Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Masawa, Nobuhide; Yoshida, Yasuhiko; Yamada, Takashi; Joshita, Takashi; Sato, Shinichi; Mihara, Ban

doi:10.1161/01.str.25.1.122

Cited by 46 publications

(33 citation statements)

References 15 publications

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“…In hypertension and aging, the number of smooth muscle cell nuclei decreases in the larger medullary arteries. 23 However, in the present investigation, there were no quantitative differences in the smooth muscle actin immunoreactive areas in the larger vessels. This might have been due to the hypertrophic changes in cell size compensating for the decrease in the number of cell bodies.…”

Section: Discussioncontrasting

confidence: 71%

Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains

Lin

Tomimoto

Akiguchi

et al. 2000

Stroke

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Background and Purpose-It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. Methods-A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. Results-The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (PϽ0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of Ͻ100 m (PϽ0.0001), there was no corresponding increase in the arteries of Ͼ100 m. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. Conclusions-The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains. (Stroke. 2000;31:1838-1842.)Key Words: Binswanger's disease Ⅲ dementia Ⅲ leukoencephalopathy Ⅲ white matter S ubcortical arteriosclerotic encephalopathy, or Binswanger's disease (BD), is characterized pathologically by widespread white matter lesions, multiple lacunae, and fibrohyalinosis of the medullary arteries. [1][2][3][4] There is a longstanding assumption that white matter lesions are pathogenically attributable to changes in the small vessel of the white matter. 5 Because small arteries and arterioles are the main vessels that resist the intraluminal perfusion pressure, especially in hypertension, 6 it is conceivable that fibrohyalinosis in these vessels has an influence on vascular resistance and flow.Although numerous studies have characterized the white matter lesions in BD, which consist of myelin degeneration, gliosis, edema, and necrotic foci, 4,7-11 the vasculopathy associated with thi...

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Section: Discussioncontrasting

confidence: 71%

Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains

Lin

Tomimoto

Akiguchi

et al. 2000

Stroke

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“…Arterial stiffness is caused by structural changes, including fibrosis, medial smooth muscle necrosis, breaks in elastin fibers, calcifications, and diffusion of macromolecules into the arterial wall, which have also been described at the site of the cerebral vasculature. 32 Finally, thromboembolism subsequent to plaque rupture may increase the risk of stroke.…”

Section: Discussionmentioning

confidence: 99%

Arterial Stiffness and Risk of Coronary Heart Disease and Stroke

Mattace-Raso

Cammen²,

Hofman³

et al. 2006

Circulation

1,745

1,167

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Background-Arterial stiffness has been associated with the risk of cardiovascular disease in selected groups of patients.We evaluated whether arterial stiffness is a predictor of coronary heart disease and stroke in a population-based study among apparently healthy subjects. Methods and Results-The present study included 2835 subjects participating in the third examination phase of the Rotterdam Study. Arterial stiffness was measured as aortic pulse wave velocity and carotid distensibility. Cox proportional hazards regression analysis was performed to compute hazard ratios. During follow-up, 101 subjects developed coronary heart disease (mean follow-up period, 4.1 years), and 63 subjects developed a stroke (mean follow-up period, 3.2 years). The risk of cardiovascular disease increased with increasing aortic pulse wave velocity index. Hazard ratios and corresponding 95% CIs of coronary heart disease for subjects in the second and third tertiles of the aortic pulse wave velocity index compared with subjects in the reference category were 1.72 (0.91 to 3.24) and 2.45 (1.29 to 4.66), respectively, after adjustment for age, gender, mean arterial pressure, and heart rate. Corresponding estimates for stroke were 1.22 (0.55 to 2.70) and 2.28 (1.05 to 4.96). Estimates decreased only slightly after adjustment for cardiovascular risk factors, carotid intima-media thickness, the ankle-arm index, and pulse pressure. The aortic pulse wave velocity index provided additional predictive value above cardiovascular risk factors, measures of atherosclerosis, and pulse pressure. Carotid distensibility as measured in this study was not independently associated with cardiovascular disease. Conclusions-Aortic pulse wave velocity is an independent predictor of coronary heart disease and stroke in apparently healthy subjects. (Circulation. 2006;113:657-663.)

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“…10 In particular, high BP accelerates atherosclerosis in large arteries and causes hypertrophy and thickening of the media of intracerebral vessels, leading to hypoperfusion and ischemic rarefaction of white matter. 11,12 This is not an "all-or-none" phenomenon, as was once thought. In fact, a reduction in cerebral blood flow can produce any degree of brain injury, from an asymptomatic condition, such as "silent" cerebral infarction, 13 to a reversible or persistent loss of function, such as transient ischemic attack and stroke.…”

mentioning

confidence: 85%

Left Ventricular Hypertrophy Is Associated With Asymptomatic Cerebral Damage in Hypertensive Patients

Selvetella

Notte

Maffei

et al. 2003

Stroke

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Background and Purpose-It has been demonstrated that left ventricular hypertrophy (LVH) confers an increased risk for major cerebrovascular events. However, it is still uncertain whether there is an association between LVH and asymptomatic cerebrovascular damage in hypertensive patients. In this study, we investigated the relation between LVH, evaluated by both echocardiography (Echo-LVH) and electrocardiography (ECG-LVH), and preclinical cerebral damage, as identified by magnetic resonance imaging. Methods-One hundred ninety-five consecutive patients were enrolled in the study. We evaluated other risk factors such as age, sex, presence of diabetes, cholesterol levels, smoking status, heart rate, and systolic and diastolic blood pressure. Asymptomatic cerebrovascular damage was considered silent cerebral lesions: punctate lesions, lacunes, and territorial lesions. Patients were divided into 2 groups according to the presence of asymptomatic brain lesions. Results-The 2 groups of patients differed only in terms of age and systolic pressure. More importantly, the prevalence of Echo-LVH (83% versus 47.7%, PϽ0.001) and ECG-LVH (56% versus 22%, PϽ0.001) was significantly higher in patients with asymptomatic brain lesions. A multivariate analysis allowed us to recognize LVH as the only independent predictor for the presence of ischemic lacunes (PϽ0.001). Moreover, we evaluated the impact of left ventricular geometry on asymptomatic cerebrovascular damage, and we found that hypertensives with concentric hypertrophy displayed more pronounced asymptomatic cerebrovascular damage compared with patients with eccentric hypertrophy. Conclusions-Our study demonstrates that LVH is associated with cerebral damage even in the absence of clinical symptoms. Thus, the presence of cardiac damage provides important prognostic clues about the presence of asymptomatic cerebral damage.

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Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.

Cited by 46 publications

References 15 publications

Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains

Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains

Arterial Stiffness and Risk of Coronary Heart Disease and Stroke

Left Ventricular Hypertrophy Is Associated With Asymptomatic Cerebral Damage in Hypertensive Patients

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