Vitamin C for preventing atrial fibrillation in high risk patients: a systematic review and meta-analysis

Vitamin C for preventing atrial fibrillation in high risk patients: a systematic review and meta-analysis

Abstract
Background

Atrial fibrillation (AF), a common arrhythmia contributing substantially to cardiac morbidity, is associated with oxidative stress and, being an antioxidant, vitamin C might influence it.
Methods

We searched the Cochrane CENTRAL Register, MEDLINE, and Scopus databases for randomised trials on vitamin C that measured AF as an outcome in high risk patients. The two authors independently assessed the trials for inclusion, assessed the risk of bias, and extracted data. We pooled selected trials using the Mantel-Haenszel method for the risk ratio (RR) and the inverse variance weighting for the effects on continuous outcomes.

Results

We identified 15 trials about preventing AF in high-risk patients, with 2050 subjects. Fourteen trials examined post-operative AF (POAF) in cardiac surgery patients and one examined the recurrence of AF in cardioversion patients. Five trials were carried out in the USA, five in Iran, three in Greece, one in Slovenia and one in Russia.

There was significant heterogeneity in the effect of vitamin C in preventing AF. In 5 trials carried out in the USA, vitamin C did not prevent POAF with RR = 1.04 (95% CI: 0.86–1.27). In nine POAF trials conducted outside of the USA, vitamin C decreased its incidence with RR = 0.56 (95% CI: 0.47–0.67). In the single cardioversion trial carried out in Greece, vitamin C decreased the risk of AF recurrence by RR = 0.13 (95% CI: 0.02–0.92).

In the non-US cardiac surgery trials, vitamin C decreased the length of hospital stay by 12.6% (95% CI 8.4–16.8%) and intensive care unit (ICU) stay by 8.0% (95% CI 3.0–13.0%). The US trials found no effect on hospital stay and ICU stay. No adverse effects from vitamin C were reported in the 15 trials.

Conclusions

Our meta-analysis indicates that vitamin C may prevent post-operative atrial fibrillation in some countries outside of the USA, and it may also shorten the duration of hospital stay and ICU stay of cardiac surgery patients. Vitamin C is an essential nutrient that is safe and inexpensive. Further research is needed to determine the optimal dosage protocol and to identify the patient groups that benefit the most.

http://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-017-0478-5

I wonder what this tells us? American vitamin C is not actually vitamin C???

Low potassium is a major cause of Afib, but nothing seems to stop my permanent Afib. D.

Isn't that the sort of thing they used to implant pacemakers for? I haven't met anyone with a pacemaker for years if not decades now.

chris c wrote:Isn't that the sort of thing they used to implant pacemakers for? I haven't met anyone with a pacemaker for years if not decades now.

I have a pacemaker Chris and I met another birder with one the other week, he was 70 and had been a marathon runner.  
Most people have rapid Afib and they give them betablockers to slow their hearts down, beta blockers would kill me!

On a monitor my heart was pausing overnight repeatedly up to four seconds and when beating in the day was irregular and slow at rest.

But my heart problems are not caused by high blood glucose, or high insulin, they have been caused by 30 years of undiagnosed Conn's syndrome and c.20x normal aldosterone.

I have been referred to a Cardiologist because I have difficulty breathing when laid down and my brain peptide test was 937.  Now for over a week I have doubled my aldosterone antagonist intake (epleronone) to stop blood sodium going in lung and heart tissue..hence difficulty breathing before due to retained fluid. The above indicates a measure of heart failure.

I have not had the breathing difficulty since I increased the potassium sparing diuretic.
atb
D.

Sympathies!

Goes to show how complex and multifactorial things can be.

My father had Graves (hyperthyroid) when he was young. This damaged his heart to the extent he was considered too ill to go to France to be killed - but not so much that it stopped him driving a fire engine during the Blitz. Or living to 82.

In those days the treatment was to wait until it became really bad and hack out most of the thyroid.

Predictably (in retrospect) he later became hypOthyroid. One of his symptoms was "palpitations" - missed beats - which he had for years if not decades.

When I went hyperthyroid my heart was pounding like a jackhammer. Taking too much carbimazole and oversuppressing the thyroid also makes me have "missed beats" mainly when falling asleep or sitting still. They seem to go away when I get the dose right. Even so I have become more leery of Lo-Salt (potassium) and less so of ordinary salt (sodium) in case that's also involved. Have you had your thyroid checked? Though the NHS version of "underactive" is actually "hugely underactive" so even if it's a player they might not have considered it, or bothered to tell you.

Hi Chris,
No problems with thyroid when tested.
Conn's is well document since discovered by Conn in the 1950's.

Conn's damages tissue, particularly the left ventricle.  It remodels tissue because it blocks the natural sodium/potassium balancing affect of the adrenals.  The feedback system for electrolyte is blocked by excessive aldosterone causing a potassium leak and sodium retension.   The removal of the offending adrenal stops hypertension in its tracks if one has unilateral disease and the normal feedback system works again. Too late for me, the problem has probably given me secondary htn by now and the op is risky.
Using an aldosterone receptor blocker helps reduce bp and damage to tissue with receptors, but it causes the tumour to generate more aldosterone that damages non genomic receptor tissue.  Some aldosterone synthase inhibitors are being developed but it is probably going to be too late, perhaps, for me.
The aldosterones feedback system works in conjuction with the other hormone renin.  
Hence most people can eat salt with impunity, they just pee it out because their aldosterone drops with high sodium intake.
regards
Derek

Thanks for the further info, not something I've come across before, other than you.

I think I'm more aware of the other side of the coin - renin - as being one of the targets of various BP-lowering meds.

chris c wrote:Thanks for the further info, not something I've come across before, other than you.

I think I'm more aware of the other side of the coin - renin - as being one of the targets of various BP-lowering meds.

Hi Chris this may be the reason why low salt diets are damaging and self defeating for those without adrenal disease. They increase renin and therefore increase adosterone by c.3x and aldosterone damages tissue when the natural feedback system is bypassed.If high it causes left ventricular hypertrophy and many other problems. D.

Once again the recommendations are making work for the cardiologists