Lipoxin A4 may function as an endogenous anti-arrhythmic molecule.
Cardiac arrhythmias cause significant morbidity and mortality in patients with coronary heart disease, hypertension, and congestive cardiac failure and in the elderly. Inflammation, oxidative injury, altered myocyte metabolism, extracellular matrix remodeling and fibrosis initiate and perpetuate cardiac arrhythmias, especially atrial fibrillation. Enhanced myeloperoxidase (MPO) activity by infiltrating activated leukocytes could bind to myocardial cells and cause fibrosis resulting in the initiation and progression of arrhythmias. Supplementation of eicosapentaenoic and docosahexaenoic acids (EPA and DHA, respectively) suppresses arrhythmias. EPA and DHA form precursors to anti-inflammatory lipid molecules: lipoxins, resolvins, protectins and maresins that are known to suppress inflammation, have anti-fibrotic actions and inhibit MPO activity. Hence, it is likely that leukocyte and/or myocardial deficiency of EPA and DHA and consequent reduced formation of lipoxins, resolvins, protectins and maresins enhance inflammation and MPO activity that leads to myocardial damage and fibrosis and initiation and progression of cardiac arrhythmias. Based on these evidences, I propose that lipoxins, resolvins and protectins function as endogenous anti-arrhythmic molecules and their stable synthetic analogs could be useful in the management of cardiac arrhythmias.
Das
Undurti N
UN
School of Biotechnology, Jawaharlal Nehru Technological University, Kakinada 533 003, India. Undurti@hotmail.com
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D015777:Eicosanoids / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D006801:Humans; D044045:Lipoxins / Q000502:physiology*
D015777:Eicosanoids; D005231:Fatty Acids, Unsaturated; D044045:Lipoxins; C040527:lipoxin A4