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By N. Asam. Institute for Transpersonal Psychology. 2018.

The level of free tracer in plasma (F) can be mea- (i discount 5mg eldepryl otc. From a practical concentration of tracer in plasma is measured with the as- Chapter 31: In Vivo Molecular Imaging 417 sumption that free concentration in plasma equals that in surements of both the tracer and the competing displacer brain generic eldepryl 5mg without prescription. An alternate out- in conjunction with D2-receptor imaging and a stimulant come measure for each of these three methods uses the non- challenge (25 buy generic eldepryl 5mg on line,26) discount 5mg eldepryl overnight delivery. Although D2-ligand displacement corre- displaceable activity in a background region of brain as a lated with the increase in extracellular dopamine measured value proportional to free tracer concentration eldepryl 5mg with mastercard. The reasons that the changes in binding are ESTIMATION OF ENDOGENOUS so much lower (although still, it is hoped, linear) relative NEUROTRANSMITTER LEVELS to the increase in extracellular dopamine are unclear. For exam- brain region occurs over a much slower time course than ple, a D2-receptor probe can be used not only to measure the relatively rapid changes in extracellular dopamine. Nevertheless, these stimulant-induced displacement studies D2 receptors but also the extent of competition of this bind- appear to provide some reflection of changes in synaptic ing caused by endogenous dopamine. In fact, the most ex- dopamine levels because they are relatively well correlated tensively studied indirect measurements have been the inter- and because depletion of tissues levels of dopamine can action of dopamine with D2-receptor ligands. These studies block the effects of amphetamine (27). The percentage of unmasking reflects the Dopamine transmission in striatum is thought to occur in percentage of D2 receptors occupied by dopamine under two different modes, tonic and phasic (22,23). Dopamine depletion has been mine release represents the steady-state level of dopamine induced in both animals and humans, with a resulting in- in the extracellular space, which is estimated to be in the crease in D2 radiotracer binding (28,29). On the other hand, in phasic release, high of these studies, especially in humans, is the difficulty of extracellular concentrations of dopamine (millimolar range) knowing whether depletion is essentially complete, so that are released within or near a synapse during an action poten- the full extent of dopamine occupancy of the receptor has tial. Close relationships have been proposed between abnor- been measured. For example, if differences in unmasking malities in phasic and tonic dopamine release and the symp- are found in two subjects, does that reflect different levels toms of schizophrenia. Namely, excessive phasic release of endogenous dopamine—or just different levels of dopa- causes psychosis, and decreased tonic release causes cogni- mine depletion? A second limitation of this depletion para- tive deficits and negative symptoms (24). These agents elevate synaptic dopamine One mechanism to minimize this potential confound is to concentrations either by releasing dopamine in a reverse perform the measurements as soon after dopamine deple- manner via a dopamine transporter (amphetamine) or by tion as possible. However, one clear advantage of the deple- blocking dopamine transporter-mediated reuptake of dopa- tion paradigm in comparison with the stimulant-induced mine (methylphenidate). In an imaging study, the elevation increase is that the depleted levels can typically be stably of synaptic dopamine levels is estimated by the decrease in maintained during the scan. Thus, the relative slowness of D2 radiotracer binding following stimulant administration the imaging measurements does not present a pharmacoki- in comparison with control conditions. Just as careful quan- netic confound, as it does in studies with stimulant-induced tification is required for direct radiotracer binding to a mo- release of dopamine. In addition, stimulant depletion studies have tors (39,40). Thus, the endogenous agonist dopamine pre- found greater unmasking of striatal D2 receptors in patients sumably facilitates the intracellular trafficking of D2 recep- with schizophrenia, which suggests that basal/tonic synaptic tors (41), and radiotracers may differ in their affinity for dopamine levels are higher in this disorder (33). Thus, neurotransmitters may occupy The relationship between affinity of the radiotracer and the a smaller percentage of extrasynaptic receptors than of re- sensitivity of its binding to endogenous dopamine is a source ceptors within the synapse, and the in vivo measurement of confusion. Under in vitroequilibrium conditions and at may not truly reflect synaptic neurotransmitter levels. Abnormalities in psychiatric disorders likely represent the However, such equilibrium binding conditions are achieved complex interaction of several neurotransmitter systems in for neither the tracer nor the displacer if each is injected the brain. PET imaging has recently been used to examine as a bolus. Even under these conditions, the sensitivity of aspects of neurotransmitter interactions. For example, Dewy radioligand binding to endogenous dopamine levels is theo- and colleagues (44–46) have pioneered studies on interac- retically (at least based on the in vitro theories) independent tions among dopamine, GABA, and acetylcholine (ACh) of the affinity of the radioactively labeled ligand when both systems in striatum. GABA neurons in the striatum have the tracer and the displacer have achieved equilibrium bind- inhibitory effects on nigral dopamine neurons, nigral dopa- ing conditions.

However purchase eldepryl 5 mg line, universal coverage cannot be hundreds of published studies that focus on spe- achieved without technology buy 5mg eldepryl with mastercard, systems and ser- cifc diseases and conditions – across a range of vices buy eldepryl 5mg line, and research is the mechanism by which communicable and noncommunicable diseases the hardware and sofware are created cheap 5 mg eldepryl amex. In contrast purchase 5mg eldepryl, there are relatively few studies that attempt to set research priorities, across all aspects of health, from the perspective Growing unevenly of national governments (Chapter 4) (62, 63). Tis is because few appraisals of research needs Research is on the rise, and the results are deliv- have been initiated by national governments, ering benefts for health worldwide. However, even though such appraisals are a vital part of the process of doing research – setting research planning for universal health coverage. Private- and public-sector investment in R&D, classifed as basic, applied and experimental development research, for six African countries ranked in ascending order of gross national income (left to right) R&D, research and development. Note: For defnitions of types of research, see Box 2. The four poorest countries focused on applied research. The two wealthi- est, Nigeria and South Africa, had a more balanced portfolio (35). Te 2010 African Innovation thumb, for every 10-fold increase in GNI per Outlook found that four lower-income countries person, the number of scientifc publications per focused on applied research, whereas two richer person increases by a factor of about 50 at best ones spread resources more evenly across basic, (Fig. Tis disproportionate applied and experimental studies (Fig. A increase also holds for other measures of research more systematic look at research in these coun- output such as the number of researchers and the tries might fnd that the balance is right, or that number of patents per head of population. Te point is that some questions These data also show that while some coun- about universal health coverage have answers that tries exploit the empirical maximum (lying are widely applicable (e. For this reason, are nations with small populations (< 20 mil- all nations need to become producers of research lion), who may choose not to invest in research, as well as consumers of it. Local expertise and but not all underinvestors are small nations. By local processes, initiatives and institutions should comparing countries, it can be said that there be valued rather than bypassed (64, 66). Thus greater wealth appears turning research priorities into research studies, to open up the potential for research, but other and the constraints on fundraising come in vari- factors are needed to fulfil that potential. At the level of national wealth, gross those factors need to be understood, it is clear national income (GNI) is an empirical measure that nations and their governments have a of research potential. National wealth facilitates, but does not guarantee, national research productivity PPP, purchasing power parity. Note: For every 10-fold increase in gross national income (GNI) per person, the number of scientifc publications (per person) increases by a factor of about 50 at best (actually by 105/3 = 46, diagonal line). While some countries exploit maximum productivity, lying close to the diagonal line, many lie well below it, indicating that there is unfulflled research potential, given their national wealth. Some of these coun- tries have smaller populations (< 20 million, blue circles), but not all. The unfulflled potential for research in one large country (Philippines) is indicated by the vertical arrow. Private companies engaged in R&D in low- However, the products are sold to people who can income countries frequently cite lack of funding aford them, ofen excluding those in greatest and the shortage of skilled researchers as major need. Both free knowledge (as a public good) and barriers to innovation (35). Te shortage of trained highly restricted knowledge (limited by its pro- researchers emerges as a general constraint in prietary nature) can be obstacles to improving R&D, but it is also found in specifc areas such as health; the former may discourage innovation health systems research (36). A disincentive for and the latter may limit access to the products private technological research is the domination of innovation. A market failure in diferent settings present some further impediment in low-income countries is critical questions for research (Box 2. The Global Strategy and Plan of Action on Public Health, Innovation and Intellectual Property Born out of concern among low- and middle-income countries about inequitable access to the products of research, the Commission on Intellectual Property Rights, Innovation and Public Health was established to promote innovation and access to medicines. The work of the Commission led to the Global Strategy and Plan of Action on Public Health, Innovation and Intellectual Property (GSPA-PHI), which was approved by the World Health Assembly in 2009 (68). The GSPA-PHI consists of eight elements that aim to promote innovation, build capacity, improve access and mobilize resources. Work is under way in several areas related to GSPA-PHI, such as the local production of medical products and technology transfer (element 4), building capacity in the management and use of intellectual property in favour of public health (element 5), reporting on models for sustainable financing and better coordination of research and development (element 7) through WHO expert working groups; and the establishment of monitoring and reporting systems (element 8), such as research observatories (Chapter 4) (69, 70). Effective implementation of the GSPA-PHI depends on the robustness of the national health research system in each country.

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Indeed purchase 5 mg eldepryl mastercard, most of the animal models of nine trusted eldepryl 5 mg, a nitric oxide synthase inhibitor that disrupts neuronal schizophrenia have relied on dopaminergic psychostimu- maturation (89) buy 5mg eldepryl with mastercard, or the antimitotic agent methyazoxymeth- lants and have proved to be largely limited to the detection anol (54 purchase eldepryl 5mg amex,90) generic 5mg eldepryl with mastercard. These models produce morphologic changes of dopamine antagonists. The major message of the fact relevant to schizophrenia, such as altered neurogenesis and that clozapine is effective, even at doses that achieve low reduced cortical volume. They also produce some of the levels of dopamine receptor occupancy, is that new treat- behavioral characteristics associated with schizophrenia, ments can be identified for patients with schizophrenia, and such as stereotypy, cognitive impairments, and deficits in that these novel treatments may not involve dopamine an- PPI. As yet, the predictive validity of this model in terms tagonism. The isolation-rearing manipulation presumably of sensitivity to antipsychotic treatments remains to be de- produces a deficit in PPI by virtue of a substantial reorgani- termined. Chapter 50: Animal Models Relevant to Schizophrenia Disorders 697 Hence, such a model has the potential to identify completely receptor transduction) are associated with substrates that novel antipsychotic treatments simply because it does not regulate both PPI and latent inhibition, which are transmit- require the administration of a drug. In another approach, comparisons of several inbred strains of rats identified some strains that exhibit deficits in PPI (103). Because these strains did not exhibit GENETIC MODELS hearing impairments, the genetically determined deficit in PPI likely represents a deficit in sensorimotor gating pro- Genetic contributions to schizophrenia have been clearly cesses. Although the focus of consid- erable research, the application of linkage analyses to schizo- GeneticallyModified Animals phrenia has not generally proved successful, perhaps because schizophrenia does not represent a single phenotype. Never- Other examples of nonpharmacologically based models rele- theless, it remains possible that genetic approaches will lead vant to schizophrenia are emerging from the field of molecu- to etiologically based models lar biology, in which genetic engineering is being used to generate transgenic and knockout animals. In the absence of established candidate genes, the use of mutant animals Strain Differences in models of schizophrenia has focused on the identification Genetic factors appear to be critical determinants of both of phenotypic differences in behaviors considered relevant sensory and sensorimotor gating in rats. For example, schizophrenia-like deficits in PPI of of the P50 gating deficit seen in schizophrenia. Indeed, a startle have been observed in specific strains of mice (104) linkage between the P50 gating deficit in patients with and in 'knockout' mice in which specific genes have been schizophrenia and a specific chromosomal marker associated deleted (105). The focus of genetic engineering in the with the gene for the 7 subunit of the nicotinic acetylcho- mouse is beginning to prompt extensions of pharmacologic line receptor has been demonstrated in a series of elegant studies from the rat to the mouse. The potential power of cross-species studies of such work is needed, it is already abundantly clear that specific behavioral abnormalities in psychiatric disorders is species differences in pharmacologic effects between mice exemplified by the parallel between these human linkage and rats will complicate the application of some schizophre- studies and the observation that the strain of mice that is nia-related rat models to mice. For example, in rats, antipsy- most deficient in gating of the N40 event-related potential chotic drugs by themselves have minimal effects on PPI, in is also the most deficient in 7-nicotinic receptors (17). Hence, rat PPI an exemplar for the application of modern molecular bio- models can identify antipsychotic effects only if a drug re- logical techniques to the generation and validation of animal verses the effects of a disruption in PPI produced by another models of psychiatric disorders. However, this genetically drug, a lesion, or a developmental manipulation such as related deficit in sensory gating does not extend to studies isolation rearing. In mice, however, it appears that antipsy- of sensorimotor gating as measured by PPI of the startle chotics improve PPI in mice that have not been manipulated response. Thus, mice in which the 7-nicotinic receptors (106). This important difference means that it may be easier have been deleted by genetic engineering exhibit normal to detect antipsychotic effects in mice, but also that it will levels of PPI (99). Nevertheless, other evidence indicates be much more difficult to demonstrate a reversal of a PPI that PPI is regulated by genetic factors. For example, strain- deficit produced by an experimental manipulation. More relevant to the recent indi- date gene approach, genetically modified mice have been cations that PPI deficits are evident in family members of used to test specific hypotheses of relevance to animal schizophrenia patients (101), Ellenbroek et al. For example, although most phar- pharmacogenetic selective breeding to produce strains of macologic evidence in rat had implicated the D2 subtype rats that were either sensitive (APO-SUS) or insensitive of the family of dopamine receptors in the PPI-disruptive (APO-UNSUS) to the effects of apomorphine on gnawing effects of dopamine agonists, gene knockout mice proved behavior. Within either a single generation or after many useful in testing this conclusion more definitively. Ralph et generations of selective breeding, APO-SUS rats and their al. Only the mice lacking the D2 subtype of logic substrates that regulate behavioral sensitivity to apo- receptor failed to show the normal effect of amphetamine morphine (presumably some feature related to dopamine- on PPI. Although knockout manipulations are confounded 698 Neuropsychopharmacology: The Fifth Generation of Progress by developmental adaptations, such a study takes advantage cal Center (MG); and the Veterans Administration National of the specificity that represents the fundamental strength Center for Schizophrenia (BM). Another model with relevance to the etiology and patho- 1.

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NEUROBIOLOGY OF TOURETTE SYNDROME Aggressive and sexual obsessions are also associated with more severe motor and phonic tics buy cheap eldepryl 5 mg, even in patients with Interconnected cortico-striato-pallido-thalamic (CSPT) cir- TS who do not meet full diagnostic criteria for OCD (15) eldepryl 5mg low price. The 'motor' loops of CSPT circuitry are known to patients with TS generic eldepryl 5mg on line. Clinical studies vary according to setting be the locus of disease in primary movement disorders such and established referral patterns buy discount eldepryl 5 mg on line, but it is not uncommon as Huntington disease (31) discount 5 mg eldepryl otc, Parkinson disease (32) and to see reports of 50% or more of referred children with TS hemiballism (33), and the 'limbic' CSPT loops have been diagnosed with comorbid ADHD (16). In contrast, epide- proposed as the source of disease in schizophrenia (29), miologic studies typically indicate a much lower incidence depression (29), OCD (34,35), ADHD (36), substance of comorbidity (14,16). Similar to the functional impact of abuse disorders (37), temporal lobe epilepsy (38), and many comorbid OCD, patients with comorbid ADHD and TS other seemingly disparate forms of psychopathology (39). Longitudinal studies confirm that children range of CSPT disorders, based on variations in responses to with comorbid TS and ADHD are at high risk of anxiety 'generalized' or 'epigenetic' early developmental insults, and mood disorders, oppositional defiant disorder, and con- from neonatal hypoxia to bacterial infections. Despite this duct disorder (17,18), whereas children who only have TS departure from the notion of discrete, specific 'lesions' and tend to fare better (17,19,20). Levels of tic severity are less circumscribed clinical presentations, the prevailing model predictive of peer acceptance than is the presence of ADHD in the search for the pathophysiology of TS is perhaps closest (19,20), and rates of subsequent psychiatric morbidity in to that previously applied to Huntington disease, in which comorbid TS and ADHD are nearly identical to those seen a unique mutation in a single gene causes—by as yet un- in prior cross-sectional and longitudinal studies of 'pure' known cellular mechanisms—a characteristic disease that ADHD (21,22). Yet the actual pathophysiology of TS remains quite elusive. The scant tangible evidence of the pathophysiology of TS Natural History and Epidemiology comes primarily from studies in neuropathology and neu- Tics typically begin between 3 and 8 years of age. For per- roimaging; supportive evidence comes from other fields of sons who go on to develop TS, the tics typically follow a investigation, including neuropsychology and psychophy- waxing and waning course, usually with a progressive pat- siology, and from ties between TS and other disorders, such tern of tic worsening. On average, the period of greatest tic as OCD and ADHD, providing indirect evidence based on severity occurs between 8 and 12 years of age. The onset what is known about the pathophysiology of these other of puberty is not associated with either the timing or the disorders. The early teens are generally followed by a The published literature of TS neuropathology studies steady decline in tic severity, and by 18 years of age, perhaps now includes seven presumed TS cases; of these, informative as many as 50% of patients with TS are nearly tic free (23). Symptoms in adulthood may typically settle into a more Interpretation of the findings from even these five cases is 1688 Neuropsychopharmacology: The Fifth Generation of Progress clouded by issues of diagnostic uncertainty, comorbidity, regions (56). The single greatest consistency across meta- and potentially confounding neurologic insults. Preliminary bolic imaging studies in TS—that of distributed hypome- findings have identified four different locations of potential tabolism—contrasts sharply with the observed corticostria- pathology within CSPT circuitry: (a) intrinsic striatal neu- tal hypermetabolism reported by many groups in patients ron abnormalities, including increased packing density of with OCD (33,34). The only suggestion of regional activa- neurons in the striatum (n 1) (40); (b) a diminished tion in TS comes during active tic suppression, which is striatopallidal 'direct' output pathway, with reduced associated with increased right caudate neuronal activity, as dynorphin-like immunoreactivity in the lenticular nuclei measured by functional magnetic resonance imaging (n 5) (41,42); (c) increased dopaminergic innervation (fMRI) (57); however, tic suppression is also accompanied of the striatum, with increased density of dopamine trans- by bilaterally diminished neuronal activity on fMRI mea- porter sites (n 3);(43); and (d) reduced glutamatergic sures, in the putamen, globus pallidus, and thalamus. The output from the subthalamic nucleus, based on reduced most analogous paradigm in OCD—obsession provoca- lenticular glutamate content (n 4) (44). Thus, in a man- tion—is associated with increased metabolic activity at ner more reminiscent of neuropathologic findings in schizo- every level of CSPT circuitry (35), in sharp contrast to the phrenia than, for example, Huntington disease, these pre- pattern observed in TS. Some of these find- other measures of CSPT biology in TS, including amine ings have not been replicated (61,62), others await replica- levels and receptors, have been reported to be normal, also tion, even internally (60), and others are evident only in a in these preliminary, small studies. Clearly, postmortem small subgroup of TS, such as four of 20 patients (58), studies are hampered by limitations in the nature and num- issues raising concern about their generalizability to the ber of the brains that have been studied (46). A potentially important report of Tourette Syndrome Association (TSA) to secure adequate 17% greater caudate D2 receptor binding among more material for neuropathologic studies are currently under way symptomatic TS identical twins (63) was based on five twin and should allow a new generation of tissue-based research pairs and reached statistical significance at the p. Significant correlations between Neuroimaging findings may ultimately provide informa- symptom severity and D2 binding were obtained using ag- tion critically important to our understanding of the patho- gregate symptom scores from three clinical measures. Volumetric imaging studies demonstrate latter findings do not directly address the brain mechanisms minimal, if any consistent, abnormalities in persons with that distinguish persons with TS from those without TS, TS. Among reports of enlarged corpus callosum volume but rather, point to the need to understand specific factors (47), reduced caudate volume (48), or diminished right-to- that contribute to the heterogeneity of the TS phenotype left asymmetry for the caudate nucleus (49) and left-to-right among affected persons. The specific cellular or structural pro- hormones in blood, cerebrospinal fluid and urine of patients cesses that may be responsible for these anatomic abnormali- with TS, compared with controls (64–66). Concerns regarding sample heterogene- derstand the relation of these abnormalities to the patho- ity, comorbidity, and effects of chronic medication physiology of TS have ranged from a proposed causal role exposure, described earlier in relation to neuropathologic ascribed to a single metabolic abnormality, such as the re- studies, are equally applicable to neuroimaging studies in ported cerebrospinal fluid elevation of the potential excito- TS. In general, these studies in TS report reduced of psychopathology.

In all four studies maintenance of sinus rhythm was greater with amiodarone than with sotalol buy eldepryl 5mg online, but the differences were statistically significant only in some studies and at some of the assessed time points (see Table 16) generic eldepryl 5mg visa. One of these studies showed no significant difference in the rate of this 245 outcome purchase eldepryl 5 mg line, while the other two found that the propafenone groups had rates of maintenance of sinus rhythm that were almost twice that of the sotalol groups discount eldepryl 5 mg free shipping, although statistical analyses 258 safe 5mg eldepryl,261 comparing the groups were not reported. Two studies compared amiodarone with propafenone and evaluated a composite outcome of 259,261 maintenance of sinus rhythm free from adverse effects from medication. In both studies, at 1 year amiodarone was better than propafenone for this outcome, but at 2 years propafenone was better. In both studies, investigators described the rate of recurrence of AF as being constant throughout followup for amiodarone, but they described the rate of recurrence of AF on propafenone as being high early on during therapy and then decreasing over time. One study compared bisoprolol with sotalol and found no significant difference in the rate of 269 maintenance of sinus rhythm. The final study found that the addition of verapamil to treatment with either amiodarone or flecainide increased the rate of AF-free survival compared with 249 treatment with either antiarrhythmic agent alone. These studies suggest that amiodarone appears to be better sotalol but no different from propafenone, but given the diversity in comparisons and the imprecision of the findings, the strength of evidence was considered low. Studies assessing maintenance of sinus rhythm with or without adverse effects Study Sample Time Point Results P-Value Size (N) a Kochiadakis, 214 1 year Amiodarone: 70. Studies assessing maintenance of sinus rhythm with or without adverse effects (continued) Study Sample Time Point Results P-Value Size (N) a Kochiadakis, 254 30 months Propafenone: 47% NR 258 2004 Sotalol: 25% a Kochiadakis, 146 12 months Amiodarone: 72% NR 259 2004 Propafenone: 56% a 24 months Amiodarone: 42% NR Propafenone: 51% Vijayalakshmi, 94 1. Abbreviations: AE=adverse event; CI=confidence interval; HR=hazard ratio; N=number of participants; NR=not reported Recurrence of AF Ten studies comparing primarily pharmacological interventions for AF included recurrence 180,224,230,241,245,249,256,259,261,269 (or prevalence) of AF as an outcome (Table 17). Three of these 180,241,261 studies compared amiodarone with sotalol. Of these three studies, one showed no 241 statistically significant difference between treatment arms at 4 months or 1 year; however, the other two studies reported a higher rate of recurrence of AF among those on sotalol compared with amiodarone—68 percent versus 33 percent at 2 years of followup in one study (no statistical 261 180 test reported), and 68 percent versus 48 percent at 1 year in the other study (p=0. The rate of recurrence of AF for sotalol versus propafenone was not statistically significantly different in 1 study at 12 months 245 (23% vs. Another study reported a higher rate with sotalol than with 261 propafenone at 2 years (68% vs. Two studies compared the effects of amiodarone versus propafenone; one found a 261 statistically significantly higher monthly rate of recurrence with propafenone; the other found 259 no significant difference in recurrence between the two drugs. In line with the results of these two studies, another study evaluated the risk of recurrence of AF for amiodarone compared with either sotalol or propafenone over approximately 1 year and found a significantly lower risk 230 among those on amiodarone, with a hazard ratio (HR) of 0. One compared amiodarone versus flecainide, with and without verapamil added to either treatment. The rate of recurrence of AF did not differ at 3 months between amiodarone and flecainide (no statistical test reported). The addition of verapamil to flecainide reduced the rate of recurrence significantly compared with flecainide alone (21% vs. One study compared amiodarone with dronedarone and found a higher rate of recurrence with 224 dronedarone, but the statistical analysis was not reported. Finally, two studies compared the beta-blocker bisoprolol with either another beta-blocker or 256,269 an antiarrhythmic agent. One study showed no significant difference between rates of 256 recurrence at 1 year between bisoprolol and carvedilol; the other showed no significant 269 difference between rates of recurrence of AF with bisoprolol versus sotalol. These findings suggest that amiodarone appears to be better than dronedarone or sotalol, but no different from propafenone (low strength of evidence). Studies assessing recurrence of AF Study Sample Time Point Results P-Value Size (N) Kochiadakis, 214 2 years Amiodarone: 33. Amiodarone + Verapamil: 20% Amiodarone + Flecainide + Verapamil: 21% Verapamil) p=0. Flecainide + Verapamil) 256 Katritsis, 2003 90 12 months Bisoprolol: 46% p=0. Three of the studies compared amiodarone with sotalol, and statistical comparisons were either not performed or treatments were not found to be statistically significantly 180,181,241 different. In one study, amiodarone was compared with sotalol or propafenone and no 230 statistical analyses were done. In another study amiodarone was compared with dronedarone 224 but no statistical analyses were done Differences in followup, comparisons, and findings resulted in insufficient strength of evidence for this outcome. Studies reporting all-cause mortality as an outcome Study Sample Time Point Results P-Value Size (N) 230 Roy, 2000 403 Mean followup 468 days Amiodarone: 4% NR Sotalol or propafenone: 4% Anonymous, 256 5 years (mean followup 3. Three studies compared amiodarone with sotalol and found no difference between these 180,241,260 treatment arms.

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