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      The effects of omega-3 polyunsaturated fatty acids on cardiac rhythm: a critical reassessment.

      1
      Pharmacology & therapeutics
      AF, AFL, ALA, APD, Atrial fibrillation, BP, CICR, Ca-ATs, DADs, DHA, DPA, Docosahexaenoic acid, EADs, EPA, ERP, Eicosapentaenoic acid, HR, HRV, Heart rate variability, ICDs, MI, MSNA, Omega-3 polyunsaturated fatty acids, RBC, RYRs, SR, VF, VT, Ventricular fibrillation, action potential duration, alpha-linolenic acid, atrial fibrillation, atrial flutter, blood pressure, calcium aftertransients, calcium induced calcium release, delayed afterdepolarizations, docosahexaenoic acid, docosapentaenoic acid, early afterdepolarizations, effective refractory period, eicosapentaenoic acid, heart rate, heart rate variability, implantable cardioverter defibrillators, muscle sympathetic nerve activity, myocardial infarction, n−3 PUFAs, n−6 PUFAs, omega-3 polyunsaturated fatty acids, omega-6 polyunsaturated fatty acids, red blood cell, ryanodine receptors, sarcoplasmic reticulum, ventricular fibrillation, ventricular tachycardia

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          Abstract

          Although epidemiological studies provide strong evidence for an inverse relationship between omega-3 polyunsaturated fatty acids (n-3 PUFAs) and cardiac mortality, inconsistent and often conflicting results have been obtained from both animal studies and clinical prevention trials. Despite these heterogeneous results, some general conclusions can be drawn from these studies: 1) n-PUFAs have potent effects on ion channels and calcium regulatory proteins that vary depending on the route of administration. Circulating (acute administration) n-3 PUFAs affect ion channels directly while incorporation (long-term supplementation) of these lipids into cell membranes indirectly alter cardiac electrical activity via alteration of membrane properties. 2) n-3 PUFAs reduce baseline HR and increase HRV via alterations in intrinsic pacemaker rate rather than from changes in cardiac autonomic neural regulation. 3) n-3 PUFAs may be only effective if given before electrophysiological or structural remodeling has begun and have no efficacy against atrial fibrillation. 5) Despite initial encouraging results, more recent clinical prevention and animal studies have not only failed to reduce sudden cardiac death but actually increased mortality in angina patients and increased rather than decreased malignant arrhythmias in animal models of regional ischemia. 6) Given the inconsistent benefits reported in clinical and experimental studies and the potential adverse actions on cardiac rhythm noted during myocardial ischemia, n-3 PUFA must be prescribed with caution and generalized recommendations to increase fish intake or to take n-3 PUFA supplements need to be reconsidered.

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          Author and article information

          Journal
          Pharmacol. Ther.
          Pharmacology & therapeutics
          1879-016X
          0163-7258
          Oct 2013
          : 140
          : 1
          Affiliations
          [1 ] Department of Physiology and Cell Biology, The Ohio State University, 304 Hamilton Hall, 1645 Neil Ave., Columbus, OH 43210-1218, United States. Electronic address: billman.1@osu.edu.
          Article
          S0163-7258(13)00126-5
          10.1016/j.pharmthera.2013.05.011
          23735203
          23017b1e-23cc-4e9a-baf9-dcd7032c3835
          Copyright © 2013 Elsevier Inc. All rights reserved.
          History

          AF,AFL,ALA,APD,Atrial fibrillation,BP,CICR,Ca-ATs,DADs,DHA,DPA,Docosahexaenoic acid,EADs,EPA,ERP,Eicosapentaenoic acid,HR,HRV,Heart rate variability,ICDs,MI,MSNA,Omega-3 polyunsaturated fatty acids,RBC,RYRs,SR,VF,VT,Ventricular fibrillation,action potential duration,alpha-linolenic acid,atrial fibrillation,atrial flutter,blood pressure,calcium aftertransients,calcium induced calcium release,delayed afterdepolarizations,docosahexaenoic acid,docosapentaenoic acid,early afterdepolarizations,effective refractory period,eicosapentaenoic acid,heart rate,heart rate variability,implantable cardioverter defibrillators,muscle sympathetic nerve activity,myocardial infarction,n−3 PUFAs,n−6 PUFAs,omega-3 polyunsaturated fatty acids,omega-6 polyunsaturated fatty acids,red blood cell,ryanodine receptors,sarcoplasmic reticulum,ventricular fibrillation,ventricular tachycardia

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