Deep, spontaneous intracerebral hemorrhages: Clinical differences and risk factors associated with anterior versus posterior circulation.

BACKGROUND: spontaneous intracerebral hemorrhages (ICH) in different anatomical locations are considered different clinical entities, associated with different vascular etiologies. However, such a distinction between deep ICH in the posterior vs. the anterior circulation is not well documented. OBJECTIVE: to look for different demographic, clinical, laboratory and radiological variables in order to clarify any distinction between deep ICH of the posterior versus the anterior circulations. MATERIAL AND METHODS: Retrospective study on patients diagnosed with deep, spontaneous ICH at a single tertiary center. Patients were divided into two groups: posterior circulation (group 1) and anterior circulation (group 2). Computerized medical records were extracted for multiple variables. RESULTS: A total of 142 patients with deep ICH were included in the study; 54.9 % (n = 78) with posterior (group 1) and 45.1 % (n = 64) with anterior circulation hemorrhages (group 2). In group 1, 67.9 % (n = 53) of hemorrhages were in the cerebellum and 28.2 % (n = 22) in the thalamus. Patients in group 1 were older at time of hemorrhage (68.69 ± 11.66 vs. 64.95 ± 13.34, p = 0.073) and had nearly threefold increased rate of BMI≥ 35 (22.0 % vs. 8.6 %, p = 0.071). In multivariate analysis, use of anti-aggregates (OR=2.391; 95 % CI 1.082-5.285, p = 0.031) and past medical history of HTN (OR=2.904; 95 % CI 1.102-7.654, p = 0.031) were significantly associated with ICH of the posterior circulation. When excluding patients with thalamic hemorrhages, BMI ≥ 35 was also associated with significant risk of having a deep hemorrhage in the posterior circulation vs. the anterior circulation (OR=3.420; 95 % CI 1.011-11.574, p = 0.048). No significant differences were found between the two groups in terms of functional and survival outcomes. CONCLUSION: HTN, use of anti-aggregates and morbid obesity are associated with deep ICHs of the posterior circulation and should be considered significant risk factors for this major clinical event. The growing data on pathophysiology of distinct subgroups of ICH will provide useful tools that will aid in preventing and treating these neurological emergencies. Future epidemiological and clinical studies should use the distinction between ICH subgroups based on their anatomical location and vascular territories as accurately as possible in order to reach solid conclusions.

Arterial stiffness in patients with deep and lobar intracerebral hemorrhage.

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.

Arterial Stiffness in Patients with Deep and Lobar Intracerebral Hemorrhage / 대한뇌졸중학회지

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.

Arterial Stiffness in Patients with Deep and Lobar Intracerebral Hemorrhage / 대한뇌졸중학회지

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.