Arterial Stiffness in Patients with Deep and Lobar Intracerebral Hemorrhage.
10.5853/jos.2014.16.3.184
- Author:
Maurizio ACAMPA
1
;
Francesca GUIDERI
;
Ilaria DI DONATO
;
Rossana TASSI
;
Giovanna MAROTTA
;
Giuseppe LO GIUDICE
;
Paolo D'ANDREA
;
Giuseppe MARTINI
Author Information
1. Stroke Unit, Department of Neurological and Sensorineural Sciences, Azienda Ospedaliera Universitaria Senese, "Santa Maria alle Scotte" General Hospital, Siena, Italy. M.Acampa@ao-siena.toscana.it
- Publication Type:Original Article
- Keywords:
Hemorrhagic stroke;
Intracerebral hemorrhage;
Deep cerebral hemorrhage;
Lobar cerebral hemorrhage;
Arterial stiffness;
Arterial hypertension
- MeSH:
Arteries;
Basal Ganglia;
Blood Pressure;
Brain;
Cerebellum;
Cerebral Hemorrhage*;
Complement System Proteins;
Compliance;
Elasticity;
Heart Rate;
Hemorrhage;
Humans;
Hypertension;
Incidence;
Linear Models;
Male;
Pons;
Rupture;
Stroke;
Thalamus;
Vascular Stiffness*
- From:Journal of Stroke
2014;16(3):184-188
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND PURPOSE: Intracerebral hemorrhage (ICH) accounts for approximately 10% of stroke cases. Hypertension may play a role in the pathogenesis of ICH that occurs in the basal ganglia, thalamus, pons, and cerebellum, but not in that of lobar ICH. Hypertension contributes to decreased elasticity of arteries, thereby increasing the likelihood of rupture in response to acute elevation in intravascular pressure. This study aimed to evaluate arterial stiffness (using the arterial stiffness index [ASI]) in patients with deep (putaminal and thalamic) ICH in comparison with patients with lobar ICH. METHODS: We enrolled 64 patients (mean+/-SD age: 69.3+/-10.7 years; 47 men and 17 women) among 73 who referred consecutively to our department for intraparenchymal hemorrhage and underwent brain computed tomography (CT) and cerebral angio-CT. In all the subjects, 24-hour heart rates and blood pressures were monitored. The linear regression slope of diastolic on systolic blood pressure was assumed as a global measure of arterial compliance, and its complement (1 minus the slope), ASI, has been considered as a measure of arterial stiffness. RESULTS: In the patients with deep ICH, ASI was significantly higher than in the patients with lobar ICH (0.64+/-0.19 vs. 0.53+/-0.17, P=0.04). CONCLUSIONS: Our results suggest that in deep ICH, arterial stiffening represents a possible pathogenetic factor that modifies arterial wall properties and contributes to vascular rupture in response to intravascular pressure acute elevation. Therapeutic strategies that reduce arterial stiffness may potentially lower the incidence of deep hemorrhagic stroke.
