Atrial Fibrillation and Stroke: The Evolving Role of Rhythm Control.
Atrial Fibrillation and Stroke: The Evolving Role of Rhythm Control.
Filed under: Drug and Alcohol Rehabilitation
Curr Treat Options Cardiovasc Med. 2013 Feb 9;
Patel TK, Passman RS
OPINION STATEMENT: Atrial fibrillation (AF) remains a major risk factor for stroke. Unfortunately, clinical trials have failed to demonstrate that a strategy of rhythm control–therapy to maintain normal sinus rhythm (NSR)–reduces stroke risk. The apparent lack of benefit of rhythm control likely reflects the difficulty in maintaining NSR using currently available therapies. However, there are signals from several trials that the presence of NSR is indeed beneficial and associated with better outcomes related to stroke and mortality. Most electrophysiologists feel that as rhythm control strategies continue to improve, the crucial link between rhythm control and stroke reduction will finally be demonstrated. Therefore, AF specialists tend to be aggressive in their attempts to maintain NSR, especially in patients who have symptomatic AF. A step-wise approach from antiarrhythmic drugs to catheter ablation to cardiac surgery is generally used. In select patients, catheter ablation or cardiac surgery may supersede antiarrhythmic drugs. The choice depends on the type of AF, concurrent heart disease, drug toxicity profiles, procedural risks, and patient preferences. Regardless of strategy, given the limited effectiveness of currently available rhythm control therapies, oral anticoagulation is still recommended for stroke prophylaxis in AF patients with other stroke risk factors. Major challenges in atrial fibrillation management include selecting patients most likely to benefit from rhythm control, choosing specific antiarrhythmic drugs or procedures to achieve rhythm control, long-term monitoring to gauge the efficacy of rhythm control, and determining which (if any) patients may safely discontinue anticoagulation if long-term NSR is achieved.
HubMed – drug
Cell-Specific mRNA Alterations in Na(+), K (+)-ATPase ? and ? Isoforms and FXYD in Mice Treated Chronically with Carbamazepine, an Anti-Bipolar Drug.
Filed under: Drug and Alcohol Rehabilitation
Neurochem Res. 2013 Feb 10;
Li B, Hertz L, Peng L
Evidence accumulating during almost 50 years suggests Na(+), K(+)-ATPase dysfunction in bipolar disorder, a disease treatable with chronic administration of lithium salts, carbamazepine or valproic acid. Three Na(+), K(+)-ATPase ? subunits (?1-3) and two ? subunits (?1 and ?2) are expressed in brain together with the auxiliary protein FXYD7. FXYD7 decreases K(+) affinity, and thus contributes to stimulation of the enzyme at elevated extracellular K(+) concentrations. Na(+), K(+)-ATPase subtype and FXYD7 genes were determined by RT-PCR in mice co-expressing one fluorescent signal with an astrocytic marker or a different fluorescent signal with a neuronal marker and treated for 14 days with carbamazepine. Following fluorescence-activated cell sorting of neurons and astrocytes it was shown that ?2 Expression was upregulated in astrocytes and neurons and ?1 selectively in neurons, but ?3 was unchanged. ?1 was upregulated in astrocytes, but not in neurons. ?2 was unaffected in astrocytes and absent in neurons. FXYD7 was downregulated specifically in neurons. According to cited literature data these changes should facilitate K(+) uptake in neurons, without compromising preferential uptake in astrocytes at increased extracellular K(+) concentrations. This process seems to be important for K(+) homeostasis of the cellular level of the brain (Xu et al. Neurochem Res E-pub Dec. 12, 2012).
HubMed – drug
Glia Maturation Factor Induces Interleukin-33 Release from Astrocytes: Implications for Neurodegenerative Diseases.
Filed under: Drug and Alcohol Rehabilitation
J Neuroimmune Pharmacol. 2013 Feb 10;
Kempuraj D, Khan MM, Thangavel R, Xiong Z, Yang E, Zaheer A
Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Multiple sclerosis (MS) involve activation of glial cells and release of inflammatory mediators leading to death of neurons. Glia maturation factor (GMF) is up-regulated in the central nervous system (CNS) in these neurodegenerative diseases. Interleukin-33 (IL-33) is highly expressed constitutively in the CNS. We have treated mouse astrocytes, mixed culture with glial cells and neurons, and only neurons with GMF and/or IL-33 in vitro. Both GMF and IL-33-induced chemokine (C-C motif) ligand 2 (CCL2) release in a dose and time-dependent manner. We report that GMF induced IL-33 release, and that IL-33 augments GMF-induced tumor necrosis factor-alpha (TNF-?) release from mouse astrocytes. IL-33 induces CCL2, TNF-? and nitric oxide release through phosphorylation of ERK in mouse astrocytes. Incubation of mixed culture containing glial cells and neurons or only neuronal culture with IL-33 reduced the number of neurons positive for microtubule-associated protein 2. In conclusion, IL-33 augments GMF-mediated neuroinflammation and may provide a new drug target for neurodegenerative and autoimmune diseases.
HubMed – drug
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