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Systemic Hypertension (systemic + hypertension)
Selected AbstractsEchocardiographic Estimation of Systemic Systolic Blood Pressure in Dogs with Mild Mitral RegurgitationJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2006DACVIM, Sandra P. Tou DVM Background:Systemic hypertension is likely underdiagnosed in veterinary medicine because systemic blood pressure is rarely measured. Systemic blood pressure can theoretically be estimated by echocardiography. According to the modified Bernoulli equation (PG = 4v2), mitral regurgitation (MR) velocity should approximate systolic left ventricular pressure (sLVP), and therefore systolic systemic blood pressure (sSBP) in the presence of a normal left atrial pressure (LAP) and the absence of aortic stenosis. The aim of this study was to evaluate the use of echocardiography to estimate sSBP by means of the Bernoulli equation. Hypothesis:Systemic blood pressure can be estimated by echocardiography. Animal: Seventeen dogs with mild MR. No dogs had aortic or subaortic stenosis, and all had MR with a clear continuous-wave Doppler signal and a left atrial to aorta ratio of , 1.6. Methods:Five simultaneous, blinded continuous-wave measurements of maximum MR velocity (Vmax) and indirect sSBP measurements (by Park's Doppler) were obtained for each dog. Pressure gradient was calculated from Vmax by means of the Bernoulli equation, averaged, and added to an assumed LAP of 8 mm Hg to calculate sLVP. Results:Calculated sLVP was significantly correlated with indirectly measured sSBP within a range of 121 to 218 mm Hg (P= .0002, r= .78). Mean ± SD bias was 0.1 ± 15.3 mm Hg with limits of agreement of-29.9 to 30.1 mm Hg. Conclusion: Despite the significant correlation, the wide limits of agreement between the methods hinder the clinical utility of echocardiographic estimation of blood pressure. [source] Spontaneous Feline Hypertension: Clinical and Echocardiographic Abnormalities, and Survival RateJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2003Valerie Chetboul Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic, cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 ± 3.5 years versus 9.6 ± 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%; P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 ± 34 mm Hg) than in other hypertensive animals (221 ± 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 ± 1.7 versus 3.7 ± 0.64 mm; P < .001) and left ventricular free wall (6.2 ± 1.6 versus 4.1 ± 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 ± 3.2 versus 15.8 ± 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats. [source] Enhanced survival of vascular smooth muscle cells accounts for heightened elastin deposition in arteries of neonatal spontaneously hypertensive ratsEXPERIMENTAL PHYSIOLOGY, Issue 4 2010Silvia M. Arribas Abnormal stiffening and narrowing of arteries are characteristic features of spontaneously hypertensive rats (SHR). In this strain, we have previously demonstrated an increased elastin content and abnormal organization of lamellae in conduit and resistance arteries from neonatal rats that preceded the impending inward remodelling, increased vascular stiffness and development of hypertension. The aim of this study was to assess the mechanism responsible for such excessive and aberrant elastin deposition in SHR vessels during perinatal development. We compared elastin, collagen and fibronectin production (inmunocytochemistry and quantitative assay of metabolically labelled insoluble elastin), DNA content as well as cell proliferation (proliferative cellular nuclear antigen, bromodeoxyuridine incorporation) and death rates (propidium iodide exclusion test, terminal transferase nick and labeling (TUNEL) assay) in cultures of vascular smooth muscle cells (VSMC) derived from neonatal SHR and Wistar,Kyoto (WKY) control rats. Cultures of VSMC derived from neonatal SHR exhibited hypertrophy, produced more elastin, collagen and fibronectin and contained more DNA than equally plated WKY counterparts. Further analysis revealed that the higher net DNA content in SHR-derived cultures was due to increased diploidy, but not to a heightened cell multiplication. The SHR-derived VSMC also exhibited lower rates of cell death and apoptosis, which were associated with increased levels of the anti-apoptotic protein, survivin. We therefore conclude that the peculiar heightened survival of matrix-producing VSMC in neonatal SHR is responsible for accumulation of hard-wearing elastin and other extracellular matrix elements in the growing arteries, thereby contributing to the subsequent development of systemic hypertension. [source] Clinical characteristics of normotensive renal transplant recipients with microalbuminuria and effects of angiotensin II type I receptor antagonist on urinary albumin excretionINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2004SHIGERU SATOH Abstract Aim:, Microalbuminuria is typically observed in renal transplant recipients with systemic hypertension. The effects of angiotensin II type 1 receptor antagonist (losartan) on the hypertensive recipients have been evaluated. However, the clinical background of normotensive recipients with microalbuminuria and the effect of losartan administration in those subjects have not been clarified. One of the two purposes for the present study was to investigate the clinical characteristics of normotensive recipients with microalbuminuria. The other was to evaluate the effect of losartan on urinary excretion of albumin in these patients. Methods:, The clinical data and the change of the single kidney glomerular filtration rate (GFR) for the graft by radionuclide study were assessed in 13 normotensive recipients with microalbuminuria. These were compared with the data of 13 normotensive patients without microalbuminuria. The 13 recipients with microalbuminuria were treated with losartan for one year and urine excretion of albumin, N-acetyl-,-D-glucosaminidase (NAG) and serum creatinine (S-Cr) levels were measured. Results:, The GFR of the grafts from donors to recipients significantly increased (30.9 to 55.2 mL/min) in microalbuminuric recipients, but did not significantly increase in the non-microalbuminuric recipients. Decreases of the urinary excretion rate of albumin (351 ± 261 at baseline to 158 ± 14 mg/gCr at 12 months), NAG (13 ± 5 to 10 ± 3 IU/gCr) and S-Cr (1.7 ± 0.6 to 1.5 ± 0.4 mg/dL) were observed in the microalbuminuric recipients with losartan administration. Conclusions:, The present study suggests that an increased single kidney GFR of the graft from the donor in situ to the recipient might be a cause of microalbuminuria in normotensive recipients. The one-year effects of losartan were observed in terms of the decrease in urinary excretion of albumin, NAG and S-Cr levels. [source] Mitochondrial mechanism of oxidative stress and systemic hypertension in hyperhomocysteinemiaJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2005Neetu Tyagi Abstract Formation of homocysteine (Hcy) is the constitutive process of gene methylation. Hcy is primarily synthesized by de-methylation of methionine, in which s-adenosyl-methionine (SAM) is converted to s-adenosyl-homocysteine (SAH) by methyltransferase (MT). SAH is then hydrolyzed to Hcy and adenosine by SAH-hydrolase (SAHH). The accumulation of Hcy leads to increased cellular oxidative stress in which mitochondrial thioredoxin, and peroxiredoxin are decreased and NADH oxidase activity is increased. In this process, Ca2+ -dependent mitochondrial nitric oxide synthase (mtNOS) and calpain are induced which lead to cytoskeletal de-arrangement and cellular remodeling. This process generates peroxinitrite and nitrotyrosine in contractile proteins which causes vascular dysfunction. Chronic exposure to Hcy instigates endothelial and vascular dysfunction and increases vascular resistance causing systemic hypertension. To compensate, the heart increases its load which creates adverse cardiac remodeling in which the elastin/collagen ratio is reduced, causing cardiac stiffness and diastolic heart failure in hyperhomocysteinemia. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source] Secondary Hypertension: Obesity and the Metabolic SyndromeJOURNAL OF CLINICAL HYPERTENSION, Issue 7 2008Gregory M. Singer MD The epidemic of obesity in the United States and around the world is intensifying in severity and scope and has been implicated as an underlying mechanism in systemic hypertension. Obese hypertensive individuals characteristically exhibit volume congestion, relative elevation in heart rate, and high cardiac output with concomitant activation of the renin-angiotensin-aldosterone system. When the metabolic syndrome is present, insulin resistance and hyperinsulinemia may contribute to hypertension through diverse mechanisms. Blood pressure can be lowered when weight control measures are successful, using, for example, caloric restriction, aerobic exercise, weight loss drugs, or bariatric surgery. A major clinical challenge resides in converting short-term weight reduction into a sustained benefit. Pharmacotherapy for the obese hypertensive patient may require multiple agents, with an optimal regimen consisting of inhibitors of the renin-angiotensin-aldosterone system, thiazide diuretics, ,-blockers, and calcium channel blockers if needed to attain contemporary blood pressure treatment goals. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 81JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003S Lori Symptomatic neuropathy in young patients with type 1 Diabetes Mellitus (t1DM) is rare but subclinical peripheral alterations can be assessed by electroclinical evaluation. This study aimed to assess prevalence of clinical and subclinical peripheral neuropathy in patients with t1DM. Motor and/or sensory nerve conduction studies of both median, ulnar, peroneal, tibial and sural nerves and standard clinical examination of peripheral nervous system were performed in 83 patients (27 females and 56 males) with diabetes onset since five years. The mean age of patients was 19.89 (range 9,28.3) years, the mean disease duration was 9.61(range 4.4,19.3) and the mean age at the onset of diabetes was 9.02 (range 0.8,23.5). Five patients (6.02 %) had both symptomatic (light clinical abnormalities as paresthesias and mild reduction of vibratory sensibility) and electrophysiologic neuropathy and six (7.2 %) with mild abnormal nerve conduction studies were totally asymptomatic (subclinical neuropathy). The majority of symptoms and electrophysiological alterations were found on the lower limbs. Only two patients had a minimal distal neuropathy of median nerve. No patients showed laboratory evidence of early renal complications or systemic hypertension; 5 (6.02 %) had early diabetic retinal abnormalities as microaneurisms, seen by fundus examination. Analysis of sex, age of onset, duration of diabetes, age at the date of electrophysiologic examination, Hemoglobin A1c (mean level of the last two years), association with retinal abnormalities and clinical assessment was performed (Fisher Exact Test, ANOVA). No correlation was found with the age at the onset, retinal abnormalities and glycaemic control index. Peripheral neuropathy was significantly related with patient age at the date of electrophysiological study and duration of t1DM. [source] Plasma Asymmetric Dimethylarginine, Symmetric Dimethylarginine, l -Arginine, and Nitrite/Nitrate Concentrations in Cats with Chronic Kidney Disease and HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008R.E. Jepson Background: Chronic kidney disease (CKD) and hypertension have been associated with decreased bioavailability of nitric oxide (NO) and endothelial dysfunction. Increased concentrations of the endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) are implicated. Hypothesis: Plasma ADMA concentration is increased in cats with CKD and systemic hypertension corresponding to a decrease in total plasma nitrate/nitrite (NOx) availability. Decrease in systolic blood pressure (SBP) and proteinuria during treatment of hypertension with amlodipine besylate may be associated with increased NOx availability. Animals: Sixty-nine client-owned normotensive and hypertensive cats with variable azotemia. Methods: Plasma ADMA, symmetric dimethylarginine (SDMA), and l -arginine were measured simultaneously by hydrophilic-interaction liquid chromatography-electrospray tandem mass spectrometry in cats from 6 groups: normotensive nonazotemic (n = 10), normotensive mildly azotemic (n = 10), hypertensive mildly azotemic with hypertensive retinopathy (n = 20), hypertensive mildly azotemic without hypertensive retinopathy (n = 10), normotensive moderately azotemic cats (n = 10), and hypertensive nonazotemic cats (n = 9). Plasma NOx concentrations were measured. Results: A moderate correlation between plasma creatinine and ADMA (n = 69, r= .608, P < .001), SDMA (n = 69, r= .741, P < .001), and NOx concentrations (n = 69, r= .589, P < .001) was observed. There was no association among plasma ADMA, SDMA, and NOx concentrations and SBP. Conclusions and Clinical Importance: Plasma ADMA and SDMA concentrations are increased in cats with CKD and correlate with plasma creatinine concentration. This may imply the presence of endothelial dysfunction in cats with CKD. Plasma ADMA concentrations were not associated with systemic hypertension. Treatment of systemic hypertension with amlodipine besylate did not affect plasma ADMA or NOx concentrations. [source] New Expression Profiles of Voltage-gated Ion Channels in Arteries Exposed to High Blood PressureMICROCIRCULATION, Issue 4 2002Robert H. Cox The diameters of small arteries and arterioles are tightly regulated by the dynamic interaction between Ca2+ and K+ channels in the vascular smooth muscle cells. Calcium influx through voltage-gated Ca2+ channels induces vasoconstriction, whereas the opening of K+ channels mediates hyperpolarization, inactivation of voltage-gated Ca2+ channels, and vasodilation. Three types of voltage-sensitive ion channels have been highly implicated in the regulation of resting vascular tone. These include the L-type Ca2+ (CaL) channels, voltage-gated K+ (KV) channels, and high-conductance voltage- and Ca2+ -sensitive K+ (BKCa) channels. Recently, abnormal expression profiles of these ion channels have been identified as part of the pathogenesis of arterial hypertension and other vasospastic diseases. An increasing number of studies suggest that high blood pressure may trigger cellular signaling cascades that dynamically alter the expression profile of arterial ion channels to further modify vascular tone. This article will briefly review the properties of CaL, KV, and BKCa channels, present evidence that their expression profile is altered during systemic hypertension, and suggest potential mechanisms by which the signal of elevated blood pressure may result in altered ion channel expression. A final section will discuss emerging concepts and opportunities for the development of new vasoactive drugs, which may rely on targeting disease-specific changes in ion channel expression as a mechanism to lower vascular tone during hypertensive diseases. [source] Renal impairment in deoxycorticosterone acetate-salt hypertensive ratsNEPHROLOGY, Issue 4 2000Catherine Dallemagne Summary: This study has compared renal function in deoxycorticosterone (DOCA)-salt hypertensive Wistar rats (uninephrectomy followed by administration of DOCA 25 mg subcutaneously every fourth day and 1% NaCl in the drinking water) with various control rats using the isolated perfused kidney preparation. The systolic blood pressure of DOCA-salt hypertensive rats was 180 ± 10 mmHg (uninephrectomy controls: 136 ± 9 mmHg) while normalization of calcium intake (DOCA-Ca rats, 1% CaCl2 in water) attenuated this increase (systolic blood pressure, 146 ± 5 mmHg). Renal mass corrected for body weight increased by 25% after uninephrectomy, 55% in uninephrectomized rats given NaCl, 152% in DOCA-salt rats and 147% in DOCA-Ca rats. At a renal perfusion pressure of 135 mmHg, isolated perfused kidneys from DOCA-salt rats showed decreases of 48% in glomerular filtration rate and 69% in sodium excretion with an increase of 44% in renal vascular resistance compared with uninephrectomized rats. There were no significant differences in renal function between DOCA-salt and DOCA-Ca rats. Histological assessment of renal pathology showed proximal tubular hypertrophy and hyperplasia, marked focal distal tubular atrophy, interstitial fibrosis and glomerular hypercellularity in DOCA rats compared with UNX rats. Lesions were less obvious in UNX-salt or DOCA-Ca rats. The lack of direct correlation between alterations in function and pathology may be explained by the compensatory effect of remaining healthy or hypertrophied nephrons. Thus, the DOCA-salt model of hypertension in rats is associated with marked structural kidney damage and severely decreased kidney function. Marked attenuation of systemic hypertension by normalizing calcium intake in DOCA-salt rats did not prevent impairment of kidney function. [source] Stent implantation for long-segment coarctation of aorta in infant with facial and mediastinal hemangiomaCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 4 2002Abraham Matitiau MD Abstract We report a case of an infant with an extensive hemangioma encompassing the thoracic aorta, associated with complex coarctation. Surgical approach was abandoned for fear of bleeding. The complexity of the coarctation made it unsuitable for balloon dilation. We implanted a stent with significant angiographic improvement and resolution of systemic hypertension. Cathet Cardiovasc Intervent 2002;55:510,512. © 2002 Wiley-Liss, Inc. [source] 2325: Dynamic retinal vessel analysis , how different parameters create the whole pictureACTA OPHTHALMOLOGICA, Issue 2010I LANZL Purpose Dynamic vessel analysis is usually associated with the observation of the reaction of retinal vessels to a defined stimulus. The data which is generated this way may be further analysed with respect to the dynamic unstimulated and stimulated vessel behaviour. Assessment of different parameters may highlight different aspects of the underlying disease. Methods Vessel diameters of retinal vessel segments were assessed by Dynamic Vessel Analyzer (DVA) in healthy volunteers of different age groups and patients with diabetes, glaucoma and systemic hypertension. Mathematical analysis of unstimulated vessels was used to describe vessel wall characteristics. Methods of signal analysis including Fourier Transformation, spectral filtration, auto- and cross correlation were applied to evaluate characteristic oscillations and pulse wave propagation along the vessel. Results Characteristic different vessel behaviour and vessel wall conformation are obtained by dynamic quantitative evaluations from the unstimulated vessels in physiologic aging and disease. Conclusion Dynamic vessel analysis includes information which may lead to further understanding of the vascular status and underlying disease pathology. It is also feasible to assess pulse wave velocities in retinal arterioles und thus clinically characterize the elasticity of the upstream vasculature in health and disease. [source] Effect of glaucoma and glaucoma risk factors on choroidal hemodynamicsACTA OPHTHALMOLOGICA, Issue 2009W ABOU SAMRA Purpose a) to determine subfoveal choroidal hemodynamics in patients with primary open angle glaucoma (POAG) and patients with ocular hypertension (OH); b) to assess the effects of diabetes (DM), systemic hypertension (SHT) and myopia on subfoveal choroidal hemodynamics Methods Laser Doppler flowmetry (LDF) was used to determine the subfoveal choroidal blood velocity (ChBVel), volume (ChBVol), and flow (ChBF) in 1) patients with POAG (n=85) and patients with OHT (n=25); 2) patients with glaucoma risk factors which were further subdivided into three subgroups; DM (n=93), SHT (n=57) and myopia (n=29) respectively. Subjects with each risk factor were further subdivided into two subgroups (without and with POAG), 3) age matched healthy controls (n=100). Results All LDF parameters were significantly reduced in all groups of patients compared with age matched controls. No statistically significant differences in the LDF parameters among HTG, NTG and OHT subgroups were detected. No significant difference in the LDF parameters between the two subgroup of each risk factor (without and with POAG) was noted. The LDF data of glaucomatous patients with risk factors demonstrated a significant reduction of ChBF and an increase in resistance in comparison to glaucomatous patients without risk factors Conclusion Subfoveal choroidal LDF parameters are reduced in subjects with POAG, OHT and patients with glaucoma risk factors, such as DM, SHT (under antihypertensive therapy) and myopia when compared with age matched healthy controls. However, the role of these choroidal circulatory alterations in the development or progression of the glaucomatous optic neuropathy remains to be clarified. [source] Major eye diseases and risk factors associated with systemic hypertension in an adult chinese population: the Beijing Eye StudyACTA OPHTHALMOLOGICA, Issue 2009T LIBONDI Purpose To assess the relationship of hypertension with major eye diseases and other ocular parameters. Methods The Beijing Eye Study is a population-based study. Examination at baseline in 2001; follow-up examination in 2006; 3222 subjects had blood pressure measurements. All participants underwent a thourough ophthalmic examination and blood pressure measurement. Hypertension was defined as a systolic blood pressure ,140 mm Hg and/or a diastolic blood pressure ,90 mm Hg, and/or self-reported current treatment for hypertension with antihypertensive medication. Results Mean age of participants in the present study was 60.4±10.0 years. Hypertension was present in 1500 (46.6%) of the 3222 subjects who had their blood pressure measured. In multiple regression analysis, hypertension was associated with higher intraocular pressure (P = 0.005), arterio-venous nicking (P = 0.009),retinal vein occlusions (P = 0.02), and diabetic retinopathy (P = 0.02). Hypertension was not significantly associated with the prevalence of open-angle glaucoma (P = 0.19) or angle-closure glaucoma (P = 0.15), age-related macular degeneration (P = 0.73), nuclear cataract (P = 0.88), posterior subcapsular cataract (P = 0.30), cortical cataract (P = 0.10), or area of alpha zone (P=0.05) or beta zone of parapapillary atrophy (P = 0.95). Conclusion In Chinese persons, while controlling for other systemic parameters, hypertension was associated with increased intraocular pressure, retinal microvascular abnormalities, and prevalence of retinal vein occlusion and diabetic retinopathy. Hypertension was not associated significantly with age-related macular degeneration, age-related cataract, or glaucoma [source] Central serous retinopathy complicating systemic lupus erythematosus: a case seriesCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 4 2000CGYW Khng FRCS Ed ABSTRACT Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder with widespread manifestations including the eye. Central serous retinopathy (CSR) has been associated as a complicating event in SLE, although it is uncommon. We present a case series of four female Chinese SLE patients who developed CSR during the course of their systemic disease. All four presented clinically with typical CSR. Angiographic findings did not show evidence of choroidal ischaemia or delayed choroidal filling. Resolution of the serous retinal detachment occurred in all four patients. Recovery of vision was seen in three patients. The clinical outcome was similar to that occurring in the usual male population. Central serous retinopathy as a manifestation of SLE may be caused by various factors. These include SLE-associated choroidopathy, systemic hypertension, renal disease, retinal pigment epithelial dysfunction and glucocorticoid therapy. [source] | |||||||||||||