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Calvo et al.                                                                                                                                                              Omega-3 fatty acids in cardiovascular health

           evidence  highlights  that the effect n-3 PUFAs exert   of transmembrane potentials during episodes  of
           on the electrophysiology  of the ventricles  and  atria   ischemia. [133]
           relies on their favorable action on cell-cell connections
           by modulating the expression and phosphorylation of   A study on 211 patients  with ST segment  elevation
           connexin-43 [125,126]  [Figure 6].                 myocardial infarction who underwent reperfusion by
                                                              percutaneous coronary intervention found patients with
           Ischemia/reperfusion                               higher levels of n-3 PUFAs (EPA + DHA ≥ 155 mg/mL)
           Although the restoration of blood flow in the ischemic   had a lower incidence  of reperfusion  injury than
           myocardium  is essential  for tissue survival  during   those with lower levels of n-3 PUFAs (EPA + DHA <
           acute myocardial infarction, its reperfusion  may   155 mg/mL). [134]  Although the antiarrhythmic effect may
           directly accelerate the ischemic process or increase   exert the most potent impact in ischemia/reperfusion
           the myocardial  injury in a phenomenon  known as   injury, [135]  other supplementary  actions may also
           “reperfusion injury”. [127-129]  Important studies have   intervene,  including  antithrombotic,  anti-inflammatory
           reported that this event is responsible for up to 50%   and vasoactive effects. [136-138]
           of  the  final  infarction  size. [130]  PUFAs appear  to be
           associated  with reduced  ischemic/reperfusion  injury   CONCLUSION
           and thus with a better recovery after a coronary event. [131]
                                                              As has been described  in review, n-3 PUFAs boast
           During ischemia/reperfusion,  increased n-3 PUFA   several  beneficial  effects  in  CV  physiology  and
           content in the mitochondrial membrane may contribute   pathophysiology  [Figure 7].  Notwithstanding  current
           to stabilization and thus lower myocardial  oxygen   available  evidence  supporting  the administration  of
           consumption  (MVO ),  thereby attenuating the      n-3 PUFAs as a therapeutic intervention in CVD,
                              2
           thermodynamic inefficiency caused by hypoxia. [132,133]    further research is required to better characterize the
           In addition, a lower MVO  could diminish vulnerability   underlying  molecular  mechanisms,  as  well  as  refine
                                  2
           to arrhythmia through the energetic maintenance    recommendations  for  their clinical use.  Indeed, one









































           Figure 6: Antiarrhythmic effects of polyunsaturated fatty acids. n-3 PUFAs show several potential antiarrhythmic properties: (1) membrane
           potential stabilization by decreasing transmembrane io trafficn; (2) inhibition of the activity and expression of connexins, decreasing the
           conductivity of myocardial tissue; (3) increase in vagal tone, decreasing heart rate, conductivity and myocardial excitability. NCX: sodium-
           calcium exchanger; Cx43: connexin-43; PUFA: polyunsaturated fatty acids
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