 32:000–000 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins. DOI:10.1097/HJH.0000000000000137 Journal of Hypertension www.jhypertension.com 1 Original Article