Idosos hipertensos apresentam menor desempenho cognitivo do que idosos normotensos / Elderly hypertensives show decreased cognitive performance compared with elderly normotensives

FUNDAMENTO: A hipertensão arterial tem sido associada à redução do desempenho cognitivo, contudo a literatura é conflitante. OBJETIVO: Comparar o desempenho cognitivo entre idosos normotensos ("N"; n = 17; idade 68 ± 1; pressão arterial = 133 ± 3/74 ± 2 mmHg) e hipertensos ("H"; n = 28; idade 69 ± 1, pressão arterial = 148 ± 4/80 ± 1 mmHg) com pelo menos cinco anos de escolaridade. MÉTODOS: A avaliação neuropsicológica ampla constou do "Cambridge Cognition-Revised" (CAMCOG-R), dos "Trail Making Test A and B" (TMT A e B) e do "Rey Auditory Verbal Learning Test" (RAVLT). RESULTADOS: Os idosos hipertensos apresentaram menor escore do CAMCOG-R (N = 87,6 ± 1,8; H = 78,6 ± 1,4; p = 0,002). Os idosos hipertensos necessitaram de maior tempo para realizar o TMT A e B (TMT A: N = 39 ± 3s; H = 57 ± 3,4s; p = 0,001; TMT B: N = 93 ± 7s; H = 124 ± 7s; p = 0,006), o que também é demonstrado pelos percentis significativamente menores obtidos nestes testes. O somatório do RAVLT foi significativamente menor nos idosos hipertensos (N = 51,8 ± 1,7; H = 40,7 ± 1,5; p < 0,0001). Mesmo ajustado para idade, sexo, escolaridade e sintomas de depressão, a hipertensão arterial foi um fator preditor independente do desempenho cognitivo medido pelo CAMCOG-R, TMT A e o somatório do RAVLT. CONCLUSÃO: O desempenho cognitivo em idosos hipertensos é menor do que em idosos normotensos.

BACKGROUND: Essential hypertension has been associated with decreased cognitive performance; however, the literature is conflicting. OBJECTIVE: This study aims at comparing cognitive performance between elderly normotensives ("N"; n = 17; age 68 ± 1; blood pressure = 133 ± 3/74 ±2 mmHg) and hypertensives ("H"; n = 28; age 69 ± 1, blood pressure = 148 ± 4/80 ± 1mmHg) with at least 5 years of education. METHODS: The comprehensive neuropsychological assessment was comprised of the Cambridge Cognition-Revised (CAMCOG-R), the Trail Making Test A and B (TMT A and B) and the Rey Auditory Verbal Learning Test (RAVLT). RESULTS: Elderly hypertensives presented lower CAMCOG-R global scores (N = 87.6 ± 1.8; H = 78.6 ± 1.4; p = 0.002). The hypertensive's performance was slower in the TMT A and B (TMT A: N = 39 ± 3s; H = 57 ± 3s; p = 0.001; TMT B: N = 93 ± 7s; H = 124 ± 7s; p = 0.006), which was also reflected in smaller percentiles achieved by hypertensives in these tests. Hypertensive subjects exhibited a significantly lower RAVLT summation score (N = 51.8 ± 1.7; H = 40.7 ± 1.5; p < 0.0001). Even when adjusted for age, sex, education and depression symptoms, hypertension was an independent predictor of cognitive performance as measured by CAMCOG-R global score, TMT A and RAVLT summation score. CONCLUSION: Cognitive performance is lower in elderly hypertensives as compared with elderly normotensives.

Elderly hypertensives show decreased cognitive performance compared with elderly normotensives.

BACKGROUND: Essential hypertension has been associated with decreased cognitive performance; however, the literature is conflicting. OBJECTIVE: This study aims at comparing cognitive performance between elderly normotensives ("N"; n = 17; age 68 ± 1; blood pressure = 133 ± 3/74 ±2 mmHg) and hypertensives ("H"; n = 28; age 69 ± 1, blood pressure = 148 ± 4/80 ± 1mmHg) with at least 5 years of education. METHODS: The comprehensive neuropsychological assessment was comprised of the Cambridge Cognition-Revised (CAMCOG-R), the Trail Making Test A and B (TMT A and B) and the Rey Auditory Verbal Learning Test (RAVLT). RESULTS: Elderly hypertensives presented lower CAMCOG-R global scores (N = 87.6 ± 1.8; H = 78.6 ± 1.4; p = 0.002). The hypertensive's performance was slower in the TMT A and B (TMT A: N = 39 ± 3s; H = 57 ± 3s; p = 0.001; TMT B: N = 93 ± 7s; H = 124 ± 7s; p = 0.006), which was also reflected in smaller percentiles achieved by hypertensives in these tests. Hypertensive subjects exhibited a significantly lower RAVLT summation score (N = 51.8 ± 1.7; H = 40.7 ± 1.5; p < 0.0001). Even when adjusted for age, sex, education and depression symptoms, hypertension was an independent predictor of cognitive performance as measured by CAMCOG-R global score, TMT A and RAVLT summation score. CONCLUSION: Cognitive performance is lower in elderly hypertensives as compared with elderly normotensives.

Maternal high-fat diet programs for metabolic disturbances in offspring despite leptin sensitivity.

A fatty diet during pregnancy in mouse dams causes metabolic abnormalities (similar to metabolic syndrome in humans) in the rodents' offspring. We tested the hypothesis that the offspring of dams fed a high-fat diet during pregnancy and lactation develop metabolic abnormalities and leptin resistance. Pregnant C57BL/6 mice (n = 20) were fed either standard chow (SC; 19% fat) or a high-fat diet (HF; 49% fat). After weaning, male offspring were divided into four groups, according to the diet of dams and offspring: SC(dams)/SC(offspring), SC/HF, HF/SC and HF/HF (n = 30/group). For a metabolic analysis, we evaluated body mass, fat mass depots, blood plasma and adipocyte structure at 12 weeks of age. To analyse leptin sensitivity, each group was divided into two groups (vehicle or leptin) to identify the feeding response and pSTAT3 expression after acute intracerebroventricular (ICV) treatment. The offspring of mothers fed a high-fat diet presented increased body mass and visceral fat, adipocyte hypertrophy and insulin resistance. This phenotype was not associated with central leptin resistance. Thus, maternal programming by HF predisposes offspring to metabolic abnormalities despite leptin sensitivity.

Dissociation between sympathetic nerve traffic and sympathetically mediated vascular tone in normotensive human obesity.

Obesity increases the risk of hypertension and its cardiovascular complications. This has been partly attributed to increased sympathetic nerve activity, as assessed by microneurography and catecholamine assays. However, increased vasoconstriction in response to obesity-induced sympathoactivation has not been unequivocally demonstrated in obese subjects without hypertension. We evaluated sympathetic alpha-adrenergic vascular tone in the forearm by brachial arterial infusion of the alpha-adrenoreceptor antagonist phentolamine (120 microg/min) in normotensive obese (daytime ambulatory arterial pressure: 123+/-1/77+/-1 mm Hg; body mass index: 35+/-1 kg/m(2)) and lean (daytime ambulatory arterial pressure: 123+/-2/77+/-2 mm Hg; body mass index: 22+/-1 kg/m(2)) subjects (n=25 per group) matched by blood pressure, age, and gender. Microneurographic sympathetic nerve activity to skeletal muscle was significantly higher in obese subjects (30+/-3 versus 22+/-1 bursts per minute; P=0.02). Surprisingly, complete alpha-adrenergic receptor blockade by phentolamine (at concentrations sufficient to completely inhibit norepinephrine and phenylephrine-induced vasoconstriction) caused equivalent vasodilatation in obese (-57+/-2%) and lean subjects (-57+/-3%; P=0.9). In conclusion, sympathetic vascular tone in the forearm circulation is not increased in obese normotensive subjects despite increased sympathetic outflow. Vasodilator factors or mechanisms occurring in obese normotensive subjects could oppose the vasoconstrictor actions of increased sympathoactivation. Our findings may help to explain why some obese subjects are protected from the development of hypertension.

Leptin, obesity and cardiovascular disease.

PURPOSE OF REVIEW: Obesity is a risk factor for cardiovascular diseases. Leptin levels are increased in obesity and leptin exhibits cardiovascular actions that may contribute to increased cardiovascular risk. We review the sympathetic, renal and vascular actions of leptin and their relevance to cardiovascular disease. RECENT FINDINGS: Leptin possesses cardio-renal actions potentially contributing to obesity-related hypertension including generalized sympathoactivation. However, given that leptin resistance occurs in obesity, it has been difficult to link hyperleptinemia with hypertension. One possibility is that leptin resistance is confined to the metabolic effects of leptin, with preservation of its sympathoexcitatory actions. Other mechanisms may contribute to the pressor effects of leptin. For instance, angiotensin II induces leptin generation. Leptin also potentiates the pressor effect of insulin. Therefore, interactions between angiotensin II and insulin with leptin could have deleterious cardiovascular effects in obesity. Additionally, leptin appears to stimulate vascular inflammation, oxidative stress and hypertophy. These actions may contribute to the pathogenesis of hypertension, atherosclerosis, and left ventricular hypertrophy. SUMMARY: The potential actions of leptin in the pathophysiology of cardiovascular complications of obesity are diverse, despite evidence of leptin resistance to its metabolic actions. However, most information about cardiovascular actions of leptin derives from in-vitro and animal studies. Future research in humans is widely awaited.

Incontinência pigmenti: síndrome de Bloch Sulzberger; relato de um caso / Incontinentia pigmenti: Bloch Sulzberger syndrome; report of a case

Incontinentia pigmenti IP) é uma genodermatose rara que afeta primordialmente crianças do sexo feminino. Trata-se de uma síndrome multissistêmica com alteraçöes dermatológicas, neurológicas, oftálmicas e dentárias. Descrevemos um caso de IP em uma menina de dois anos