Beneficial Actions of Statins in the Reduction of Atrial Fibrillation and Stabilization and Regression of Coronary Plaques: But How and Why?

Das, Undurti N.

doi:10.1253/circj.cj-10-0939

Cited by 5 publications

(6 citation statements)

References 22 publications

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“…22 Although the effects of other statins on these enzyme activities were not evaluated fully, statins increase the formation of DHLA, AA, EPA, and DHA by these enzymes. 23 We speculate that the effects of statins on the formation and conversion of PUFAs are different among specific types of statins and these differences partly explain the various pleiotropic effects of statins. The AA, EPA, and DHA give rise to anti-inflammatory molecules such as lipoxins, resolvins, protectins, and maresins.…”

Section: Discussionmentioning

confidence: 90%

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Effects of Statins on Serum n-3 to n-6 Polyunsaturated Fatty Acid Ratios in Patients With Coronary Artery Disease

Nozue

Yamamoto

Tohyama

et al. 2013

J Cardiovasc Pharmacol Ther

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Section: Discussionmentioning

confidence: 90%

“…The AA, EPA, and DHA give rise to anti-inflammatory molecules such as lipoxins, resolvins, protectins, and maresins. 23 Thus, PUFAs form precursors of both pro- and anti-inflammatory molecules and the balance between these mutually antagonistic compounds could determine the process of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of Statins on Serum n-3 to n-6 Polyunsaturated Fatty Acid Ratios in Patients With Coronary Artery Disease

Nozue

Yamamoto

Tohyama

et al. 2013

J Cardiovasc Pharmacol Ther

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“…Jula et al reported that simvastatin increases serum AA levels due to an increase in Δ6- and Δ5-desaturase enzyme activities [ 13 ]. Although the effects of other statins on these enzyme activities have not been evaluated, statins increase the formation of AA, EPA, and DHA by these enzymes [ 14 ]. The AA, EPA, and DHA give rise to anti-inflammatory molecules such as lipoxins, resolvins, and protectins [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Although the effects of other statins on these enzyme activities have not been evaluated, statins increase the formation of AA, EPA, and DHA by these enzymes [ 14 ]. The AA, EPA, and DHA give rise to anti-inflammatory molecules such as lipoxins, resolvins, and protectins [ 14 ]. Some of beneficial actions of statins are explained by the formation of these anti-inflammatory molecules [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Statin treatment alters serum n-3 to n-6 polyunsaturated fatty acids ratio in patients with dyslipidemia

Nozue

Michishita

2015

Lipids Health Dis

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BackgroundThe effects of statins on serum n-3 to n-6 polyunsaturated fatty acids (PUFAs) levels have not been fully evaluated. We examined the effects of two types of statins (rosuvastatin and pitavastatin) on serum PUFAs levels and their ratios in patients with dyslipidemia.FindingsA total of 46 patients who were not receiving lipid-lowering therapy were randomly assigned to receive either 2.5 mg/day of rosuvastatin or 2 mg/day of pitavastatin. Serum PUFAs levels were measured at baseline, at 4 weeks, and at 12 weeks. Rosuvastatin was used to treat 23 patients, and the remaining 23 patients were treated using pitavastatin. Serum docosahexaenoic acid (DHA) levels decreased significantly at 12 weeks in both groups (rosuvastatin: from 169.6 to 136.3 μg/mL, p = 0.006; pitavastatin: from 188.6 to 153.9 μg/mL, p = 0.03). However, serum levels of eicosapentaenoic acid (EPA) and arachidonic acid (AA) did not change. In addition, the EPA/AA ratio did not change, whereas the DHA/AA ratio decreased significantly at 12 weeks in both groups (rosuvastatin: from 0.99 to 0.80, p = 0.01; pitavastatin: from 1.14 to 0.91, p = 0.003). No adverse events were observed during the study period.ConclusionsIn this small, open-label, pilot study, rosuvastatin and pitavastatin decreased serum DHA levels and the DHA/AA ratio in patients with dyslipidemia.

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“…As discussed above, VNS and PUFAs seem to interact with each other such that they potentiate each other's actions. Both VNS and PUFAs (and their products lipoxins, resolvins, protectins, maresins and PGI 2 ) have anti-inflammatory actions, reduce insulin resistance, and are useful in the prevention and management of cardiovascular diseases and cardiac arrhythmias [ 7 , 8 , 11 , 26 - 28 , 34 , 36 , 45 - 50 ]. It is likely that in patients with RA, lupus and other autoimmune diseases and inflammatory conditions such as inflammatory bowel diseases, vagal tone will be subnormal and sympathetic tone is high; synovial fibroblasts, infiltrating (into the involved joints) macrophages, T cells and leukocytes may show reduced number or defective expression of alpha7nAChR and their content of PUFAs (especially AA, EPA and DHA) and ability to form adequate amounts of lipoxins, resolvins, protectins and maresins will be defective; and even the plasma and synovial fluid content of PUFAs and concentrations of lipoxins, resolvins, protectins and maresins are likely to be low.…”

Section: Hypothesismentioning

confidence: 99%

Can vagus nerve stimulation halt or ameliorate rheumatoid arthritis and lupus?

Das

2011

Lipids Health Dis

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Acetylcholine, the principal vagus neurotransmitter, inhibits inflammation by suppressing the production of proinflammatory cytokines through a mechanism dependent on the α7 nicotinic acetylcholine receptor subunit (alpha7nAChR) that explains why vagus nerve stimulation is anti-inflammatory in nature. Strong expression of alpha7nAChR in the synovium of rheumatoid arthritis and psoriatic arthritis patients was detected. Peripheral macrophages and synovial fibroblasts respond in vitro to specific alpha7nAChR cholinergic stimulation with potent inhibition of proinflammatory cytokines. Fibroblasts balance inflammatory mechanisms and arthritis development through feedback cholinergic stimulation by nearby immune cells. Collagen induced arthritis in alpha7nAChR (-/-) mice was significantly severe and showed increased synovial inflammation and joint destruction compared to the wild-type mice. Similar to vagal nerve stimulation and alpha7nAChR agonists, polyunsaturated fatty acids: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also suppress inflammation. In view of their similar anti-inflammatory actions, it is proposed that vagal nerve stimulation, alpha7nAChR agonists and EPA and DHA may augment the formation of anti-inflammatory lipid molecules: lipoxins, resolvins, protectins and maresins. This implies that therapies directed at regulation of the cholinergic and alpha7nAChR mediated mechanisms and enhancing the formation of lipoxins, resolvins, protectins and maresins may halt and/or ameliorate rheumatoid arthritis, lupus and other rheumatological conditions.

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Beneficial Actions of Statins in the Reduction of Atrial Fibrillation and Stabilization and Regression of Coronary Plaques: But How and Why?

Cited by 5 publications

References 22 publications

Effects of Statins on Serum n-3 to n-6 Polyunsaturated Fatty Acid Ratios in Patients With Coronary Artery Disease

Effects of Statins on Serum n-3 to n-6 Polyunsaturated Fatty Acid Ratios in Patients With Coronary Artery Disease

Statin treatment alters serum n-3 to n-6 polyunsaturated fatty acids ratio in patients with dyslipidemia

Can vagus nerve stimulation halt or ameliorate rheumatoid arthritis and lupus?

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