NYT article today misleading in one respect

Not sure if this is behind paywall

[well.blogs.nytimes.com]

But even when all traces of A-fib are eliminated, Dr. Ruff said, continued treatment with an anticoagulant is needed to guard against stroke. “Once a person has had A-fib, there is an increased risk of stroke even if their heart is in normal rhythm,” he said.

This just supports the importance of awareness about the 'thick, sticky blood' prevalence (hyperviscosi/hypercoaguability) issue that relates to silent inflammation and other influences such as toxins, systemic bacterial overload, iron overload, methylation dysfunction, heavy metal exposure and so on.

Note this article doesn't mention that every person should be tested for the specific key markers that evaluate blood for the "thick, sticky tendencies"... but goes right for the Rx drug rememdy as is so typical and then the patient is stuck with the adverse effects of LT anticoag drugs rather than remediating the core issue in the first place... ie, what is causing the silent inflammation that leads to the thick, sticky, hyperviscous blood?

Of course, Dr. Ruff's advice will greatly improve the bottom line of the drug companies.

Jackie

If his statement is backed up by some studies, I'll buy it. Until I see the facts, I don't buy it. I doubt that "sticky" blood is a result of errant electrical signals in the heart....or even correlates to afib. But...show me...if I'm wrong -

Typical NYT health related article filled with some generally accurate very basic info mixed in with some very misleading or outright wrong misconceptions.

'When every trace of AFIB has truly been eradicated the ONLY possible need for life long Anti-coagulation is if a TEE confirms that so much scarring from long term remodeling due to years of unaddressed AFIB might have slowed down the emptying velocity out of the LAA and/or caused an inconsistent A-wave at the mitral inflow such that the LAA based clot formation and subsequent stroke risk remains elevated even when the person is in normal sinus rhythm... This too can happen as a result of LAA isolation ablation about 50% to 60% of the time after LAA isolation.

There can be other conditions that might warrant staying on a blood thinner, of course, but implying that a strictly AFIB related stroke risk is on going even when there is no more AFIB and when the two conditions noted above are not present is misleading.

Other than those two scenarios, there is definitely ZERO good reason to continue anti-coagulation drugs due solely to a supposed 'AFIB -related' elevated stroke risk even after AFIB has been rendered dormant for the long term.

He probably meant to say "I prefer to keep every afibber on warfarin or an NOAC even when 'it seems' they might not be having much active AFIB just in case they are having silent undetected AFIB episodes" which is a valid concern, but then we are not talking about truly being free of AFIB.

Perhaps Dr Ruff deems the story easier for people to remember , and perhaps even also considers that he'll get more Brownie points from the makers of these AC drugs, if he just 'rounds off' the real truth a bit and gives the easier to convey declaration that 'everyone who ever had any amount of AFIB should be relegated to anticoagulation for life even if they are not totally free of any arrhythmia!!

Or maybe it's just a lazy medical journalist who took what Dr Ruff really meant to say out of context and came up with that handy, though highly misleading, 'sound bite' to end his AFIB article?

Anyway, this is an all too typical lay press story, and often the sort found in the NYT, that conveys some good info while also sewing a thread of confused and flat out wrong ideas throughout and in between the good parts.

Alas, probably 90% of their large volume of lay readers lack the lingo and understanding in this area to be able to discriminate what parts are fact and what fiction since it all sounds so plausible, if you didn't know any better.

Shannon



Edited 3 time(s). Last edit at 01/01/2014 05:20PM by Shannon.

The focus should be on reversing or correcting the underlying cause(s) of inflammation that contribute to sticky blood since hyperviscosity is the precursor to adverse clotting and is stimulated by the various conditions mentioned previously… most specifically silent inflammation…. and of course free-radical damage from prolonged aerobic exercise. The stimulation of inflammatory cytokines is an important factor and should be managed preventively.

Hemodynamics studies the impact of elevated whole blood viscosity and examines the risk factors of hyperviscous blood’s effect on flow velocity…especially in the areas of shear stress such as arterial branches of which there are many. When these branches are affected by hyperviscous blood, there is injury at the junctions which brings about the inflammatory response and all that ensues downstream from that as a protective mechanism to the injury and includes plaque formation and then the potential consequences of plaques breaking off the causing a blockage or an clot that flows right to the brain …etc.

It’s proven that hyperviscosity causes clots which result in TIAs, strokes, MIs and DVT, etc. Why not correct the problem at the source and take preventive action by eliminating the initiators of silent inflammation?

As mentioned in the other post on Fire in the Heart and silent inflammation, quoting Barry Sears:

Chronic inflammation = pain
Silent inflammation … kills.

If there is a tendency for silent afib…which many EPs claim is a threat even post ablation… then thick, sticky blood from causes other than errant electrical signals can be a threat because thick, sticky blood tends to have poor or slow clearance out of the heart chambers and can form clots.

This fostered the saying “Churn cream, you get butter. Churn blood, you get a clot.”

Thus, the importance of regularly monitoring all of the inflammatory markers that contribute to thick, sticky blood is a better method than just thinning the blood because it will manage the total body silent inflammation rather than just thin the blood while the inflammation continues to smolder.

Researchers examining the causes and effects of silent inflammation indicate the process is the basis of aging and age-related diseases such as CV disease, diabetes, some cancers, MS, Parkinson’s, Alzheimer’s, autoimmune disorders, asthma and arthritis. Elevated markers such as C-reactive protein and Interleukin 6 are found to be present long before the onset of cardiovascular disease.

Author of C-Reactive Protein, Board Certified cardiologist Scott J. Deron, DO, FACC, notes that people with high CRP suffer recurrent heart attacks and angina. He says CRP may not be just a marker for inflammation, but a cause and cites a study that CRP inflames arteries by triggering the formation of clots and plaque.

He says (in 2004) that “studies of more than 85,000 people show that over the last 10 years inflammation is always present in the heart’s blood vessel walls among heart attack patients whose cholesterol levels were normal or near normal.” And that elevated CRP is a warning sign or risk factor for heart disease.

So.. we can expand that to indicate that when this inflammatory marker is elevated it makes sense that some people might manifest with atrial fibrillation as a result. Again, as I like to say, Afib is the Canary in the Coal Mine that something is amiss in the body and it makes sense to check all the markers of silent inflammation.

Taking an anticoag may help with the prevention of adverse clotting, but it doesn’t address the inflamed heart issue which most certainly can be a trigger for afib.

Dr. Deron also mentions one study showing those with the highest CRP levels were three times more likely to develop Alzheimer’s disease over a 20-year period and in patients with many forms of cancer, high levels of CRP correspond to a lower survival rate.

This supports what many others have been promoting for years… eliminate the source of the inflammation rather than just thin the blood to prevent a potential for adverse clotting.

Jackie


C-Reactive Protein by Scott J. Deron, D.O., FACC, McGraw-Hill; New York, NY, 2004

The Anti-Inflammation Zone by Barry Sears, PhD, Harper Collins Publishers; New York, NY, 2005.

The Inflammation Syndrome: The Complete Nutritional Program to Prevent and Reverse Heart Disease, Arthritis, Diabetes, Allergies, and Asthma by Jack Challem, John Wiley & Sons; Hoboken, NJ, 2003.

Silent Inflammation - The root cause of many of the major chronic diseases is inflammation and there are many nutraceuticals that can play a role in curbing this risk factor.
By Dr. Barry Sears
[www.nutraceuticalsworld.com]

It's good to get the opinion of others on this site regarding the recent article on A-Fib in the NYT. With everything that has been said here in response to the article, my initial thought is this: "What post ablation precautions do top electrophysicists take to ensure that the risk of a stroke or other debilitating medical condition is eliminated or dramatically reduced?" Also, I'm curious about follow-up monitoring, post ablation. I'm sure that there are initial follow-up appointments, but how frequent are those appointments and for what period of time? Are we talking months or years? It's my understanding that the medical industry defines a "successful" ablation as being A-Fib free for one (1) year. The one year threshold seems to be very low to me. I would like to think that some day the medical community will define a successful ablation as being A-Fib free for five (5) years or more.

Happy New Year!

Chuck

Ironically Jackie, Coumadin for example and likely the NOAC class of drugs, don't have much direct bearing on reducing elevated true whole blood viscosity readings. You can have an ideal therapeutic INR of day 2.5 and still have an severely high whole blood viscosity reading using the new and only reliable Hemothix WBV machine that tests WBV in both the systolic and diastolic phases of cardiac cycle.

The typical Pharma blood thinners don't really deal with all aspects that continue to think sticky blood., but instead are more intended to prevent thrombus clot formation from happening.

This fact was underscored in my own experience not long after my LAA isolation ablation while I was still on a large dose of a Coumadin at 13.5mg/day and then at that point I had stopped all Nattokinase, Serrapeptidase and a few other natural blood viscosity lowering agents not wanting to possibly cause a risky scenario with the larger Coumadin dose I needed with my Coumadin resistance and As a result Intested very high on the WBV test at Meridian Valley Labs!

A good couple consults with Dr Holsworth and Dr Jonathan Wright reassured me that Nattokinase and several other natural anti-oxidant anti-inflammatory agents the help lower WBV could safely be taken with Coumadin under the watch of a knowledgable Doc and by using weekly at home INR testing to insure that marker isn't getting too high or low.

I was able to drop my WBV by around 38% reintroducing all those agents plus paying better attention to hydration every day.

The moral of this story is that while Coumadin and NOACs have merit when needing to address a serious embolic stroke risk, when it comes to lowering overall WBV with all the many cardiovascular as well as many other health benefits beyond embolic stroke risk protection, a collection of key natural agents plus strong daily hydration win hands down over anything Big Pharma has to offer to reduce WBV.

Perhaps it's not so ironic after all why testing for WBV directly has never really been emphasized in western medicine since the drug classes they have available to work with are more targeted toward more isolated effects of thick turgid blood like platelet aggregation or embolic clot prevention. And to address the huge amount of endothelial wear and tear that is a major direct result if too high WBV for too long leading as well to accelerated plaque formation and arteriosclerosis allopathic medicine mainly has only statins, stents and open heart surgery to try to save the horse once he has galloped far away from the barn!

Shannon

Lots of replies to that NYT article.. 145 so far

From the article

"Researchers at the University of California, San Francisco, reported this month in Annals of Internal Medicine that people with a high rate of premature atrial contractions, which can be detected by a Holter monitor worn for 24 hours, face a significantly increased risk of developing A-fib. Dr. Gregory M. Marcus, the senior author and director of clinical research at U.C.S.F.’s cardiology division, theorized that eradicating these premature contractions with drugs or a procedure that destroys the malfunctioning area of the heart may reduce the risk of the rhythm disorder."

So how about giving people mag instead before you give them meds or ablate them for PAC's???

HI George,

Of course that would be the preferred first step when seeing new patients is to run a full intra-celular Ion tests like the Exatest and they start to treat accordingly.

The problem being, that most Docs still look at this issue only through the lens of Magnesium serum testing and thus many of their studies and anecdotal attempts to achieve results have seemed like a mixed bag due to been unknowingly mislead by that very reliance on serum testing to determine whether or not magnesium dosing is correct or whether a patient should even be started on it.

A large percentage of middle aged Americans will likely still show a serum magnesium level with the overall reference range. And yet many of these still have serious intracellular mag deficiency as we all know. That being the case, when only considering serum Mag, the typical MD will either assume the patient doesn't really need any more if their levels are about say 1.8 or so, or they will consider it a waste of time because so many of their patients who do have ongoing AFIB also have what appears to be 'normal levels of serum Magnesium.

Since they mistakenly equate any serum Magnesium levels within the reference range as optimal, they naturally draw the wrong conclusion that improving magnesium status is an unreliable tool for helping to control AFIB, becuase they are looking at the wrong measure of Magnesium to begin with!

This fundamental mistake has led to the confusion where most EPs will acknowledge the theoretical and even practical role of magnesium in the cardiac contraction cycle, but assume its not worth supplementing for most folks who are already apparently within a 'normal range'.

A simple shift to correlating intracellular Magnesium stores with clinical status would likely open many eyes to the potential value of magnesium as a front line agent in the management of AFIB and other arrhythmias.

Another problem, as you well know too, is that magnesium is notoriously difficult to absorb from both food and oral supplementation, especially for anyone with any digestive challenges which are also rampant from middle age onward.

That, and the fact that it can take many months of relatively high dose Magnesium supplementation, or use of IV mag to bring stores up more quickly, has made it not a very friendly or useful tool for Docs so used to using drugs with much more immediate effects as well as unwanted side effects.

Hopefully. with more and more of these reports on magnesium and potassiums role in rhythm control come out the impression of a larger number of Cardio's and EPs will start to change and open up more.

Shannon

Don't forget that some people (like me) actually do worse with magnesium supplementation. Virtually every time I'd take in extra supplemental magnesium regardless of brand or compound, I would afib in one or two days.

It's hard for me to buy into the ion-based cure theories as a general rule....the complexity of most arrhythmia-sources is greater than that IMO.

Tom,

I certainly am aware that ions aren't a panacea. However they do help many and have fewer side effects than putting everyone on meds and ablating them.

George

TomB,I definitely would not label any ion replacement protocol a 'cure' for AFIB. But when done correctly and consistently, for those of course that can tolerate them and don't have some other underlying issue or reaction to them as you report.

I do know from experience with many patients seen at several clinics of progressive functional medicine MDs that commonly when you find people that are highly reactive to both mineral and vitamin supplements and so often do much worse when taking them, they also have an underlying adrenal dysfunction, and not always necessarily a deficiency , though often so,
one of the hallmarks of true adrenal dysfunction is a much heightened reactivity to many stressors, and most especially certain supplements and medications for which the adrenally challenged so often are overly sensitive and often have the kind of over-reaction making the condition or symptoms they are trying to address even worse.

Anyway, its food for thought.

Cheers!
Shannon