RESUMO

The relation between hypertension and cognitive impairment is an undisputable fact. The aims of this study were to determine the prevalence of cognitive impairment in hypertensive patients, to identify the most affected cognitive domain, and to observe the association with different parameters of hypertension and other vascular risk factors. A multicentre study was carried out, and 1281 hypertensive patients of both genders and ≥21 years of age were included. Data on the following parameters were obtained: cognitive status (Minimal Cognitive Examination), behavioural status (Hospital Anxiety and Depression Scale), blood pressure, anthropometry, and biochemical profile. The average age was 60.2±13.5 years (71% female), and the educational level was 9.9±5.1 years. Global cognitive impairment was seen in 22.1%, executive dysfunction in 36.2%, and semantic memory impairment in 48.9%. Cognitive impairment was higher in males (36.8% vs. 30.06%) within both the 70-79-year-old and the ≥80-year-old (50% vs. 40%) age groups. Abnormal Clock Drawing Test results were related to high pulse pressure (p<0.0036), and abnormal Mini-Boston Naming Test results to both high systolic blood pressure (p<0.052) and pulse pressure (p<0.001). The treated/uncontrolled hypertensive group showed abnormal results both in the Mini Mental State Examination (OR, 0.73; p=0.036) and the Mini-Boston Naming Test (OR, 1.36; p=0.021). Among patients without cognitive impairment (MMSE >24), 29.4% presented executive dysfunction, and 41.5% semantic memory impairment. Cognitive impairment was higher in hypertensive patients than in the general population. Executive functions and semantic memory were the most affected cognitive domains. High systolic blood pressure and pulse pressure were associated with abnormal results in cognitive tests.

Assuntos

RESUMO

Although a variety of factors have been proposed as key factors of the atherosclerotic plaque vulnerability, the mechanisms that contribute to this problem are not yet fully characterized. In previous works we demonstrated that changes in arterial wall viscosity and elasticity and/or in the filtering function (FF) could be in the basis of arterial wall alterations. If these properties are altered in arterial wall with atherosclerotic plaques remain to be analyzed. Our aims were to analyze, the arterial wall visco-elasticity and FF of human carotid arteries with atherosclerotic plaques. To this end, instantaneous arterial diameter waveforms were obtained non-invasively (B-Mode Echography), in five sites (S1-S5) on the carotid artery. After that, diameter waveform obtained in S1 (first segment of the common carotid artery) was calibrated using pressure values, and used to quantify the pressure-diameter relationship for each segment. From pressure-diameter relationships, viscosity, elasticity and FF were quantified. Central portions of atherosclerotic plaques showed a reduced FF. At least in theoretical terms, the FF reduction could be related with the plaque vulnerability.

Assuntos

Assuntos

RESUMO

OBJECTIVE: To determine whether angiotensin converting enzyme inhibition by perindopril can reduce cardiac transforming growth factor beta1 (TGFbeta1) and plasminogen activator inhibitor 1 (PAI-1) and therefore control collagen accumulation in an animal model with the metabolic syndrome such as the obese Zucker rat (OZR). ANIMALS: Male OZR (group 1, n = 10); OZR treated with perindopril (group 2, n = 10); and lean Zucker rats (group 3, n = 10). METHODS: During six months, group 2 received 3 mg/kg/day of perindopril orally and group 1 and group 3 were given a vehicle. Hearts were processed for pathology studies including immunohistochemical analysis with antibodies to PAI-1, TGFbeta1, collagen type I, and collagen type III. RESULTS: Group 2 had lower blood pressure (126.7 (2) v 148.6 (2.7) mm Hg, p < 0.01) than untreated OZR and had decreased cardiac PAI-1 (3.6 (0.4) v 13.5 (1.7)% of positive area/field, p < 0.01), TGFbeta1 in myocytes (0.13 (0.1) v 9.14 (4.7)%/area, p < 0.01) and in interstitium (19.8 (6.8) v 178.9 (27.4) positive cells/area, p < 0.01), collagen I (3 (0.8) v 13.3 (1)%/area, p < 0.01), collagen III (5 (0.6) v 9.5 (0.9)%/area, p < 0.01), and collagen I to collagen III ratio (0.59 (0.13) v 1.40 (0.15) p < 0.01) compared with untreated OZR. CONCLUSION: These results suggest that perindopril reduces cardiac PAI-1 and TGFbeta1 and ameliorates cardiac fibrosis in a rat model with multiple cardiovascular risk factors.

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Seventeen patients with coronary disease submitted to myocardial revascularization were studied. Ten patients had a hypertrophied ventricle, and 7 had normal ventricular mass. Myocardial biopsies were obtained before ischemia and at the time of reperfusion and were assessed for: volume fraction of fibrous tissue, myocyte diameter, morphometric mitochondrial studies and ultrastructural changes. The volume fraction of fibrous tissue in patients with hypertrophied ventricle was 1.9 +/- 0.04, and in patients with normal ventricular mass was 0.9 +/- 0.01 (p less than 0.05). The diameter of the myocyte was 23 +/- 0.3 microns and 18 +/- 1.2 microns for patients with hypertrophied and normal ventricular mass, respectively (p less than 0.01). The value of volumetric density for pre-ischemia samples in patients with a hypertrophied ventricle was 23 +/- 2.2 and in patients with normal ventricular mass was 35 +/- 2.7 (p less than 0.02). Grades 3 and 4 of damaged mitochondria were significantly increased in reperfusion samples from patients with a hypertrophied ventricle compared to pre-ischemia samples. Collagen growth was increased in hypertrophied hearts which were also more sensitive to the ischemia/reperfusion mechanism.

Assuntos

RESUMO

To assess a possible free-radical scavenging action of taurine during coronary artery bypass grafting, 12 patients were randomly divided into two equal groups. One to 3 hours before surgery, they received a rapid intravenous infusion of either placebo (group 1) or taurine (5 gm) (group 2). During surgery, biopsy samples were taken before ischemia (preischemic samples) and after 10 minutes of reperfusion (reperfusion samples). Lipoperoxidation was determined by hydroperoxide-initiated chemiluminescence of heart homogenates, and myocardial cell damage was assessed by electron microscopy. The values for chemiluminescence in preischemic and reperfusion samples from group 1 were 7500 +/- 1600 and 18,600 +/- 4600 cpm/mg of protein, respectively (p less than 0.03). This difference was not observed in group 2 where the values were 10,050 +/- 2700 and 11,800 +/- 4200 cpm/mg of protein, for preischemic and reperfusion samples, respectively. The number of severely damaged mitochondria (grades 3 and 4) in reperfusion samples from group 1 increased significantly compared to preischemic samples (25 +/- 8% vs 12 +/- 3%, p less than 0.01). Conversely no differences were observed between the number of severely damaged mitochondria in reperfusion and preischemic samples from group 2 (8 +/- 3% vs 8 +/- 2%). The number of damaged and necrotic myocytes increased in group 1 after reperfusion from 22 +/- 9% to 34 +/- 10% (p less than 0.03) and from 10 +/- 7% to 26 +/- 20% (p = NS), respectively. No changes were observed between reperfusion and preischemic samples in group 2. Treatment with taurine seems to reduce lipoperoxidation and decrease cell damage at the time of reperfusion.

Assuntos