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      Elevated blood lipids are uncommon in patients with post-polio syndrome – a cross sectional study

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          Abstract

          Background

          The post-polio syndrome occurs in people who previously have had poliomyelitis. After the initial recovery, new or increasing neurologic symptoms occur. Inflammation and dyslipidaemia may play an important role in the development of atherosclerotic complications, for example myocardial infarction and angina pectoris. Previous studies on cardiovascular risk factors in the post-polio syndrome have found a higher prevalence of hypertension, ischemic heart disease, hyperlipidaemia, and stroke in these patients. The present study was undertaken in order to evaluate whether post-polio patients have elevated lipid values, and if blood lipid abnormalities could be correlated to signs of inflammation.

          Methods

          Cross-sectional study of 89 consecutive post-polio patients, (53 women, mean age 65 years) from the Post-Polio Outpatient Clinic, Danderyd University Hospital, Stockholm, Sweden. The lipid profiles of post-polio patients were compared to age and sex matched reference values from two earlier studies. Statistical analyses were performed by the Student’s t-test, and linear regression analyses were assessed by Pearson’s correlation coefficient.

          Results

          Mean total cholesterol levels (5.7 mmol/L) were low or normal in post-polio patients, whereas low density lipoprotein levels (3.6 mmol/L) were normal, and high density lipoprotein (1.5 mmol/L) and triglycerides (1.4 mmol/L) lower than reference values. The prevalence of diabetes (7%), hypertension (38%), concomitant cardiovascular disease, (including angina pectoris, myocardial infarction, heart failure, atrial fibrillation and stroke) (7%), and calculated 10 year risk of coronary heart disease according to Framingham risk score algorithm (8%) was not increased in post-polio patients.

          Conclusions

          Compared to reference populations, post-polio patients in Sweden appear to have low or normal total cholesterol and low density lipoprotein levels, whereas high density lipoprotein and triglyceride levels are low. Hence, a possible persisting inflammatory process in post-polio syndrome does not seem to be associated with increased lipids and an increased risk for coronary heart disease events.

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          Most cited references22

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          Inflammation in atherosclerosis: from pathophysiology to practice.

          Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells would then elaborate an extracellular matrix that would entrap lipoproteins, forming the nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
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            Statin-associated myopathy.

            Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are associated with skeletal muscle complaints, including clinically important myositis and rhabdomyolysis, mild serum creatine kinase (CK) elevations, myalgia with and without elevated CK levels, muscle weakness, muscle cramps, and persistent myalgia and CK elevations after statin withdrawal. We performed a literature review to provide a clinical summary of statin-associated myopathy and discuss possible mediating mechanisms. We also update the US Food and Drug Administration (FDA) reports on statin-associated rhabdomyolysis. Articles on statin myopathy were identified via a PubMed search through November 2002 and articles on statin clinical trials, case series, and review articles were identified via a PubMed search through January 2003. Adverse event reports of statin-associated rhabdomyolysis were also collected from the FDA MEDWATCH database. The literature review found that reports of muscle problems during statin clinical trials are extremely rare. The FDA MEDWATCH Reporting System lists 3339 cases of statin-associated rhabdomyolysis reported between January 1, 1990, and March 31, 2002. Cerivastatin was the most commonly implicated statin. Few data are available regarding the frequency of less-serious events such as muscle pain and weakness, which may affect 1% to 5% of patients. The risk of rhabdomyolysis and other adverse effects with statin use can be exacerbated by several factors, including compromised hepatic and renal function, hypothyroidism, diabetes, and concomitant medications. Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin plasma concentration. How statins injure skeletal muscle is not clear, although recent evidence suggests that statins reduce the production of small regulatory proteins that are important for myocyte maintenance.
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              Atrial fibrillation prevalence revisited.

              The estimate of 0.4-1.0% prevalence of atrial fibrillation in the most recent American guidelines is based mainly on studies including patients with permanent atrial fibrillation (AF), although recent evidence shows that the stroke risk is similar with paroxysmal and persistent AF. Our objective was to determine the prevalence of AF in Sweden, irrespective of type and to what extent patients with AF receive adequate stroke prophylaxis. Retrospective study of patients with a clinical diagnosis of atrial fibrillation between 2005 and 2010 in the national Swedish Patient Register matched with data from the National Prescribed Drugs Register. We identified 307 476 individuals with a diagnosis of atrial fibrillation. Of these, 209 141 were still alive on the last day of the inclusion period, signifying a prevalence of clinically diagnosed AF in Sweden of 2.9% of the total adult (≥20 years) population. Only 42% of them had purchased an oral anticoagulant within 6 months of the first presentation with AF during the study period. Those at the highest risk of stroke were those least likely to receive anticoagulant treatment. Undertreatment was common amongst women and individuals >80 years, whilst overtreatment was common amongst young men without risk factors. The prevalence of atrial fibrillation is at least 2.9% of the Swedish adult population, not counting 'silent atrial fibrillation'. The official US figures probably underestimate the magnitude of the problem by a factor of 3-5. More than 80% had risk factors motivating anticoagulation therapy. © 2013 The Association for the Publication of the Journal of Internal Medicine.
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                Author and article information

                Contributors
                eva.melin@ki.se
                thomas.kahan@ds.se
                kristian.borg@ki.se
                Journal
                BMC Neurol
                BMC Neurol
                BMC Neurology
                BioMed Central (London )
                1471-2377
                29 April 2015
                29 April 2015
                2015
                : 15
                : 67
                Affiliations
                [ ]Division of Rehabilitation Medicine, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden
                [ ]Division of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden
                Article
                319
                10.1186/s12883-015-0319-z
                4429706
                25924966
                f56f5539-4d33-48cf-9263-8f0378af3b47
                © Melin et al.; licensee BioMed Central. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 5 May 2014
                : 14 April 2015
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2015

                Neurology
                post-polio syndrome,neuromuscular disease,dyslipidaemia,cardiovascular risk
                Neurology
                post-polio syndrome, neuromuscular disease, dyslipidaemia, cardiovascular risk

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