Loading

skip to Main Content
contact@ecoteer.com
whitetube.cc
Colospa

By Y. Jose. State University of New York College of Agriculture and Technology, Cobleskill.

In this regard generic 135 mg colospa amex muscle relaxant lorazepam, Apo E In this chapter purchase colospa 135 mg free shipping muscle relaxant vs anti-inflammatory, a discussion of Alzheimer neuropathology is particularly critical to A deposition (101–103) discount colospa 135mg online muscle relaxant definition. Cellular provides the starting point for understanding how the diag- uptake and clearance of A involve interactions of an Apo nosis of AD is made and how clinical symptoms arise and E/A complex with LRP colospa 135 mg on line yorkie spasms. Later sections address the neuroanatomic and cel- loid deposition is underscored by the observation that Apo lular basis for dementia and the molecular events that lead E gene ablation abolishes amyloid deposition in transgenic to neuropathologic lesions and, ultimately, to the death of mice overexpressing APP containing the London mutation neurons. A consideration of current hypotheses on the evo- (104). Microglial function also seems to be critical to A lution of cellular pathology identifies common features that removal (15). In transgenic models of FAD, A deposition help to reconcile the differing views of disease pathogenesis. Although a sequence of events after A deposi- tion has not been confirmed, it is hypothesized that A I am grateful to Janet Rosdil for expert assistance in the accumulation within diffuse plaques eventually leads to local preparation of this manuscript. A -initiated inflammatory and DISCLAIMER neurotoxic processes generate excessive free radicals and per- oxidative injury to proteins and alterations of ionic homeo- Dr. Nixon has received research support from Johnson and stasis, particularly excessive calcium entry into neurons ac- Johnson (Janssen). Alzheimer neuro- growth of arbuscular mycorrhizal fungi is induced by a branch- pathologic alterations in aged cognitively normal subjects. J ing factor partially purified from plant root exudates. Lithium reduces amyloid load in individuals with mild cognitive impairment. Active site-directed gender effects on Alzheimer disease in 100 adults with Down antibodies identify calpain II as an early-appearing and pervasive syndrome. Neuro- endocytosis and protease delivery to early endosomes in sporadic biol Aging 1997;18:S55–65. Consensus recommendations for the postmortem of increased beta-amyloidogenesis. Aging, and Reagan Institute Working Group on Diagnostic 29. Application of the in Proc Natl Acad Sci USA 1992;89:2509]. Proc Natl Acad Sci National Institute on Aging (NIA)–Reagan Institute criteria for USA 1991;88:10998–11002. Gene expression pathol Exp Neurol 1999;58:1147–1155. Amyloid beta protein evidence for early up-regulation of the endosomal-lysosomal (A beta) deposition in dementia with Lewy bodies: predomi- system. Sense and senility: the neuropathology of the aged human meganeurite formation and phosphorylated tau abnormalities brain. Enzymatically active lysosomal pro- sis factor alpha converting enzyme is involved in regulated alpha- teases are associated with amyloid deposits in Alzheimer brain. Soluble amyloid beta peptide ties in degenerating neurons link neuronal compromise to senile concentration as a predictor of synaptic change in Alzheimer plaque development in Alzheimer disease. The pathogenesis of Alzheimer disease: an alternative 19. J Neuropathol Exp Neurol 1996;55: cellular A beta 42 is related to apoptosis but not necrosis. Neuropathological stageing of Alzheimer- levulinic acid uptake. Some cytoarchi- phism of cathepsin D is strongly associated with the risk for tectural abnormalities of the entorhinal cortex in schizophrenia. Neurosci Lett 1999; Arch Gen Psychiatry 1991;48:625–632. Alpha-2 macroglobulin high molecular mass subunit of neurofilaments in axons of reti- is genetically associated with Alzheimer disease [see Comments]. Interaction between amyloid Cell Biol 1988;107:2689–2701. The topographical and tions for the pathogenesis of Alzheimer disease. Proc Natl Acad neuroanatomical distribution of neurofibrillary tangles and neu- Sci USA 1997;94:8208–8213. Proc Natl Acad Sci USA 1999;96: ronal vulnerability in neurodegenerative diseases. Mutagenesis identifies toxicity in rat hippocampal pyramidal neuronal cultures. J Neu- new signals for beta-amyloid precursor protein endocytosis, rosci 1998;18:195–204. Eur J Biochem 1997; low density lipoprotein receptor-related protein gene. Processing of the Chapter 85: Cell and Molecular Neuropathology of Alzheimer Disease 1229 pre–beta-amyloid protein by cathepsin D is enhanced by a fa- 95. Eur J Biochem 1994;224: presenilin-1 exon 9 deletion and L250S mutations sensitize SH- 265–271. SY5Y neuroblastoma cells to hyperosmotic stress-induced 79. Impairment of glucose apolipoprotein E3 or E4 in the brains of Apoe / mice: iso- and glutamate transport and induction of mitochondrial oxida- form-specific effects on neurodegeneration. J Neurosci 1999;19: tive stress and dysfunction in synaptosomes by amyloid beta 4867–4880. Cellular actions of beta-amyloid precursor protein 1 antichymotrypsin apolipoprotein E promotes amyloid beta and its soluble and fibrillogenic derivatives. Beta-amyloid precur- (A beta) binding proteins in A beta aggregation. J Neurosci Res sor protein metabolites and loss of neuronal Ca2 homeostasis 1996;46:58–66. Calcium as sculptor and destroyer of neural circui- apolipoprotein E reduces amyloid-beta deposition in a mouse try. Lack of apolipoprotein to p25 deregulates Cdk5 activity and promotes neurodegenera- E dramatically reduces amyloid beta-peptide deposition. Immunization with human disease and transgenic mouse models. Neuron 1999;24: amyloid-beta attenuates Alzheimer-disease–like pathology in 507–510. Curr Opin Chem Biol Alzheimer disease: a potential molecular basis for neuronal de- 1997;1:260–267. Calpains and calpas- rodegeneration in Alzheimer disease. In: Terry R, Katzman R, tatin in SH-SY5Y neuroblastoma cells during retinoic acid–in- Bick K, eds. New York: Raven, 1994: duced differentiation and neurite outgrowth: comparison with 305–315. Possible role of tau toxicology of calcium-dependent protease. Loss of endo- precursor protein mutation increases amyloid beta42(43) pep- somal/lysosomal membrane impermeability is an early event tide levels and induces apoptosis. Ann Neurol 2000;47: in amyloid Abeta1–42 pathogenesis.

Two transmembrane transgenic Alzheimer mice [Abstract 636 generic 135mg colospa otc muscle relaxant medication prescription. The protein tyrosine kinase colospa 135 mg line spasms movie, fyn buy colospa 135 mg low cost muscle relaxant 4211, in Alzhei- pressing FAD-linked presenilin 1 discount colospa 135mg on-line muscle relaxant reversals. Functional phenotype in non-receptor tyrosine kinases. Presenilin 1 is required for tyrosine kinase, pp125FAK. Notch1 and DII1 expression in the paraxial mesoderm. Notch1 is required for the able to amyloid -protein neurotoxicity. Presenilin 1 interaction helical filaments from mouse tau: implications for the neurofibril- in the brain with a novel member of the Armadillo family. Characterization of pathol- catenin by mutations in presenilin-1 potentiates neuronal ogy in transgenic mice over-expressing human genomic and apoptosis. Association of missense Chapter 84:Transgenic Mouse Models of Alzheimer Disease 1219 and 5′-splice-site mutations in tau with the inherited dementia and progression of a tauopathy in transgenic mice overexpressing FTDP-17. Prominent tion in familial progressive subcortical gliosis. The prevalence and incidence of AD increase aggression, and wandering), and problems with self-care (ac- with age. The prevalence of the disease broadly doubles for tivities of daily living) (1–3). Caring for a person with de- every 5 years of age, increasing from less than 1% of the mentia places a huge strain on both formal (paid, profes- population ages 65 to 69 years to between 10% and 40% sional) and informal careers (4). The age-specific incidence Alzheimer disease is associated with significant and excess rates of AD are between 51 and 161 cases per 100,000 morbidity and mortality. Approximately 30% of elderly person-years for ages 65 to 69; they increase to between people with dementia are severely disabled and require in- 1,000 and 2,855 cases per 100,000 person-years for ages tensive or specialized care and support (2). Studies also indi- 80 to 84 and to between 1,456 and 5,420 cases per 100,000 cate that 50% of an incident cohort with dementia will be person-years for ages 85 and over. The length of survival depends on the age at diagnosis, comorbid conditions, setting of care, Two theoretically distinct treatment options are available family situation, and gender (5,6). Symptomatic treatments are aimed mated that AD accounts for 2. The demographic trend toward an aging population Stabilization treatments are directed at altering the underly- means that the burden of the condition will increase in the ing disorder (characterized by the deposition of amyloid next 25 years. Population estimates suggest that the ex- and the presence of neurofibrillary tangles and abnormally pected number of people with AD will rise from less than phosphorylated tau protein); they do not necessarily pro- half a million in 1999 to more than 600,000 in 2020 in duce symptomatic improvement but may delay the progres- the United Kingdom (8). Similar increases are predicted in sion of the disorder. Canada, from 161,000 people in 1991 to 314,000 people Symptomatic Treatment Andrea Manca: Centre for Health Economics, University of York, York, United Kingdom. The most successful agents to provide symptomatic improve- Linda Davies: School of Psychiatry and Behavioural Sciences, University ment are the acetylcholinesterase drugs. AD is associated of Manchester, Manchester, United Kingdom. Alistair Burns: Department of Old Age Psychiatry, Withington Hospital, with a number of neurologic and neurochemical abnormali- West Disbury, Manchester, United Kingdom. Acetylcholines- 1268 Neuropsychopharmacology: The Fifth Generation of Progress TABLE 89. AGE-SPECIFIC PREVALENCE OF DEMENTIA AND ALZHEIMER DISEASE (%) Eurodem (10) Framingham (11) Jorm et al. The evidence of a symptomatic improvement cholinergic neurotransmission by inhibiting the breakdown in patients taking these drugs is inconsistent. Estrogen appears to have a signifi- suggested that physostigmine has short-term efficacy in im- cant protective effect against the development of AD and proving memory. However, the results of trials vary substan- may work through a number of different mechanisms. In addition, the drug is associated with a high inci- Small-scale studies have shown minor benefits in terms of dence of side effects (13). Tacrine requires a complex dosing improved cognitive function. A growing body of evidence regime and has toxic side effects (3). Systematic reviews indicates that free radical formation is a mediator of the suggest that the drug has a modest but not clinically or excessive lipid peroxidation and cell damage seen in AD. Because administration of shown to have biological activity in acting as scavengers for the drug has been accompanied by a high rate of adverse free radicals. Therefore, Second-generation anticholinesterases include donepezil of the three stabilization agents currently available, only vi- hydrochloride (Aricept, Pfizer) and rivastigmine (Exelon, tamin E is supported by evidence that it can delay deteriora- Novartis). Overall, patients taking the drug show an im- nificant potential to cause gynecologic cancer and currently provement in cognition, global clinical state, and carer rat- is suitable only for women, and antiinflammatory agents ings of activities of daily living. Drugs that have a stabilization effect on the progress of AD are nonsteroidal antiinflammatory agents (NSAIDs), ECONOMIC PERSPECTIVE estrogen, and antioxidant agents. There is good evidence of an inflammatory component in AD, and it is well docu- Given the constraints on health and social care budgets, mented that NSAIDs are protective against the develop- those responsible for the provision and financing of such Chapter 89: Cost-Effectiveness of Therapeutics for Alzheimer Disease 1269 services need to ensure that resources are used efficiently. Two approaches have been used to evaluate the economic conse- Cost-Effectiveness Analysis quences of AD. These are (a) cost-of-illness or burden-of- A cost-effectiveness analysis compares the direct costs of disease studies to assess the costs and consequences of a health and social care resources of two or more interventions disease to society and (b) full economic evaluations to com- with patient outcomes, measured in terms of clinical effec- pare the costs and consequences of alternative health or tiveness. For AD, measures such as years of life with mild social care interventions. Cost-of-Illness Analyses If one intervention, such as a new drug to control symp- toms or delay progression, leads to lower direct costs and From an economic perspective, the aim of cost-of-illness or improved patient outcomes, it is the dominant and pre- burden-of-disease studies is to describe and value the costs ferred option. In other words, it clearly saves resources to and consequences of a disease to society. A cost-of-illness provide care and is more beneficial to the patient. More study should describe and value the direct costs of health often, a new therapy is associated with improved patient and social care for people with the disease. Incremental cost effectiveness describe the mortality and morbidity consequences. These ratios (ICER) provide a measure of the cost of gaining a should be valued in either monetary terms (as indirect and unit of health improvement, such as cost per life-year intangible costs) or by utility-based measures such as qual- gained. The ICER is calculated as follows: (Cost of A ity-adjusted life-years (QALYs). Cost-of-illness studies can be used to estimate the total Cost-effectiveness analysis is limited by the use of effec- burden of disease for a given year. In this approach, known tiveness measures, which may not capture the total impact as the prevalence approach, the costs and health outcomes of health and social care on quality of life or overall well- of all people with the disease in a given year are included. This is particularly important in AD, in which the An alternative approach is to estimate the lifetime costs and impact of the disease and patient care is multidimensional. Cost–utility analysis is similar to cost-effectiveness analysis, but utility is used as the outcome measure. Cost–utility Full Economic Evaluation analysis is used to estimate QALYs.

Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Since the KQ was removed after the original Embase searches were performed on December 16 buy 135 mg colospa with visa muscle relaxant egypt, 2011 order colospa 135 mg with visa muscle relaxant for stiff neck, we have included documentation of the search strategy below colospa 135 mg lowest price muscle relaxant little yellow house. This portion of the search was not included in the final search update on August 1 buy colospa 135mg with amex muscle relaxant starting with b, 2012. The results from this search are reflected in the totals depicted in the literature flow diagram. Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Anti-Arrhythmia Agents explode all trees OR MeSH descriptor Adrenergic beta- Antagonists explode all trees OR MeSH descriptor Calcium Channel Blockers explode all trees OR ((antiarrhythmic:ab,ti OR antiarrhythmia:ab,ti) AND (agent:ab,ti OR agents:ab,ti OR drug:ab,ti OR drugs:ab,ti)) OR metoprolol:ab,ti,kw OR atenolol:ab,ti,kw OR carvedilol:ab,ti,kw OR bisoprolol:ab,ti,kw OR timolol:ab,ti,kw OR esmolol:ab,ti,kw OR nebivolol:ab,ti,kw OR verapamil:ab,ti,kw OR diltiazem:ab,ti,kw OR digoxin:ab,ti,kw OR beta-blocker:ab,ti OR beta-blockers:ab,ti OR Acebutolol:ab,ti,kw OR Nadolol:ab,ti,kw OR Amiodarone:ab,ti,kw OR dronedarone:ab,ti,kw #3 #1 AND #2 #4 #3, Limits: Cochrane Reviews, 2000-2012 KQ 2—What are the comparative safety and effectiveness of a strict rate-control strategy versus a more lenient rate-control strategy in patients with atrial fibrillation? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 ((rate:ab,ti OR heart rate:ab,ti,kw) AND control:ab,ti) AND (strategy:ab,ti OR lenient:ab,ti OR strict:ab,ti) #3 #1 AND #2 #4 #3, Limits: Cochrane Reviews, 2000-2012 KQ 3—What are the comparative safety and effectiveness of newer procedural and other nonpharmacological rate-control therapies compared with pharmacological agents in patients A-10 with atrial fibrillation who have failed initial pharmacotherapy? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Pacemaker, Artificial explode all trees OR MeSH descriptor Cardiac Pacing, Artificial explode all trees OR MeSH descriptor Atrioventricular Node explode all trees OR MeSH descriptor Catheter Ablation explode all trees OR nonpharmacological:ab,ti OR non-pharmacological:ab,ti OR pacemaker:ab,ti OR (cardiac:ab,ti AND (pace:ab,ti OR pacing:ab,ti) AND artificial:ab,ti) OR AVN:ab,ti OR ((atrioventricular:ab,ti OR atrio-ventricular:ab,ti) AND (nodal:ab,ti OR node:ab,ti)) OR “catheter ablation”:ab,ti #3 rate:ab,ti OR heart rate:ab,ti,kw #4 #1 AND #2 AND #3 #5 #4, Limits: Cochrane Reviews, 2000-2012 KQ 4—What are the comparative safety and effectiveness of available antiarrhythmic agents and electrical cardioversion for conversion of atrial fibrillation to sinus rhythm? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Anti-Arrhythmia Agents explode all trees OR ((antiarrhythmic:ab,ti OR antiarrhythmia:ab,ti) AND (agent:ab,ti OR agents:ab,ti OR drug:ab,ti OR drugs:ab,ti)) OR flecainide:ab,ti,kw OR propafenone:ab,ti,kw OR amiodarone:ab,ti,kw OR sotalol:ab,ti,kw OR ibutilide:ab,ti,kw OR dofetilide:ab,ti,kw OR dronedarone:ab,ti,kw OR Disopyramide:ab,ti,kw #3 MeSH descriptor Electric Countershock explode all trees OR electrical:ab,ti OR cardioversion:ab,ti #4 #1 AND (#2 OR #3) #5 #4, Limits: Cochrane Reviews, 2000-2012 KQ 5—What are the comparative safety and effectiveness of newer procedural rhythm- control therapies, other nonpharmacological rhythm-control therapies, and pharmacological agents for maintenance of sinus rhythm in atrial fibrillation patients? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Catheter Ablation explode all trees OR MeSH descriptor Cardiac Resynchronization Therapy explode all trees OR MeSH descriptor Electric Countershock explode all trees OR non- pharmacological:ab,ti OR nonpharmacological:ab,ti OR ablation:ab,ti OR “surgical maze”:ab,ti OR (surgical:ab,ti AND maze:ab,ti) OR resynchroni*:ab,ti OR (ganglionic:ab,ti AND ablation:ab,ti) OR (ganglionated:ab,ti AND ablation:ab,ti) OR denervation:ab,ti OR “pulmonary vein isolation”:ab,ti OR (pulmonary:ab,ti AND isolation:ab,ti) OR electrical:ab,ti OR cardioversion:ab,ti #3 MeSH descriptor Anti-Arrhythmia Agents explode all trees OR ((antiarrhythmic:ab,ti OR antiarrhythmia:ab,ti) AND (agent:ab,ti OR agents:ab,ti OR drug:ab,ti OR drugs:ab,ti)) OR flecainide:ab,ti,kw OR propafenone:ab,ti,kw OR amiodarone:ab,ti,kw OR sotalol:ab,ti,kw OR ibutilide:ab,ti,kw OR dofetilide:ab,ti,kw OR dronedarone:ab,ti,kw OR Disopyramide:ab,ti,kw #4 rhythm:ab,ti #5 #1 AND (#2 OR #3) AND #4 #6 #5, Limits: Cochrane Reviews, 2000-2012 A-11 KQ 6—What are the comparative safety and effectiveness of rate-control therapies versus rhythm-control therapies in patients with atrial fibrillation? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Pacemaker, Artificial explode all trees OR MeSH descriptor Cardiac Pacing, Artificial explode all trees OR MeSH descriptor Atrioventricular Node explode all trees OR MeSH descriptor Catheter Ablation explode all trees OR MeSH descriptor Anti-Arrhythmia Agents explode all trees OR MeSH descriptor Adrenergic beta-Antagonists explode all trees OR MeSH descriptor Calcium Channel Blockers explode all trees OR ((nonpharmacological:ab,ti OR non-pharmacological:ab,ti OR pacemaker:ab,ti OR (cardiac:ab,ti AND (pace:ab,ti OR pacing:ab,ti) AND artificial:ab,ti)) OR AVN:ab,ti OR ((atrioventricular:ab,ti OR atrio-ventricular:ab,ti) AND (nodal:ab,ti OR node:ab,ti)) OR “catheter ablation”:ab,ti OR ((antiarrhythmic:ab,ti OR antiarrhythmia:ab,ti) AND (agent:ab,ti OR agents:ab,ti OR drug:ab,ti OR drugs:ab,ti) AND (heart rate:ab,ti,kw OR rate:ab,ti)) OR metoprolol:ab,ti,kw OR atenolol:ab,ti,kw OR carvedilol:ab,ti,kw OR bisoprolol:ab,ti,kw OR timolol:ab,ti,kw OR esmolol:ab,ti,kw OR nebivolol:ab,ti,kw OR verapamil:ab,ti,kw OR diltiazem:ab,ti,kw OR digoxin:ab,ti,kw OR OR beta- blocker:ab,ti OR beta-blockers:ab,ti OR Acebutolol:ab,ti,kw OR Nadolol:ab,ti,kw #3 MeSH descriptor Catheter Ablation explode all trees OR MeSH descriptor Cardiac Resynchronization Therapy explode all trees OR MeSH descriptor Electric Countershock explode all trees OR MeSH descriptor Anti-Arrhythmia Agents explode all trees OR non-pharmacological:ab,ti OR nonpharmacological:ab,ti OR ablation:ab,ti OR “surgical maze”:ab,ti OR (surgical:ab,ti AND maze:ab,ti) OR resynchroni*:ab,ti OR (ganglionic:ab,ti AND ablation:ab,ti) OR (ganglionated:ab,ti AND ablation:ab,ti) OR denervation:ab,ti OR “pulmonary vein isolation”:ab,ti OR (pulmonary:ab,ti AND isolation:ab,ti) OR electrical:ab,ti OR cardioversion:ab,ti OR ((antiarrhythmic:ab,ti OR antiarrhythmia:ab,ti) AND (agent:ab,ti OR agents:ab,ti OR drug:ab,ti OR drugs:ab,ti)) AND rhythm:ab,ti) OR flecainide:ab,ti,kw OR propafenone:ab,ti,kw OR amiodarone:ab,ti,kw OR sotalol:ab,ti,kw OR ibutilide:ab,ti,kw OR dofetilide:ab,ti,kw OR dronedarone:ab,ti,kw OR Disopyramide:ab,ti,kw #4 #1 AND #2 AND #3 #5 #4, Limits: Cochrane Reviews, 2000-2012 Eliminated KQ*—What are the comparative diagnostic accuracy, diagnostic thinking, therapeutic, and patient outcome efficacy of echocardiographic studies and other clinical parameters for predicting successful conversion, successful ablation, successful maintenance of sinus rhythm, and improved outcomes in patients with atrial fibrillation? Since the KQ was removed after the original Cochrane searches were performed on December 9, 2011, we have included documentation of the search strategy below. This portion of the search was not included in the final search update on August 1, 2012. The results from this search are reflected in the totals depicted in the literature flow diagram. Set # Terms #1 MeSH descriptor Atrial Fibrillation explode all trees OR MeSH descriptor Atrial Flutter explode all trees OR “atrial fibrillation”:ab,ti OR (atrial:ab,ti AND fibrillation:ab,ti) OR afib:ab,ti OR “atrial flutter”:ab,ti #2 MeSH descriptor Prognosis explode all trees OR MeSH descriptor Sensitivity and Specificity explode all trees OR MeSH descriptor Treatment Outcome explode all trees OR MeSH descriptor Diagnosis explode all trees OR predictors:ab,ti OR predict:ab,ti OR predicting:ab,ti OR predicts:ab,ti OR predicted:ab,ti OR prognosis:ab,ti OR prognostic:ab,ti OR accurately:ab,ti OR accuracy:ab,ti OR accurate:ab,ti OR reliability:ab,ti OR sensitivity:ab,ti OR specificity:ab,ti OR diagnostic:ab,ti #3 maintain:ab,ti OR maintenance:ab,ti OR maintained:ab,ti OR success:ab,ti OR successful:ab,ti OR conversion:ab,ti OR restoration:ab,ti OR restored:ab,ti A-12 #4 #1 AND #2 and #3 #5 #4, Limits: Cochrane Reviews, 2000-2011 Grey Literature Searches ClinicalTrials. Data Abstraction Elements Study Characteristics • Study Identifiers o Study Name or Acronym o Last name of first author o Publication Year • Additional Articles Used in This Abstraction • Study Objectives • Study Dates o Enrollment Start (Mon and YYYY) o Enrollment End (Mon and YYYY) o Follow-up End (Mon and YYYY) • Study Sites o Single Center, Multicenter, Unclear/Not reported, Other (specify) o Number of sites • Geographic Location (Select all that apply) o US, Canada, UK, Europe, S. America, Asia, Africa, Australia/NZ, Unclear/Not reported, Other (specify) • Study Design o Prospective RCT o Prospective cohort o Retrospective cohort o Case-control o Cross-sectional o Other (specify) • Funding Source (Select all that apply) o Government, Industry, Non-govt/Non-industry, Unclear/Not reported, Other (specify) • Setting (Select all that apply) o In-patient, Out-patient, Emergency Room, Unclear/Not reported, Other (specify) • Enrollment Approach (Select all that apply) o Consecutive patients, Convenience sample, Unclear/Not reported, Other (specify) • Study Inclusion and Exclusion Criteria o Copy/paste inclusion and exclusion criteria as reported o Is the study entirely composed of patients with any of the following characteristics/ conditions? Record the following elements for Total Population, Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Number of Patients, Age, Ethnicity, and Race o Number of Patients  Total  Female  Male o Percentage  Female  Male o Age  Mean  Standard Deviation  Standard Error  Median  IQR  Min  Max  NR o Ethnicity  Hispanic or Latino  Not Hispanic or Latino  NR o Race  Black/African American  American Indian or Alaska Native  Asian  Native Hawaiian or other Pacific Islander B-2  White  Multiracial  Other (specify)  NR • Co-morbidities and Previous Treatment Failures o Diabetes  N  % o Heart failure, All types (define)  N  % o Heart failure, Systolic (define)  N  % o Heart failure, Diastolic (define)  N  % o Hypertension  N  % o Kidney disease (define)  N  % o Hypertrophic cardiomyopathy (define)  N  % o Thyroid disease (define)  N  % o Pulmonary disease (define)  N  % o Coronary artery disease  N  % o Enlarged left atrium (define)  N  % o LVEF, Mean or median  Mean  Median  SD  SE  IQR o LVEF, Number of patients (<35% or other [define])  N B-3  % o Previously failed rate-control pharmacological therapy (define)  N  % o Previously failed rhythm-control pharmacological therapy (define)  N  % o Duration of AF (include units)  mean  Median  SD  SE  IQR o Permanent AF  N  % o Paroxysmal AF  N  % o Persistent AF  N  % • Comments Intervention Characteristics. Record the following elements for Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Intervention Characteristics o Intervention Components (check all that apply)  Placebo or control  Pharmacological agents for rate control  Procedures for rate control  Pharmacological agents for rhythm control  Procedures for rhythm control o Placebo/Control Details  Placebo  Usual care control/optimal medical therapy  Other (specify) o Rate-control Pharmacological Agent Details  Beta-blockers • Acebutolol • Atenolol • Bisoprolol • Carvedilol • Esmolol • Metoprolol • Nadalol B-4 • Nebivolol • Timolol • Specific medication not reported  Calcium channel blockers • Diltiazem • Verapamil • Specific medication not reported • Other o Amiodarone o Digoxin o Dronedarone o Specific medication not reported o Rate-control Procedure Details  AVN ablation and permanent pacemaker implantation o Rate-control Target  Strict (define)  Lenient (define)  Other (define)  NA o Rhythm-control Pharmacological Agent Details  Amiodarone  Beta-blockers • Acebutolol • Atenolol • Carvedilol • Esmolol • Metoprolol • Nadalol • Nebivolol • Timolol • Specific medication not reported  Calcium channel blockers • Diltiazem • Verapamil • Specific medication not reported  Disopyramide  Dofetilide  Dronedarone  Flecainide  Ibutilide  Propafenone  Sotalol o Rhythm-control Procedure Details  Electrical cardioversion  Pulmonary vein ablation – open surgical B-5  Pulmonary vein ablation – minimally invasive  Pulmonary vein ablation – transcatheter  Surgical Maze  Cardiac resynchronization • Intervention Descriptors o Describe the intervention received by patients in Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) • Duration of Follow-up - Record the following elements for Arm 1, Arm 2, Arm 3, and Arm 4 (as applicable) o Mean follow-up o Mean Variability (SD, SE, IQR) o Median follow-up o Median Variability (SD, SE, IQR) • Comments Outcomes • Select the outcome reported on this form o Restoration of sinus rhythm (conversion) o Maintenance of sinus rhythm o Recurrence of AF (specify time period) o Development of cardiomyopathy o All-cause mortality o Cardiac mortality o Myocardial infarction o CV hospitalizations o AF Hospitalizations o Heart failure symptoms o Control of AF symptoms (e. B-11 • Overall Study Rating (Good/Fair/Poor) o Good (low risk of bias). These studies have the least bias, and the results are considered valid. These studies adhere to the commonly held concepts of high quality, including the following: a clear description of the population, setting, approaches, and comparison groups; appropriate measurement of outcomes; appropriate statistical and analytical methods and reporting; no reporting errors; a low dropout rate; and clear reporting of dropouts. These studies are susceptible to some bias, but not enough to invalidate the results. They do not meet all the criteria required for a rating of good quality because they have some deficiencies, but no flaw is likely to cause major bias. The study may be missing information, making it difficult to assess limitations and potential problems. These studies have significant flaws that may have invalidated the results. They have serious errors in design, analysis, or reporting; large amounts of missing information; or discrepancies in reporting. Use the PICOS format to identify specific issues, if any, that may limit the applicability of the study to this review. List of Included Studies Abreu Filho CA, Lisboa LA, Dallan LA, et al. Effectiveness of the maze procedure using cooled- tip radiofrequency ablation in patients with permanent atrial fibrillation and rheumatic mitral valve disease. Combined radiofrequency modified maze and mitral valve procedure through a port access approach: early and mid-term results. Prospective, randomized comparison of two biphasic waveforms for the efficacy and safety of transthoracic biphasic cardioversion of atrial fibrillation. Randomized study of surgical isolation of the pulmonary veins for correction of permanent atrial fibrillation associated with mitral valve disease. Randomised comparison of antero-lateral versus antero- posterior paddle positions for DC cardioversion of persistent atrial fibrillation. A randomized controlled trial of efficacy and ST change following use of the Welch-Allyn MRL PIC biphasic waveform versus damped sine monophasic waveform for external DC cardioversion. Maintenance of sinus rhythm in patients with atrial fibrillation: an AFFIRM substudy of the first antiarrhythmic drug. Small or large isolation areas around the pulmonary veins for the treatment of atrial fibrillation? Exercise capacity in atrial fibrillation: a substudy of the Sotalol-Amiodarone Atrial Fibrillation Efficacy Trial (SAFE-T). Pharmacological conversion of recent atrial fibrillation: a randomized, placebo-controlled study of three antiarrhythmic drugs. Thyroid function abnormalities during amiodarone therapy for persistent atrial fibrillation. Long-term efficacy and safety of propafenone and sotalol for the maintenance of sinus rhythm after conversion of recurrent symptomatic atrial fibrillation. Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm; a randomized study. Randomized study comparing duty-cycled bipolar and unipolar radiofrequency with point-by-point ablation in pulmonary vein isolation. Blomstrom-Lundqvist C, Johansson B, Berglin E, et al. A randomized double-blind study of epicardial left atrial cryoablation for permanent atrial fibrillation in patients undergoing mitral valve surgery: the SWEDish Multicentre Atrial Fibrillation study (SWEDMAF). Atrial Fibrillation Catheter Ablation Versus Surgical Ablation Treatment (FAST): A 2-Center Randomized Clinical Trial. DC cardioversion of persistent atrial fibrillation: a comparison of two protocols. Higher energy monophasic DC cardioversion for persistent atrial fibrillation: is it time to start at 360 joules?.

pornplaybb.com siteripdownload.com macromastiavideo.com shemalevids.org
Back To Top