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The Benefits of Marine Omega-3S for Preventing Arrhythmias

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The Benefits of Marine Omega-3S for Preventing Arrhythmias Open access Editorial Open Heart: first published as 10.1136/openhrt-2018-000904 on 4 February 2020. Downloaded from The benefits of marine omega- 3s for preventing arrhythmias James J DiNicolantonio, James OKeefe To cite: DiNicolantonio JJ, MARINE OMEGA-3S FOR THE PREVENTION OF polyunsaturated fatty acids (PUFAs) can also OKeefe J. The benefits of marine ARRHYTHMIAS be liberated from lipoproteins via lipoprotein omega- 3s for preventing and hepatic lipase and picked up by albumin arrhythmias. Open Heart Omega- 3s have been theorised to increase 2020;7:e000904. doi:10.1136/ membrane fluidity by reducing compression via fatty acid- binding sites. The omega- 3s are openhrt-2018-000904 of the acyl chains of membrane phospholipid then carried by albumin to the heart, brain fatty acids, which can lead to a reduction in and other tissues for entrance into membrane 4 Received 17 July 2018 the ‘spring- like’ tension on membrane ion phospholipids and stored as triglycerides. Revised 29 September 2018 channels. This spring-like tension can reduce However, it is the liberated ‘free- fatty acid’ Accepted 12 October 2018 the ability of ions to freely move in and out form of omega-3s that are thought to produce of the ion channel and hence reduce its the antiarrhythmic properties. This free conductance. This is known as the ‘Andersen form of omega-3 can be mobilised from the membrane spring- like tension hypothesis’ plasma phospholipid during states of stress and is just one way marine omega- 3s may (severe exertion, sympathetic discharge) via prevent arrhythmias.1 This theory states that phospholipases.5 6 If consumed on a regular the phospholipid cell membrane curves near basis, omega- 3s will be adequately stored the ion protein channel in order for the in the heart waiting to be released in order hydrophobic domains of the cell membrane to protect against fatal arrhythmias. Their to match up. The hydrophobic length of storage into cellular membranes of cardiac ion channel proteins is slightly less than cells also likely provides antiarrhythmic bene- the hydrophobic length of the acyl chains fits. One group of authors suggested that in the phospholipid bilayer, which causes a omega- 3s, by accumulating into every heart slight bend in the membrane, and this bend cell, makes them resistant to arrhythmias. http://openheart.bmj.com/ compresses the ion channel decreasing the It was concluded that omega-3 benefits on space that ions can freely move in and out of arrhythmias are mainly due to ‘…the suppres- the channel. However, supplementing with sion of the L-type Ca2+ and voltage-dependent fish oil can prevent or reduce this compres- Na+ currents…’ By inhibiting the L-type Ca2+ sion increasing the movement of ions in and channels, excess calcium coming into the out of the channel.1 Other antiarrhythmic cytosol is prevented, thereby reducing the benefits of omega- 3s include eicosapentae- risk of ‘triggered arrhythmias’, whereas inhi- noic acid (EPA)’s ability to be a competitive bition of the voltage-dependent Na+ currents on October 5, 2021 by guest. Protected copyright. substrate for the enzymes that metabolise prolongs the inactivated state of the Na+ arachidonic acid (AA) to proinflammatory channel protecting the heart from ischaemia- eicosanoids, which is partly how marine induced arrhythmias (activation of the inacti- omega-3s reduce inflammation.2 EPA metab- vated state can lead to an arrhythmia).4 The olites are also antiarrhythmic, whereas almost benefits of alpha- linolenic acid (ALA) are less © Author(s) (or their all metabolites from AA (and linoleic acid) certain, especially if ingested orally, as ALA is employer(s)) 2020. Re- use 3 permitted under CC BY- NC. No are proarrhythmic. not stored to the extent long-chain omega- 3s commercial re- use. See rights Dietary omega- 3s are mainly consumed as are. Docosahexaenoic acid (DHA) is the and permissions. Published triglycerides, which are absorbed as free fatty preferred storage form of omega- 3s in both by BMJ. acids and monoglycerides. These fats then get the heart and brain. Preventive Cardiology, Saint Luke’s Mid America Heart rapidly resynthesised in the intestine and liver Despite fish oil inhibiting the Na ion Institute, Kansas City, Missouri, back to triglycerides with subsequent inte- channel, it does not lead to an upregulation USA gration into chylomicrons, very low-density of the number of Na channels per cardio- lipoprotein and low-density lipoprotein myocyte (unlike the class I antiarrhythmics Correspondence to (LDL) (LDL can actually deliver omega-3s Dr James J DiNicolantonio; some of which have been implicated in jjdinicol@ gmail. com to tissues via LDL receptors). The omega-3 increased sudden death). The Na current DiNicolantonio JJ, OKeefe J. Open Heart 2020;7:e000904. doi:10.1136/openhrt-2018-000904 1 Open Heart Open Heart: first published as 10.1136/openhrt-2018-000904 on 4 February 2020. Downloaded from can cause arrhythmias because it initiates action poten- prospective studies indicate that fish or fish oil reduces tials in heart cells and if this occurs in partially depo- cardiovascular mortality anywhere from 29% to 52% and larised myocytes, which require less depolarisation to sudden cardiac death from 45% to 81%.3 Indeed, fish oil exert an action potential, an arrhythmia can occur if this has been found to significantly reduce mortality in just 3 happens at a susceptible time in the electrical cycle of months after an acute MI.10 the heart. These susceptible times are reduced with the Although death due to coronary heart disease has consumption of fish oil. Indeed, ‘…partially depolarised decreased in the USA since the 1960s, sudden cardiac cells at the periphery of the ischaemic zone after an acute deaths due to fatal arrhythmias remains high with ventric- myocardial infarction (MI) are promptly and completely ular fibrillation making up 80% of all sudden deaths in inactivated so that their potential arrhythmogenic role the USA.13 Cardiac arrhythmias can occur early during has been aborted by the presence of the omega-3 fatty an ischaemic event or after reperfusion. Long- chain acids’. Thus, omega-3 PUFAs inhibit partially depolarised omega- 3s have been found to reduce both ischaemic myocytes from exerting an action potential during a crit- and reperfusion arrhythmias. Indeed, fish oil reduces ical time after an MI that may lead to a fatal arrhythmia. ventricular fibrillation from coronary artery occlusion in George Billman and Alexander Leaf were best known numerous animal models (rats, monkeys, pigs and dogs) for their omega-3 experiments in animals. In one study, and has also been found to reduce myocardial ischaemia- Billman and Leaf surgically induced large anterior wall reperfusion injury (reduced ischaemic damage and MIs (via ligation of the left anterior coronary artery) in fatal arrhythmias).14 Moreover, in the same experiment, dogs.4 After 1 month, the animals were run on a tread- almost twice as many animals were alive with fish oil mill and had their left circumflex artery occluded (using supplementation (76%) vs the omega-6 corn oil group a hydraulic cuff) to induce ventricular fibrillation. (41%). This may be due to their ability to penetrate into However, when they were infused with EPA, five of the endothelial cells, neutrophils, platelets, myocytes, and seven dogs were completely protected from fatal ventric- monocytes reducing inflammation, platelet aggregation, ular arrhythmias (p<0.02). Similar results were found and the pro-arr hythmic effects of the 2-series eicosanoids with DHA and ALA (six of eight dogs were protected, from AA.13 p<0.004 for each). Billman and Leaf concluded, ‘These Around 300 000 people die every year in the USA from results indicate that purified omega-3 fatty acids can non- traumatic out- of- hospital sudden cardiac arrest with prevent ischaemia- induced ventricular fibrillation in this the majority of cases being caused by ventricular fibril- dog model of sudden cardiac death’. In other studies lation due to thrombotic events.15 16 Marine omega- 3s from these authors, similar results were found. Indeed, have evidence for reducing the risk of this complication. infusing fish oil intravenously just prior to exercise- plus- Studies suggest that if your intake of omega-3s is low, or ischaemia prevented ventricular fibrillation (in seven of intake of omega-6 is high, then you are at a greater risk eight dogs), which was not found with soybean oil (all of having a heart attack as well as death due to a heart http://openheart.bmj.com/ five of five dogs developed ventricular fibrillation).7 The attack. Indeed, the reduction in sudden cardiac death in same results occurred in a subsequent study, whereby 10 patients supplemented with marine omega-3s who had of 13 dogs did not develop ventricular fibrillation when experienced a MI in GISSI- P became significant in just 4 provided with omega-3 PUFAs.8 It is important to note months and this accounted for almost 60% of the mortality that infusing omega-3 PUFAs allows them to be delivered benefit.10 Approximately 50%–60% of all sudden deaths right into the cardiac phospholipid membranes within that occur within 1 hour of an acute MI are attributable seconds getting them to the site of action so they can to sustained ventricular arrhythmias, suggesting that quickly exert their antiarrhythmic effects. The benefits of omega- 3s prevent fatal ventricular arrhythmias after an omega- 3s for preventing ischaemia-induced fatal ventric- MI. In one randomised controlled trial
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