These results suggest that global 2D strain might provide useful information on myocardial fibrosis and cardiac events in HCM patients with normal chamber function.

Abstract-We examined the possibility that continuous activation of the human brain renin-angiotensin system causes cognitive impairment, using human renin (hRN) and human angiotensinogen (hANG) gene chimeric transgenic (Tg) mice. Cognitive function was evaluated by the shuttle avoidance test once a week from 10 to 20 weeks of age. The avoidance rate in wild-type mice gradually increased. In contrast, the avoidance rate in chimeric hRN/hANG-Tg mice also increased; however, no further increase in avoidance rate was observed from 14 weeks of age, and it decreased thereafter. Cerebral surface blood flow was markedly reduced in 20-week-old hRN/hANG-Tg mice. Superoxide anion production in the brain was already higher in 10-week-old hRN/hANG-Tg mice and further increased thereafter with an increase in NADPH oxidase activity. Moreover, expression of p47 phox and Nox4 in the brain of hRN/hANG-Tg mice also increased. Administration of an angiotensin II type 1 receptor blocker, olmesartan (5.0 mg/kg per day), attenuated the increase in blood pressure and ameliorated cognitive decline with enhancement of cerebral surface blood flow and a reduction of oxidative stress in hRN/hANG-Tg mice. On the other hand, hydralazine (0.5 mg/kg per day) did not improve the decrease in avoidance rate, and did not influence cerebral surface blood flow or oxidative stress in hRN/hANG-Tg mice, in spite of a similar reduction of blood pressure to that by olmesartan. Moreover, we observed that treatment with Tempol improved impaired cognitive function in hRN/hANG-Tg mice. These results suggest that continuous activation of the brain renin-angiotensin system impairs cognitive function via stimulation of the angiotensin II type 1 receptor with a decrease in cerebral surface blood flow and an increase in oxidative stress. Key Words: angiotensin II receptors Ⅲ cognitive function Ⅲ blood flow Ⅲ oxidative stress Ⅲ transgenic mice D ementia is a common serious health problem that impairs quality of life. A continuous decline in cognitive function occurs as the natural aging course in both humans and animal models. Hypertension is a major risk factor for cerebrovascular disease, including stroke, and contributes to the development of vascular dementia. 1 Several clinical studies, such as Perindopril Protection Against Recurrent Stroke Study, Systolic Hypertension in Europe, and Study on Cognition and Prognosis in the Elderly, have shown that antihypertensive drug treatment is associated with reduced cognitive decline. 2-4 However, it is not still clear which classes of antihypertensive drugs provide greater benefits than others.Activation of the renin-angiotensin system (RAS) plays major roles in elevated blood pressure and the development of cerebrovascular disorders. All of the components of the classic RAS have been identified in the brain. 5,6 Recent clinical trials, such as the Losartan Intervention for Endpoint Reduction in Hypertensive Study, Morbidity and Mortality After Stroke, Eprosartan Compared With Nitrendipine for Secondary Prevention, and...

These results suggest that enlargement and weakened differentiation of adipocytes are observed in atherosclerosis and diabetes, and that AT(1) receptor blockade prevented adipocyte enlargement and promoted adipocyte differentiation in these models.

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