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Angiotensin-converting-enzyme Inhibitors (angiotensin-converting-enzyme + inhibitor)
Selected AbstractsNon-adherence to antihypertensive medication and impaired cognition: which comes first?INTERNATIONAL JOURNAL OF PHARMACY PRACTICE, Issue 5 2010Paul R. Gard Abstract Objective, Antihypertensive medications are important in the prevention of serious consequences of hypertension, such as stroke and heart failure. Up to one-third of elderly hypertensive patients, however, do not adhere to their medication. Adherence to medication decreases with increasing age, and with decreasing cognitive ability, thus elderly, cognitively-impaired patients have poorer control of blood pressure. Good control of blood pressure is associated with decreased prevalence of dementia and Alzheimer's disease. This study assessed the evidence that antihypertensive medications have effects on the prevalence or severity of mild cognitive impairment, dementia or Alzheimer's disease. Methods, The ISI Web of Knowledge database was searched; including replicates, the nine searches identified 14 400 publications since 1952, of which 9.9% had been published in 2009. This review considers the 18 studies meeting the set criteria published in 2009 or later. Key findings, Not all antihypertensive medications are equivalent in their positive cognitive effects, with brain-penetrating angiotensin-converting-enzyme inhibitors and possibly angiotensin receptor antagonists being the most effective. Conclusions, Based on evidence of blood-pressure control and cost, UK National Institute for Health and Clinical Excellence guidelines recommend calcium-channel blockers or thiazide-type diuretics for the treatment of hypertension in patients over 55 years. These guidelines take no account of the potential cognitive effects of the antihypertensive therapies, consideration of which might lead to a review. There may be benefit in stressing that adherence to antihypertensive medication not only decreases the risk of cardiovascular disease and death, but may also decrease the risk or severity of mild cognitive impairment, dementia and Alzheimer's disease. [source] Effect of losartan on early liver fibrosis development in a rat model of nonalcoholic steatohepatitisJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2007Patricio Ibañez Abstract Background and Aim:, Nonalcoholic steatohepatitis (NASH) is a metabolic disorder of the liver that may evolve into fibrosis or cirrhosis. Recent studies have shown reduction of experimental liver fibrosis with the use of angiotensin-converting-enzyme inhibitors or angiotensin-receptor antagonists. The aim of this study was to determine whether losartan can influence the early phase of fibrogenesis in an animal model of NASH. Methods:, To induce NASH, a choline-deficient diet (CDD) was given to Sprague-Dawley rats for 12 weeks. These animals were then compared with a control group receiving choline-supplemented diet (CSD) and a group fed a CDD plus losartan (10 mg/kg/day). Biochemical (serum levels of alanine aminotransferase and aspartate aminotransferase) and histological evaluation of fatty liver was performed by conventional techniques. Hydroxyproline content in liver tissue was assayed by spectrophotometry. In addition, mRNA levels of procollagen I and transforming growth factor (TGF)-, were assessed by semiquantitative RT-PCR and stellate cell activation by ,-actin immunofluorescence stain. Results:, After 12 weeks CDD induced a marked elevation of serum aminotranferases, a severe fatty liver infiltration with mild histological inflammation and fibrosis. These findings correlated with a significant increase in mRNA levels of both procollagen I and TGF-, and significant increased liver hydroxyproline content. No differences were seen between rats receiving CDD alone and rats receiving CDD plus losartan with regard to the biochemical, morphological or molecular alterations induced by the CDD. Conclusion:, Losartan does not seem to influence liver injury and fibrogenic events in the CDD model of NASH. [source] Did thirst-blockers like angiotensin-converting-enzyme inhibitors, sartans, serotonine-re-uptake-inhibitors, dopamine agonists/antagonists, or atypical neuroleptics contribute to the exorbitant number of fatalities during the French 2003 heat wave?PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 11 2007Dr Claudia Stöllberger MD Univ. No abstract is available for this article. [source] Prevention of Atrial Fibrillation in Cardiac Surgery: Time to Consider a Multimodality Pharmacological ApproachCARDIOVASCULAR THERAPEUTICS, Issue 1 2010Kwok M. Ho Atrial fibrillation (AF) is very common within the first 5 days of cardiac surgery. It is associated with significant morbidity including stroke, ventricular arrhythmias, myocardial infarction, heart failure, acute kidney injury, prolonged hospital stay, and also short- and long-term mortality. The underlying mechanisms of developing AF after cardiac surgery are multifactorial; risk factors may include advanced age, withdrawal of beta-blockers and angiotensin-converting-enzyme inhibitors, valve surgery, obesity, increased left atrial size, and diastolic dysfunction. There are many pharmacological options in preventing AF, but none of them are effective for all patients and they all have significant limitations. Beta-blockers may reduce the incidence of AF by more than a third, but bradycardia, hypotension, or exacerbation of heart failure often limit their utility postoperatively. Recent evidence suggests that class III antiarrhythmic drugs, sotalol and amiodarone, are more effective than beta-blockers, but they both share similar hemodynamic side effects of beta-blockers. Magnesium, antiinflammatory drugs such as statins, omega fatty acids, and low-dose corticosteroids also have some efficacy and they have the advantages of not causing significant hemodynamic side effects. Data on effectiveness of calcium channel blockers, digoxin, alpha-2 agonists, sodium nitroprusside, and N-acetylcysteine are more limited. Because the pathogenesis of AF is multifactorial, a combination of drugs with different pharmacological actions may have additive or synergistic effect in preventing AF after cardiac surgery. Randomized controlled trials evaluating the effectiveness of a multimodality pharmacological approach in patients at high-risk of AF after cardiac surgery are needed. [source] Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitisCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009J. W. Cohen Tervaert Premature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible. [source] | ||||||||||