Arterial hypertension and ischaemic stroke

Droste, Dirk W.; Ritter, Martin; Dittrich, Ralf; Heidenreich, Stefan; Wichter, Th.; Freund, M.; Ringelstein, E. B.

doi:10.1034/j.1600-0404.2003.00098.x

Cited by 39 publications

(33 citation statements)

References 111 publications

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“…1,2,3 Hypertension is generally regarded as the most important risk factor for stroke in the general population. However, some individuals experience a stroke even if their BP is within the normal range.…”

Section: Discussionmentioning

confidence: 99%

“…The majority of literature is devoted to exploring the relationship between hypertension and stroke. 2,3 Few researchers have studied this association in those who are normotensive. 6 It is evidenced that apart from high BP, the pathological causes of stroke are manifold, including the formation of atheroma, embolism from the heart, intracranial small vessel disease, malformations of the vasculature in the brain, etc.…”

mentioning

confidence: 99%

“…[1][2][3] There is a continuous and linear relationship between BP and risk of stroke, 4 which holds even in individuals with a normal BP. 1,5 Yet, people are classified into those with hypertension and normal BP.…”

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confidence: 99%

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Risk Factors for Stroke in Subjects With Normal Blood Pressure

Engström

Hedblad

et al. 2005

Stroke

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Background and Purpose-Although stroke is strongly associated with hypertension, some individuals with normal blood pressure (BP) experience a stroke. This prospective study explored risk factors for stroke in subjects with normal BP. Methods-A total of 11 228 men and 17 174 women, 45 to 73 years old, were examined in a population-based cohort study. Normal BP was defined as BP Ͻ140/90 mm Hg and no treatment for hypertension. The incidence of stroke was followed over a mean period of 6 years. Results-In the cohort, 10 938 (38%) had normal BP. Of them, 56 patients experienced a first-ever stroke (12% of all stroke). Compared with subjects without stroke during follow-up, these stroke subjects were older, had lower education, were often smokers and alcohol nondrinkers, and had a history of coronary heart disease (CHD), gastric ulcer, or renal calculus. Subjects with stroke had a higher body mass index (BMI) and a high-normal BP (130 to

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Risk Factors for Stroke in Subjects With Normal Blood Pressure

Engström

Hedblad

et al. 2005

Stroke

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“…5 These alterations are believed to underlie the cognitive impairment and brain damage associated with hypertension. 6,7 Angiotensin II (Ang II) has emerged as a critical factor in the deleterious cerebrovascular effects of hypertension. 6 Ang II produces cerebrovascular remodeling, promotes vascular inflammation, and impairs CBF regulation.…”

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confidence: 99%

Angiotensin II Impairs Neurovascular Coupling in Neocortex Through NADPH Oxidase–Derived Radicals

Kazama

Anrather

Zhou

et al. 2004

Circulation Research

235

289

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Abstract-Angiotensin II (Ang II) exerts detrimental effects on cerebral circulation, the mechanisms of which have not been elucidated. In particular, Ang II impairs the increase in cerebral blood flow (CBF) produced by neural activity, a critical mechanism that matches substrate delivery with energy demands in brain. We investigated whether Ang II exerts its deleterious actions by activating Ang II type 1 (AT 1 ) receptors on cerebral blood vessels and producing reactive oxygen species (ROS) through NADPH oxidase. Somatosensory cortex CBF was monitored in anesthetized mice by laser-Doppler flowmetry. Ang II (0.25 g/kg per minute IV) attenuated the CBF increase produced by mechanical stimulation of the vibrissae. The effect was blocked by the AT 1 antagonist losartan and by ROS scavenger superoxide dismutase or tiron and was not observed in mice lacking the gp91 phox subunit of NADPH oxidase or in wild-type mice treated with the NADPH oxidase peptide inhibitor gp91ds-tat. Ang II increased ROS production in cerebral microvessels, an effect blocked by the ROS scavenger Mn(III)tetrakis (4-benzoic acid) porphyrin and by the NADPH oxidase assembly inhibitor apocynin. Ang II did not increase ROS production in gp91-null mice. Double-label immunoelectron microscopy demonstrated that AT 1 and gp91phox immunoreactivities were present in endothelium and adventitia of neocortical arterioles. Collectively, these findings suggest that Ang II impairs functional hyperemia by activating AT 1 receptors and inducing ROS production via a gp91 phox containing NADPH oxidase. The data provide the mechanistic basis for the cerebrovascular dysregulation induced by Ang II and suggest novel therapeutic strategies to counteract the effects of hypertension on the brain. T he functional and structural integrity of the brain depends on a continuous blood supply commensurate to its changing energy needs. 1 Thus, if a brain region is activated, cerebral blood flow (CBF) to that region increases to match the increased energy demands and to remove potentially deleterious byproducts of cellular metabolism. 2 This phenomenon, termed functional hyperemia, is crucial to maintain the homeostasis of the cerebral microenvironment, and its alteration leads to brain dysfunction and disease. 3 Hypertension has profound effects on the brain and its circulation. 4 Whereas hypertension alters the structure of cerebral blood vessels, it also disrupts regulation of CBF. 5 These alterations are believed to underlie the cognitive impairment and brain damage associated with hypertension. 6,7 Angiotensin II (Ang II) has emerged as a critical factor in the deleterious cerebrovascular effects of hypertension. 6 Ang II produces cerebrovascular remodeling, promotes vascular inflammation, and impairs CBF regulation. 8 -11 Importantly, Ang II attenuates the CBF increase produced by activation of the mouse somatosensory cortex. 12 Such impairment in functional hyperemia is not related to the associated elevation in arterial pressure (AP) or to actions of Ang II on neural ...

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“…Hypertension progressive neurologic deficits promote atherosclerosis in cerebral arteries [9] and induce lipohyalinosis, a pathological process characterized by fibrinoid necrosis of the vascular wall [9]. Functional changes include regionally reduced resting CBF (cerebral blood flow) and impaired cerebrovascular reactivity [10].…”

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confidence: 99%

A 55 Year Old Man with Progressive Neurologic Deficits

Senjaya¹

2015

JPP

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At least 50% of the decline in functional abilities associated with the elderly is caused by neurological conditions, particularly vascular dementia, such as occurs in Binswanger disease. Binswanger disease is a rare condition, characterized by acute strokes with symptoms and signs compatible with lacunar infarction. The disease onset is commonly between 55 and 75 years. The majority of patients with Binswanger disease have chronic hypertension and other putative factors including diabetes mellitus, polycythemia, thrombocytosis, hyperlipidemia, hyperglobulinemia and pseudoxanthoma elasticum, increased fibrinogen levels and the antiphospholipid antibody syndrome. We report the case of a 55 year old man, who suffered from involuntary movements of his right arm, slight hemiparesis on the right side, and also had dementia. He had a history of high blood pressure and laboratory tests showed that he had diabetes mellitus. The brain magnetic resonance imaging showed irregular white matter abnormalities with multiple lacunar infarcts in the basal ganglia and pons. The clinical picture is characterized by acute strokes, followed by involuntary movements and also dementia. Therefore we decided to diagnose it as Binswanger disease. After discharge from hospital, the patient has not returned for follow-up.

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Arterial hypertension and ischaemic stroke

Abstract: In the vast majority of patients and healthy individuals, target blood pressure should be as high as or below 120/80 mmHg to minimize the occurrence of stroke and other cardiovascular complications.

Cited by 39 publications

References 111 publications

Risk Factors for Stroke in Subjects With Normal Blood Pressure

Risk Factors for Stroke in Subjects With Normal Blood Pressure

Angiotensin II Impairs Neurovascular Coupling in Neocortex Through NADPH Oxidase–Derived Radicals

A 55 Year Old Man with Progressive Neurologic Deficits

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