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Guideline Latin American guidelines on hypertension. Latin American Expert Group. 2009
Sanchez RA, Ayala M, Baglivo H, Velazquez C, Burlando G, Kohlmann O, Jimenez J, Jaramillo PL, Brandao A, Valdes G, Alcocer L, Bendersky M, Ramirez AJ, Zanchetti A, Anonymous00032. · Sección Hipertensión Arterial y Unidad Metabólica, Fundación Favaloro. Belgrano 1782 P: 4, Buenos Aires, Argentina. · J Hypertens. · Pubmed #19349909 No free full text.
Abstract: Hypertension is a highly prevalent cardiovascular risk factor in the world and particularly overwhelming in low and middle-income countries. Recent reports from the WHO and the World Bank highlight the importance of chronic diseases such as hypertension as an obstacle to the achievement of good health status. It must be added that for most low and middle-income countries, deficient strategies of primary healthcare are the major obstacles for blood pressure control. Furthermore, the epidemiology of hypertension and related diseases, healthcare resources and priorities, the socioeconomic status of the population vary considerably in different countries and in different regions of individual countries. Considering the low rates of blood pressure control achieved in Latin America and the benefits that can be expected from an improved control, it was decided to invite specialists from different Latin American countries to analyze the regional situation and to provide a consensus document on detection, evaluation and treatment of hypertension that may prove to be cost-utility adequate. The recommendations here included are the result of preparatory documents by invited experts and a subsequent very active debate by different discussion panels, held during a 2-day sessions in Asuncion, Paraguay, in May 2008. Finally, in order to improve clinical practice, the publication of the guidelines should be followed by implementation of effective interventions capable of overcoming barriers (cognitive, behavioral and affective) preventing attitude changes in both physicians and patients.
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Editorial Blood-pressure-related disease is a global health priority. 2008
Macmahon S, Alderman MH, Lindholm LH, Liu L, Sanchez RA, Seedat YK. · George Institute for International Health, University of Sydney, Sydney, New South Wales, Australia. · J Hypertens. · Pubmed #18806633 No free full text.
This publication has no abstract.
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Editorial Blood-pressure-related disease is a global health priority. 2008
MacMahon S, Alderman MH, Lindholm LH, Liu L, Sanchez RA, Seedat YK. · No affiliation provided · Am J Hypertens. · Pubmed #18648355 No free full text.
This publication has no abstract.
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Article Telmisartan improves insulin resistance in high renin nonmodulating salt-sensitive hypertensives. 2008
Sanchez RA, Masnatta LD, Pesiney C, Fischer P, Ramirez AJ. · Hypertension Section and Metabolic Unit, Fundación Favaloro, Buenos Aires, Argentina. · J Hypertens. · Pubmed #19008718 No free full text.
Abstract: BACKGROUND: Nonmodulating (NMHT) is a high-renin subtype of salt sensitive hypertension, which additionally develops insulin resistance and oxidative stress. Conversely, modulating hypertensives (MHT) normally regulates renal hemodynamics after high sodium intake without metabolic impairment. We postulate that telmisartan, an angiotensin receptor blocker with partial peroxisome proliferators-activated receptorgamma partial agonist, may improve insulin resistance compared with ramipril, an angiotensin-converting enzyme inhibitor (ACEI) in NMHT. METHODS: We studied 18 NMTH (32 +/- 5y nine men, BMI 29 +/- 3 kg/m2) and 16 MHT (34 +/- 4, 10 men, BMI 28 +/- 5 kg/m2) before and after the crossover administration of ramipril 10 mg (3 months) or telmisartan 80 mg (3 months). In each patient studied we measured, before and after each treatment period, office blood pressure, glycemia and insulinemia before and 60 and 120 min after a glucose overload (75 g), total cholesterol, high-density lipoprotein and low-density lipoprotein fractions, triglycerides and highly sensitive C-protein-reactive protein. After that, HOMA-IR Index was calculated. RESULTS: Plasma renin activity was higher in NMHT 4.4 +/- 0.5 than MHT 2.6 +/- 0.9 ng.ml.h; P < 0.01. Blood pressure was similarly reduced either in MHT or NMHT by ramipril (MHT: from 159 +/- 10/102 +/- 4 to 142 +/- 6/93 +/- 3 mmHg, P < 0.05; NMHT: from 162 +/- 12/97 +/- 4 to 139 +/- 7/89 +/- 2 mmHg, P < 0.05) or telmisartan (MHT: from 154 +/- 8/96 +/- 5 to 137 +/- 6/88 +/- 4 mmHg, P < 0.05; NMHT: from 161 +/- 9/96 +/- 5 to 137 +/- 5/86 +/- 3 mmHg, P < 0.05). In NMHT, fasting glycemia (99 +/- 10 mg%) and insulinemia (16 +/- 4 microU%) and 120 min glycemia (110 +/- 2 mg%) and insulinemia (57 +/- 9 microU%) were higher than in MHT (fasting: 92 +/- 8 mg% and 9.2 +/- 2 mU%; 120 min: 95 +/- 5 and 21 +/- 5 microU%, P < 0.05). In MHT, after 3 months treatment with either ramipril or telmisartan no changes were found in fasting and 120 min glycemia and insulinemia. In NMHT, telmisartan, after 3 months treatment, significantly reduced fasting and 120 min insulinemia (fasting: 8.4 +/- 2, 120 min: 25 +/- 10 microU%; P < 0.01) compared either to basal values or ramipril treatment. Similarly, only in NMHT, compared with basal values and ramipril treatment, telmisartan improved the HOMA-IR index in both MHT (2.76 +/- 0.16 to 2.24 +/- 0.18, P < 0.05) and NMHT (from: 4.4 +/- 1 to 2.3 +/- 0.7) and triglyceride plasma levels (MHT: from 139 +/- 1.85 to 122 +/- 2.4 mg%, P < 0.05; NMHT: from: 223 +/- 12 to 146 +/- 10 mg%, P < 0.01). Finally, highly sensitive C-protein-reactive protein values were higher in NMHT (0.33 +/- 0.07 mg.dl) than in MHT (0.14 +/- 0.06 mg.dl; P < 0.01). Both treatments reduced highly sensitive C-protein-reactive protein in NMHT. (ramipril from 0.32 +/- 0.05 mg.dl to 0.26 +/- 0.06 m.dl (P < 0.05) and telmisartan from 0.34 +/- 0.05+/- to 0.20 +/- 0.05 mg.dl (P < 0.01). CONCLUSION: Our data suggest that the improvement of the insulin sensitivity by telmisartan, instead of a similar effect on blood pressure shown by both drugs, could be ascribed to the PPAR agonistic action of telmisartan. This opens an interesting therapeutic approach for patients with hypertension and altered glycemic metabolism.
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Article Blood-pressure-related disease is a global health priority. 2008
MacMahon S, Alderman MH, Lindholm LH, Liu L, Sanchez RA, Seedat YK. · George Institute for International Health, University of Sydney, Sydney, NSW 2050, Australia. · Lancet. · Pubmed #18456084 No free full text.
This publication has no abstract.
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Article Smart smooth muscle spring-dampers. Smooth muscle smart filtering helps to more efficiently protect the arterial wall. 2007
Armentano RL, Barra JG, Pessana FM, Craiem DO, Graf S, Santana DB, Sanchez RA. · Facultad de Ingeniería y Ciencias Exactas y Naturales, Buenos Aires, Argentina. · IEEE Eng Med Biol Mag. · Pubmed #17278774 No free full text.
This publication has no abstract.
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Article Studying the evolution and the magnetic resonance findings of reversible posterior leukoencephalopathy in children. free! 2006
Ferraz-Filho JR, Rocha-Filho JA, Bichuette TF, de Albuquerque RC, Sanchez RA, Souza AS. · Department of Radiology, Faculdade de Medicina Estadual de Rio Preto, Hospital de Base de São Jose do Rio Preto SP, Rua Brigadeiro Faria Lima 5544, 15090-000 São Jose do Rio Preto SP, Brazil. · Arq Neuropsiquiatr. · Pubmed #17057873 links to free full text
Abstract: PURPOSE: To describe the evolution and the magnetic resonance imaging (MRI) findings of the reversible posterior leukoencephalopathy (RLPS) in children. METHOD: Nine children with neurologic symptoms and sudden increase of the arterial pressure were studied by brain MRI. RESULTS: All children evaluated had lesions seen on FLAIR-weighted images of the parietal-occipital regions. Other regions were also involved. Four patients presented restriction on diffusion-weighted images and only two with reduction of the apparent diffusion coefficient (ADC), which evolved with neurologic sequels and persistence of the lesions on the control examination. The other patients had complete regression of the lesions after therapy. CONCLUSION: MRI is important to suggest the diagnosis of RPLS in patients with arterial hypertension and unspecific neurologic symptoms. Moreover, the outcome is not favorable all the time and the association of D-WI with ADC can be an instrument capable of predicting irreversible lesions.
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Article Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition. free! 2006
Armentano RL, Barra JG, Santana DB, Pessana FM, Graf S, Craiem D, Brandani LM, Baglivo HP, Sanchez RA. · Facultad de Ingeniería y Ciencias Exactas y Naturales, Universidad Favaloro, Buenos Aires, Argentina. · Hypertension. · Pubmed #16461847 links to free full text
Abstract: Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.
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