Tag Archives: stroke

Blood Thinners (Oral Anticoagulants) For Atrial Fibrillation: Who Should Take Them and Which One To Take

The most serious  adverse consequence of having atrial fibrillation is stroke. Since we have safe and effective ways of preventing afib-related stroke with oral anticoagulant drugs (blood thinners), a major decision for the newly diagnosed patient with atrial fibrillation is “should I take a blood thinner?”

To answer this question the afibber should engage in a lengthy discussion with his/her health-care provider which results in a shared and informed  decision. Such discussion must cover your risk of stroke, the benefits of blood thinners in preventing stroke, the bleeding risks of blood thinners and the pros and cons of the five oral anticoagulants available to prevent stroke.

Estimating Your Risk of Stroke With Afib

The best way we have of estimating a patient’s risk of stroke if they have atrial fibrillation (AF) is by the CHA2DS2-VASc scale (which I like to call the Lip scale)

Stroke Risk EstimationThis scale take the factors we know that increase the risk of stroke and assigns 1 or 2 points. The acronym comes from the first letter of the factors that are known to increase risk as listed to the left.

Most of the factors get 1 point, but prior stroke (S) and age>75 (A) get 2 points.

We then add up your points and use another chart (or app) to calculate the risk of stroke per year.

CHA2 stroke riskYour risk of stroke is very low if you have zero risk factors; it gets progressively higher as you reach the maximum number of 9.

Treatment with an oral anticoagulant (OAC),  either warfarin, or one of the four novel anticoagulant agents (NOACS), is recommended when score is >/=2 corresponding to a  risk of stroke  above 1-2% per year.

These blood thinners have consistently been shown to lower your risk of stroke or systemic embolization (when a clot from the heart goes somewhere other than the brain) by almost 70%.

The higher the risk, the more the benefit of these blood thinners in preventing stroke.

Both European and American guidelines recommend using the CHA2DS2-VASc score for initial risk stratification. The European  guideline recommends OAC therapy for males with a CHA2DS2-VASc score ≥1 and for female patients with a score ≥2., whereas the American guideline recommends use of OAC if the CHA2DS2-VASc  score is ≥2 for men and women.

I’ve been using the CHA2DS2-VASc scale for several years in my afib patients. I try to review the patient’s risk of stroke and their risk of bleeding during every office visit, and decide whether they should be on or off an OAC.

Bleeding From Blood Thinners

All OACs cause increase bleeding. They don’t discriminate between bad clots that cause strokes and good clots that stop you from bleeding.

If you’re taking one you are more likely to have nose bleeds, bleeding into the intesitnal tract or urine and you will bleed longer when cut and more profusely if in an accident. In lower stroke risk patients, the bleeding risk of OAC of 1% per year may outweigh the benefits conferred by stroke reduction.

I wrote a post entitled “Why Does The TV Tell me Xarelto Is a Bad Drug” which points out that law suits against the makers of the newer OACs are frivolous and that these NOACs are likely more safe and effective than warfarin.

In recent years, four new drugs for reducing strokes in patients with atrial fibrillation which are much less influenced by diet and medications have gained approval from the FDA. These are generally referred to as “novel anticoagulants” reflecting their newness, different effects from warfarin or aspirin, and their blood thinning properties.  The first  (brand name Pradaxa) was released to much excitement and fanfare in October, 2010.  The press release for this approval read as follows:

PRADAXA, an oral direct thrombin inhibitor2 that was discovered and developed by Boehringer Ingelheim, is the first new oral anticoagulant approved in the U.S. in more than 50 years. As demonstrated in the RE-LY® trial, PRADAXA 150mg taken twice daily has been shown to significantly reduce stroke and systemic embolism by 35 percent beyond the reduction achieved with warfarin, the current standard of care for patients with non-valvular atrial fibrillation. PRADAXA 150mg taken twice daily significantly reduced both ischemic and hemorrhagic strokes compared to warfarin

What was very clear from the study with Pradaxa  and stated very clearly in all publications and patient and doctor  information sources was that just like warfarin, patients could have severe bleeding complications, sometimes fatal. Overall serious bleeding complications were about the same (the rate of major bleeding in patients Pradaxa  in the RE-LY trial was 3.1% versus 3.4% in the warfarin group) but Pradaxa had about 50% more bleeding from the gastrointestinal tract and warfarin about 50% more bleeding into the brain.

Another big difference between the novel anticoagulants and warfarin is that we have antidotes (Vitamin K, fresh frozen plasma) that can reverse the anticoagulation state rapidly for warfarin but until recently none for the newer drugs. (There is now available an antidote for Pradaxa).  This information also was made very clear to all doctors prescribing the medications in the package insert and educational talks. Despite this, in the major trials comparing these newer agents to warfarin, the newer agents were as safe or safer than warfarin.

The most feared bleeding complication on all OACs is bleeding into the head (intracranial hemorrhage). The risk of ICH is between 0.2 to 0.4 percent per year on warfarin. Studies show with the NOACs the risk is about half of the risk on warfarin.

Should You Take a NOAC or Warfarin?

Once the decision has been made to start a blood thinner, the next question is whether to take warfarin or a NOAC. Warfarin (brand name Coumadin) has been utilized since the 1950s  and prior to 2010 was  the only drug available for doctors to reduce clot formation in the heart and susbsequent strokes.. Warfarin is only effective and safe within a narrow window and its effects are strongly influenced by Vitamin K in the diet and most medications. Thus, frequent blood testing and adjustment in dosage is needed, and close monitoring of diet and changes in medications. Even with this close monitoring, serious and sometimes fatal bleeding occurs frequently with warfarin.

Here is a patient information sheet on warfarin which gives you an idea of issues you will need to be aware of when taking the drug. (WArfar patient handout)

If you do a Google search on warfarin you will quickly discover that it is used as a rat poison. Scientists isolate the chemical from  sweet clover that was causing cows to bleed and then developed a more potent form that they named warfarin in the 1940s. After developing blood tests that allowed the drug to be used safely  to dissolve clots it was approved for human use in the 1950s.

Warfarin or more potent variations on its chemical structure have been utilized as rat poison since the 1940s.

The rats are consuming much larger quantities of the blood thinner and are clearly not being monitored for blood thinness.

Some despicable sites peddling alternative or natural products such as this “Healthy Habits” site engage in fear-mongering over the warfarin/rat poison connection in order to promote totally unproven products. Healthy Habits indirectly suggests  that Nattokinase : is a safer, more effective natural alternative to warfarin” This remarkable enzyme has the ability to dissolve blood harmful clots involved in heart disease and strokes without upsetting normal healthy clotting.”

Such misinformation is dangerous and could lead to patients stopping a life-saving medication and suffering a stroke.

By the way, in this Xarelto (another NOAC competitor) ad, Screen Shot 2016-06-29 at 2.21.20 PMKevin Nealon says he chose Xarelto over warfarin because he wanted to eat salads. This is a common misconception and the makers of Xarelto should be ashamed for promulgating it.

I tell my patients it is fine to eat green, leafy vegetables while taking warfarin. The Vitamin K in the vegetables does influence the effectiveness of warfarin thinning blood but this is why we check the blood test to determine the appropriate dosage of warfarin for you and your personal dietary Vitamin K consumption , be it high or low.

Novel Oral Anticoagulant Drugs

The newer OACs, in contrast to warfarin do not require blood tests for monitoring of their efficacy because their levels are not significantly influenced by changes in diet or most medications.

In head to head studies versus warfarin four of these NOACs have demonstrated at least similar efficacy in preventing stroke and at most similar bleeding risk.

Due to their perceived advantages most new prescriptions for OACs are for NOACs. In contrast to 2014 American afib guidelines which don’t state a preference, the most recent European afib guidelines recommend choosing a NOAC over warfarin when initiating anticoagulant therapy in patients who are eligible for NOACs. (Ineligible patients include those with mitral stenosis, mechanical heart valves and end-stage renal disease.)

The ESC guidelines published in 2016, , make choosing a NOAC over warfarin a IA recommendation. This means there is a consensus that the treatment should be recommended (Class I recommendation) and that there is strong evidence from randomized controlled trials to support it (Level A.)

I have decided to primarily use Eliquis (apixaban) as my NOAC of choice based on my comparison of the different NOAC studies. If a patient’s insurance covers another NOAC better , making it cheaper then  I am happy to switch.

Because these four NOACs are new and brand name they are significantly more expensive than warfarin. Cost varies substantially based on type of insurance coverage and we can only determine how much a patient will pay for any given NOAC based on writing a prescription and having a pharmacy check out the cost.

I have found some patients paying nothing for their NOAC whereas some are paying several hundred dollars monthly. The more NOACs cost, the more likely the patient and I are to choose warfarin.

While waiting to determine if cost is going to be prohibitive I will typically provide the patient with samples of the NOAC chosen. The pharmaceutical companies making these NOACs are clearly making substantial profits off them and they are happy to provide lots of samples to doctors to influence the doctors to utilize their product.

NOACs are being extensively promoted both to physicians and directly to patients. Physicians have to be especially careful to make sure they are presenting a true summary of the relative risks and benefits of warfarin versus NOACs in light of these constant attempts to influence them.

Despite now having four NOACs with similar benefits and ease of use compared to warfarin, the cost of these agents doesn’t seem to have declined significantly from when the first NOAC came on the market. Personally, I would love to see Medicare step in and negotiate significantly lower costs for American senior citizens.

An abstract at the ACC meeting in March of 2017 suggested  a reduction in medical costs with NOACs despite their high costs. This was related to a lower rate of major bleeding complications: Xarelto cost $542 per patient compared with warfarin’s $500, or $42 more. Pradaxa, cost $367 to warfarin’s $452, saving $85.  Eliquis cost  $286 charge against warfarin’s $537 resulting in $251 in savings. Data were from from a study of U.S. Medicare patient records.

Aspirin May Not  Prevent Stroke In Afib

Many patients consider aspirin to be  a “blood thinner” that has some benefit in preventing clots and strokes in patients with afib. However,  aspirin is not considered a blood thinner or anticoagulant and is more properly  termed an anti-platelet agent.

I used to consider aspirin at doses of 120 to 200 mg daily provided some protection against stroke in afib and put afib patients on aspirin who were low risk for stroke or would not or could not take OACs.

More and more, however, experts are reaching the conclusion that the substantial bleeding complications from aspirin usage outweigh its very slight benefit in stroke prevention.

The most recent ESC guidelines, in fact, list aspirin therapy for stroke prevention in atrial fibrillation as IIIA. That means that overall it is felt to be harmful (III) with a high level of evidence (A.)

Bleeding risks for aspirin are similar to warfarin and Eliquis. Thus, patients should not consider aspirin as a safer alternative to prevent stroke in afib.

Finally, do not take any “natural” supplement that has been promoted as a blood thinner. These are neither safe nor effective. Remember that it took years of scientific investigation and careful testing in animals then humans before warfarin (the agent in sweet clover that caused cows to bleed ) was transformed into a safe and effective anticoagulant.

Antiemboligenically yours

-ACP

Is September Really National Atrial Fibrillation Awareness Month (And Why Does It Matter?)

The skeptical cardiologist received an email from a woman telling him that September is atrial fibrillation awareness month and offering me the free use of an infographic given that I

“care deeply about helping people living with AF.”

Well, I do care about deeply about people living with atrial fibrillation and pretty much all cardiac diseases  (except perhaps Schuckenbuss syndrome.)

That’s the major reason I write this blog. I’ve written a lot about Afib and have a lot more i want to write (I really want to write about antiarrhythmic drugs, i.e. drugs that maintain you in normal sinus rhythm.)

But I don’t find it particularly helpful to assign a disease to a month or a day so my posts on atrial fibrillation come out randomly dependent on the mysterious machinations of my messy mind.

It turns out that September, 2009 was declared National Atrial Fibrillation Awareness Month (NAFAM) by Senate Resolution 262 although Stop Afib.org wants us to believe September is eternally NAFAM.

However, the email prompted me to better organize my atrial fibrillation and stroke page (now containing all that I have written on the subjects) which I have copied below.

Posts on Diagnosing Atrial fibrillation

Take your pulse and prevent a stroke

TIAs and silent atrial fibrillation. Sometimes strokes present in unusual ways, like the inability to differentiated a spade from a diamond when playing bridge and afib is often the cause.

Estimating Stroke Risk in Patients With Atrial Fibrillation You can estimate your stroke risk using an app that utilizes the CHAD2DS2-VASc score. I prefer to call the Lip score.

Posts About Using Personal Devices To Diagnose Atrial Fibrillation

Two That Work Reasonably Well

AliveCor

Using a Smart Phone Device and App To Monitor Your Pulse for Atrial Fibrillation (AliveCor)

AliveCor Is Now Kardia and It Works Well At Identifying Atrial Fibrillation At Home And In Office

AliveCor Successes and Failures.

Sustained Atrial Fibrillation or Not: The Vagaries and Inaccuracies of AliveCor/Kardia and Computer Interpretation of ECG Rhythm

AfibAlert

How Well Does The AfibAlert Remote Hand-Held Automatic ECG Device Work For Detection of Atrial Fibrillation?

AfibAlert Versus AliveCor/Kardia: Which Mobile ECG Device Is Best At Accurately Identifying Atrial Fibrillation?

And One of Several Devices To Avoid: AF Detect

Do NOT Rely on AF Detect Smartphone App To Diagnose Atrial fibrillation

Posts About Treatment Of Atrial Fibrillation

        Lifestyle Changes

How Obesity Causes Atrial Fibrillation in FatSheep and How Losing Weight helps prevent afib from coming back.

Drug Therapy: Rate Control and Anticoagulation

Foxglove Equipoise. When William Withering began treating patients suffering from dropsy in 1775 with various preparations of the foxglove plant he wasn’t sure if he would help or hurt them. After 240 years of treatment, we are still unsure if the drug obtained from foxglove is useful.

Should Digoxin Still Be Used in Atrial Fibrillation? Recent studies suggest that we should not.

Why Does the TV Tell Me Xarelto Is A BAD Drug? Anticoagulant drugs that prevent the bad clots that cause stroke also increase bleeding risk. A bleeding complication is not a valid reason to sue the manufacturer.  The lawsuit are strictly a money-making tactic for sleazy lawyers.

Cardioversion and Ablation

Cardioversion: How Many Times Can You Shock The Heart?

Ablation: Cautionary Words From Dr. John Mandrola and The Wisdom of a Team Approach

Miscellaneous Topics

What Happens If You Go Into Atrial Fibrillation On A Cruise?

Infographics

Are infographics really helpful? Someone should do a study on that. Perhaps we could use the money we spend on infographics in atrial fibrillation to research whether the left atrial appendage should be excised at the drop of a hat.

Here’s the infographic (because everyone loves an infographic!)

The first part lays out the problem of AF with patriotic bunting.

The second part uses the annoying numerical infographic approach.

 

 

 

 

 

 

 

The third part explains why I got the email. A product is being promoted. The woman who sent me the email works for MyTherapyApp.

 

 

 

Eagerly Awaiting Schuckenbuss Syndrome Day,

-ACP

 

 

 

What Pain Medications Are Safe For My Heart?

The skeptical cardiologist is frequently asked by patients if it is OK to take certain pain medications.

Yesterday, I got a variation on this  when a patient called and indicated that he had been prescribed meloxicam and tramadol by his orthopedic surgeon for arthritic leg joint pain. The orthopedic surgeon said to check with me to see if it was OK to take either of these medications. (Patients, if you want to skip to my answer skip down to the last two sections of the post and avoid the background information.)

What Is The Risk Of Pain Medications?

Cardiologists have been concerned about the increased risk of heart attack and heart failure with non steroidal anti-inflammatory drugs (NSAIDs) since Vioxx was withdrawn from the market in 2004.

NSAIDS have long been known to increase risk of gastrointestinal (GI) bleeding  by up to 4-5 fold, Scientists developed Vioxx, a COX-2 inhibitor, hoping to reduce that risk but Vioxx  turned out to  increase the risk of heart attack.

Since this revelation it has become clear that NSAIDS in general increase the risk of heart problems as well as GI problems

This includes the two over the counter (OTC) NSAIDS:

-ibuprofen (in the US marked most commonly as Motrin or Advil, internationally known as Nurofen). For extensive list of brand names see here.

-naproxen (most commonly sold as Aleve. Per wikipedia “marketed under various brand names, including: Aleve, Accord, Anaprox, Antalgin, Apranax, Feminax Ultra, Flanax, Inza, Maxidol, Midol Extended Relief, Nalgesin, Naposin, Naprelan, Naprogesic, Naprosyn, Narocin, Pronaxen, Proxen, Soproxen, Synflex, MotriMax, and Xenobid. It is also available bundled with esomeprazole magnesium in delayed release tablets under the brand name Vimovo.)

In 2015  the FDA mandated  warning labels on all prescription NSAIDs including

1) a “black box” warning highlighting the potential for increased risk for cardiovascular  (CV) events and serious life-threatening gastrointestinal  bleeding, ulceration, and perforation;

(2) statements indicating patients with, or at risk for, CV disease and the elderly may be at greater risk, and that these reactions may increase with duration of use;

(3) a contraindication for use after coronary artery bypass graft surgery on the basis of reports with valdecoxib/parecoxib;

(4) language that the lowest dose should be used for the shortest duration possible

5) wording in the warning section that there is no evidence that the concomitant use of aspirin with NSAIDs mitigates the CV risk, but that it does increase the GI risk

Since then, hardly a day goes by without me having a discussion with a patient about what drugs they can safely take for their arthritis.

A reasonable approach to using NSAIDS, balancing GI and CV risks, that I have used in the past comes from a 2014 review
This table and many authorities recommend naproxen as the NSAID of choice for patients with high CV risk.

Indeed prior to the publication of the PRECISION study in 2016 I believed that naproxen was the safest NSAID for my cardiac patients. I told them it was OK to use from a CV standpoint but to use the least amount possible for the shortest time in order to minimize side effects.

The PRECISION study compared a COX-2 NSAID (celecoxicib or Celebrex) to ibuprofen and naproxen in patients who required NSAIDS for relief of their joint pain.

The findings:

cardiovascular death (including hemorrhagic death), nonfatal MI, or nonfatal stroke, occurred in 2.3% of celecoxib-treated patients, 2.5% of the naproxen-treated patients, and 2.7% of the ibuprofen group.

There was no placebo in this trial so we can only look at relative CV risk  of the three NSAIDS and it did not significantly differ.

GI bleeding was less with celecoxib than the other two NSAIDS.

Although this study has flaws it throws into question the greater CV safety of naproxen and suggests that all NSAIDS raise CV risk.

My Current Patient Advice on Cardiac Safety of Pain Meds

Here is an infographic I came across from the Arthritis Foundation (complete PDF….here)

It’s a reasonable approach for these OTC drugs and I will start handing this out to my patients.

We should consider that all NSAIDS have the potential for increasing the risk of heart attack and heart failure, raising blood pressure, worsening renal function and causing GI bleeding.

Therefore, if at all possible avoid NSAIDS.

Acetaminophen (Tylenol) is totally safe from a heart standpoint and overall if you don’t have liver disease it is your safest drug for arthritis. However, it provides no anti-inflammatory effects and often is inadequate at pain relief.

Treating The Whole Patient

Meloxicam is an NSAID so my patient should , if at all possible, avoid it.

The other drug he was prescribed, tramadol, is an opiod. Opiods have their own set of problems including, most importantly,  addiction and abuse.

A recent review concluded

 reliable conclusions about the effectiveness of long-term opioid therapy for chronic pain are not possible due to the paucity of research to date. Accumulating evidence supports the increased risk for serious harms associated with long-term opioid therapy, including overdose, opioid abuse, fractures, myocardial infarction, and markers of sexual dysfunction; for some harms, the risk seems to be dose-dependent.

As his cardiologist I am concerned about his heart, of course, but a good cardiologist doesn’t just focus on one organ, he looks at what his recommendations are doing to the whole person.

I certainly don’t want to have him become addicted to narcotics in order to avoid a slightly increased risk of a heart attack. On the other hand, the risks of the NSAIDS involve multiple organs, most of which don’t fall in the domain of the cardiologist.

My patient’s risk of taking either the meloxicam or the tramadol is best assessed by his primary care physician, who has the best understanding of his overall medical condition and the overall risk of dangerous side effects from these drugs.

Ultimately, I think the decision of which pain pill to take for chronic arthritis has to be made by an informed patient in discussion with his  informed (and informative) primary care physician. Only the patient can decide how much pain he is having and how much risk he/she wants to assume in relieving that pain.

Analgesically Yours,

-ACP

Death Knell For Niacin For Lipids Sounded by FDA?

The skeptical cardiologist stopped writing new prescriptions for niacin extended release tablets in 2011. For any patient who was taking niacin, I recommended stopping it.

Because niacin had favorable effects on the cholesterol profile, physicians had been utilizing it for many years in high risk patients on statins who had low HDL  (good cholesterol) and/or high triglycerides.

The rationale was that, since high HDL was associated with lower risk of heart attacks, raising the HDL would lower that risk. Similarly, lowering the triglycerides would improve cardiovascular risks.

While niacin certainly improved the cholesterol profile, there was no good evidence that starting it in a patient already on statin would improve cardiovascular outcomes. The cholesterol profile is a surrogate endpoint: the actual treatment goal is reducing cardiovascular disease.

In 2011, the AIM-HIGH study proved there was no benefit to adding niacin to good statin therapy despite increasing HDL from 35 to 42 mg/dl, lowering triglycerides and lowering LDL. This and other studies showing no benefit of niacin therapy (and worrisome adverse effects) should have resulted in the total cessation of niacin prescriptions, especially  in patients on statins.

Unfortunately, old habits die hard amongst physicians, and the allure of raising HDL and lowering triglycerides with niacin persisted despite a lack of evidence of any benefit in lowering cardiovacular risk.

Yesterday, the FDA announced it was removing from the market two  drugs made by Abbvie, Advicor and Simcor, which are combinations of extended release niacin plus lovastatin or simvastatin, and removed its approved indication for niacin ER plus statin for lowering CHD risk stating:

“Based on the collective evidence from several large cardiovascular outcome trials (Refs. 1-3), the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events. Consistent with this conclusion, FDA has determined that the benefits of niacin ER tablets and fenofibric acid DR capsules for coadministration with statins no longer outweigh the risks, and the approvals for this indication should be withdrawn.”

This is good news for patients whose physicians were keeping them on the unproven brand name combination drugs, Advicor and Simcor.

There are still legitimate uses of niacin to prevent vitamin deficiencies but If you are still taking some form of niacin ER for the purpose of preventing heart disease with or without a statin I recommend presenting your doctor with the link to the FDA pronouncement above and having a good discussion with him about the rationale for staying on it.

The other drug mentioned in the announcement, fenofibric acid,  is far less often prescribed and is not available as a combination. It is the most effective drug we have for extremely high triglyceride levels over 500 mg/dl which can cause pancreatitis. I have a few patients on the generic fenofibric acid strictly for the purpose of lowering their dangerously high triglycerides but not for the indication of lowering their cardiovascular risk.

Nonsurrogateingly Yours

-ACP

 

Atrial Fibrillation: How Many Times Can You Shock The Heart?

The most effective method for getting a heart that is in atrial fibrillation back to normal rhythm is a called an electrical cardioversion.

I’ve tried to come up with a good alternative or descriptive term for this procedure for my patients, such as “resetting” or “rebooting” the heart, but the term that seems to best resonate with patients is “shocking” the heart.

How Does Electrical  Cardioversion Work?

Typically, we all can connect (excuse the pun) to the feeling of a low current electrical shock which occurs when touching an ungrounded electrical source.

Unless the current reaches a certain level, it only results in transient burns and discomfort.

However, at current levels greater than 50 mA, an AC electrical shock traveling through the chest can, if timed properly, cause the heart to go out of normal rhythm into ventricular fibrillation.

We use a “synchronized” electrical cardioversion (termed direct current or DC cardioversion (DCC)) to convert a fibrillating or fluttering atrium back to the normal rhythm by timing the electrical shock so that it doesn’t cause ventricular fibrillation but resets both ventricles and atria safely back to normal.

cardioversionAF
Recording from a recent cardioversion I performed on a patient with recurrent atrial flutter/fibrillation associated with heart failure. On the left is the heart rhythm before the shock, and on the right we can see resumption of normal sinus rhythm. The little squiggles labeled p waves represent the electrical activity of the sinus node preceding the big vertical deflections, which represent the electrical activity of the ventricles (QRS). The circled little arrow shows the timing of the shock concurrent with the QRS complexes. If the timing is not correct, the shock can cause ventricular fibrillation.

This may seem like a barbaric and unnecessarily crude and dramatic way to restore normal rhythm, but if patients are properly prepared for this procedure, it is very safe and very effective, resulting in resumption of the normal rhythm 99% of the time.

There are some medications that we can utilize to convert atrial fibrillation (afib) back to normal (antiarrhythmic drugs), but they are far less effective than the electrical cardioversion, and often can bring out more dangerous heart rhythms.

Typically, I do my cardioversions in conjunction with an anesthesiologist, who administers IV propofol (yes, this was Michael Jackson’s sleep aid, his “milk”) to obtain “deep  sedation.” At this level of anesthesia, the patient is breathing on his own but will only respond to painful stimulation. The propofol is short-acting and prevents the patient from feeling the intense pain of the cardioversion (often described as like a mule kicking one in the chest), and from recalling any of the events.

Electrical cadioversion
The skeptical cardiologist calmly prepares to push the “shock” button that will trigger the Zoll device to deliver 150 Joules of biphasic direct current to the electrodes attached to his patient’s chest thereby “ZAPPING” her back to NSR. Should the patient’s heart rhythm be too slow, the Zoll device also can serve as an external pacemaker, triggering cardiac contractions via lower level electrical currents delivered through the chest electrodes.

The electrical shock is administered through electrodes, consisting of large sticky pads with electrical conducting gel attached to the right anterior chest and the left posterior back (see this brief information from Zoll about optimal placement).
Since I began using “biphasic” energy, the initial cardioversion is successful >95% of the time in my experience, but the heart may revert back to atrial fibrillation anywhere from a few minutes to a few years after the shock. We can reduce the chances of reverting back by the use of anti-arrhythmic drugs.

Multiple Shocks: What Is The Limit?

The DCC may need to be repeated, and we may repeat it after starting one of those anti-arrhythmic drugs I mentioned, in order to increase the time that the heart stays in the normal rhythm.

A common question when I recommend a repeat cardioversion is:

“Doc, how many times can you have your heart shocked?”

One might think it is one and done with the shock but it is not a cure; it is merely a resetting of the chaotic, confused and futile activity of the atria, so that the synchronized and regular electrical pacing provided by the sinus node in the upper right atrium can again resume its rightful role as conductor of the cardiac electrical orchestra that creates the wondrous symphony of normal cardiac contraction.

The factors that brought on the afib in the first place likely are still present: if we don’t address correctable factors we are less likely to maintain the normal sinus rhythm (NSR). Correctable factors include:

  • abnormal thyroid function
  • abnormal potassium or magnesium
  • inflammation of adjacent lung or pericardium
  • severe infection
  • obesity (see my post on fat sheep and afib)
  • certain cardiac valve problems

There is no evidence that the cardioversion per se damages the heart in any way. The major risks of the procedure (again, assuming proper preparation, see below) are related to the anesthesia.

I am more inclined to recommend a repeat cardioversion if there is clear-cut evidence that the patient does poorly when the heart is in afib.

Why Shock The Heart?

In medicine, there are two reasons for giving medications and doing surgery/procedures: to make the patient feel better or to reduce the chances of dying/having a major complication.

The major complication of afib is stroke.  Proper anticoagulation is required to prevent this in patients with afib whether or not they are in normal rhythm.  Clots can form in the left atrial appendage within hours of the development of afib, and the electrical cardioversion can increase the chance of stroke as any clot present is more likely to be expelled when the quivering, ineffective atrium converts back to a normally pumping, vigorous  atrium.

Primarily, then, we utilize cardioversion for the purpose of making patients feel better.

Some patients feel terrible the moment they go into afib: symptoms of palpitations, chest pain, or shortness of breath predominate and are especially prominent if the heart rate is high. Controlling the high heart rate with beta-blockers or diltiazem will reduce many of these symptoms, but I have a large number of patients who still feel terrible when they are “out of rhythm,” even if the heart rate is normal. Such patients who persist in afib are good candidates for one or multiple cardioversions, with or without the addition of anti-arrhythmic drugs.

A second group of patients, I think, benefits the most from maintaining sinus rhythm (rhythm control strategy): patients who develop heart failure when they go into AF.

These patients may not even know they are in AF because they don’t feel the typical symptoms initially.  After a few days or weeks or months of being in afib silently, however, they develop shortness of breath, weakness and leg  swelling – classic signs of heart failure.

When we look at the heart of such a patient by echocardiography, we often find one of two things causing the heart failure: a weakening of the heart muscle (cardiomyopathy) or significant leakage/backflow from the mitral valve (mitral regurgitation). Following cardioversion and maintenance of SR for weeks to months, the heart muscle strengthens back to normal and/or the mitral regurgitation improves dramatically and the heart failure resolves.

Multiple Shocks: Rationale

Yesterday I did an electrical cardioversion on an elderly patient of mine  for atrial fibrillation/flutter; this was her fifth DCC in the last year.

She falls into the second category of afib patients; she had developed severe heart failure due to mitral regurgitation after silently going into afib a year earlier. After long-term loading on the anti-arrhythmic drug amiodarone, followed by her fourth cardioversion, she had stayed in NSR for 10 months, her MR resolved, and she felt great. In patients like her, I think it is particularly important to maintain NSR and thus, multiple shocks are definitely warranted.

On the other hand, if you feel fine in afib without any evidence that it is effecting your heart muscle or valves, then it is hard to justify multiple attempts to shock the heart.

Any patient that has recurrent symptomatic afib or afib associated with heart failure, should be considered a candidate for an atrial fibrillation ablation.  The risks and benefits of afib ablation are worthy of another blog post, but the patient-centered afib website stopafib.org has a reasonable discussion here. Suffice it to say, it is a much more complicated and risky procedure than a cardioversion, but it attempts to address the underlying cause(s) of afib, and in some cases creates what could be considered a “cure.”

Cardiovertly Yours,

-ACP

For additional reading:

Here’s a good article from the European Society of Cardiology on cardioversion (https://www.escardio.org/Guidelines-&-Education/Journals-and-publications/ESC-journals-family/E-journal-of-Cardiology-Practice/Volume-11/Cardioversion-in-Atrial-Fibrillation-Described)

and check out what Dr. John Mandrola, an electrophyiologist (cardiologist who specializes in electrical problems of the heart) has to say about afib ablations at Drjohnm.org (http://www.drjohnm.org/2015/09/a-cautionary-note-on-af-ablation-in-2015/)

Credits-Life Coach of the Skeptical Cardiologist (LCOSC) for review of electrical engineering stuff.

 

 

 

Is Green Tea Better For Your Heart Than Black Tea?

Coffee is the  caffeinated beverage most consumed by Americans and the skeptical cardiologist. It is good for the heart (unless adulterated by titanium dioxide or lots of sugar, a horror that Starbucks likes to promote).

coffee_teaWorldwide, however, as this cool graphic demonstrates (interactive at the Economist)  tea dominates over coffee in lots of places.

Tea in general and particularly green tea is perceived by many to be incredibly healthy: fighting cancer, dementia, obesity and heart disease. But is this perception justified?

The Green Tea Superfood Hype

If you Google search the health benefits of green tea you might conclude that it is a panacea for all that ails modern civilization. However, bad nutritional advice is the norm on the internet and even  websites like Web MD, which you might consider to be reliable, spread inaccurate, misleading and poorly researched information regularly.

WebMD has an article on green tea that starts off

“Green tea is so good for you that it’s even got some researchers raving.“It’s the healthiest thing I can think of to drink,” says Christopher Ochner, PhD. He’s a research scientist in nutrition at the Icahn School of Medicine at Mount Sinai Hospital.”

Who is Chris Ochner and why is he “raving” about the health benefits of green tea you might ask? That’s certainly what I wanted to know, particularly since this same quote or variations on it are all over the internet on sites like “Herbal Republic” which ups the green tea ante with the title “”Green Tea is Beyond a Superfood”-Dr. Christopher Ochner”  (by the way, any source of nutritional information that uses the term superfood should be considered bogus.)

ochnerAlthough no source is provided for this quote from Dr. Ochner, there is a Christopher Ochner, Ph.D listed on the Icahn Medical School Staff. His Ph. D. is in psychology and he works in the areas of adolescent obesity (perhaps he pushes green tea on his obese adolescents).  I can find no publications by him on the topic of green tea and no evidence that he made these comments. I have sent him an email asking for clarification and edification.

The website,  juicing for health.com lists “5 scientifically proven reasons to drink green tea” (by the way, I consider articles with headlines that start with a number, i.e.  “3 health foods that are actually killing you from the inside”,  “5 veggies that kill stomach fat”, and “35 celebs who’ve aged horribly” are worthless and should be ignored and avoided at all costs)

Green Tea and Catechins: Magical Weight Loss elixir?

It’s hard to find good studies on green tea that aren’t somehow funded by the tea, nutraceutical or food industry.  For example, one “S Wolfram” has written extensively on the benefits of green tea in marginal scientific journals. He works for DSM Nutritional Products, LTd., a Swiss food conglomerate.(“DSM Nutritional Products is the world’s largest nutritional ingredient supplier to producers of foods, beverages, dietary supplements, feed and personal care products” says one DSM PR release”).

DSM developed a highly concentrated extract of  a catechin called Epigallocatechin Gallate (EGCG) in green tea that had been identified as having potential health benefits for humans.

In one recent “review” Wolfram wrote  in somewhat vague but highly optimistic terms

“Dose-response relationships observed in several epidemiological studies have indicated that pronounced cardiovascular and metabolic health benefits can be obtained by regular consumption of 5-6 or more cups of green tea per day. Furthermore, intervention studies using similar amounts of green tea, containing 200-300 mg of EGCG, have demonstrated its usefulness for maintaining cardiovascular and metabolic health. Additionally, there are numerous in vivo studies demonstrating that green tea and EGCG exert cardiovascular and metabolic benefits in these model systems.”

I’m not sure what “model systems” he is referring to but it is certainly not humans. He may be talking about rodents, because in 2005  Wolfram published  a paper entitled:

“TEAVIGO (epigallocatechin gallate) supplementation prevents obesity in rodents by reducing adipose tissue mass”

In the conclusions of this “landmark” study performed in mice and rats he wrote

“Thus, dietary supplementation with EGCG should be considered as a valuable natural treatment option for obesity.”

Voila! From a few experiments in rodents and a few short-term, small studies in humans performed by heavily biased scientists, DSM’s version of EGCG emerged as a leading nutraceutical (I prefer the term, snakeoil) and now you can buy this online from a host of bogus supplement/nutraceutical sites as Teavigo.

The production and marketing of TeaVigo is a classic example of how the cynical food/supplement/nutraceutical industry creates a product that has a thin veneer of scientific credibility for health promotion but is considered “natural” (despite being manufactured)

teavigo
It’s Really Pure…. and Really Useless!

and therefore appeals to Americans who are seeking “natural” ways to prevent or treat the common  chronic  diseases of Western civilization.

Because there is no good scientific evidence supporting a role for green tea extracts or ECGC in preventing any specific disease, there is no FDA scrutiny of

Screen Shot 2015-12-27 at 7.51.35 AM
Teavigo: Good for everything that ails you plus can be put in anything you would like to consume and spread on your face! The perfect nutraceutical!

the drug for efficacy and safety. This is fine for nutraceutical manufacturers as they have been granted the ability to  sell their useless products without any regulatory or FDA approval.

Companies like DSM avoid making any specific health claims for their supplements (such as this drug reduces your chances of having a heart attack or stroke) because the FDA can then go after them.
Instead, the Teavigo website makes vague but optimistic statements such as
“Green tea has long been used for health benefits and Teavigo® is the purest and most natural form of the most active substance in green tea – Epigallocatechin Gallate (EGCG). EGCG contains potent natural antioxidants and efficient free-radical scavengers (free radicals being the highly reactive compounds that cause cellular damage).
Notice the key marketing buzzwords in this statement
-Purest
-Natural
-Active
-Antioxidants
-Efficient
-Free-Radical Scavengers
-Cellular Damage
Who wouldn’t want to take a pill that is pure and natural and full of those wonderful antioxidants that stop those nasty free-radicals  from causing cellular damage?
Unfortunately, any time a proposed powerful “anti-oxidant” ( b-carotene, vitamin E, vitamin C, selenium, retinol, zinc, riboflavin, and molybdenum ) has been studied in a well done scientific trial for prevention of cancer or cardiovascular disease it has failed.
We don’ know if this is because the wrong anti-oxidants have  been chosen (for example in green tea  there are hundreds of potential beneficial chemicals)  or because extracting a single chemical from its milieu in a complex food/beverage makes it inactive or if the whole idea of stopping free-radical damage is misguided.
Why take the time to actually brew and drink green tea the website points out after all:
“To get the optimal benefits from ordinary green tea would take an intake of four to eight cups of green tea a day. With Teavigo® you get the same pure, natural and healthy effects, with more convenience and without the caffeine.”
Finally, consumers of Teavigo can be reassured because it is produced using
“A patented and unique production process with constant product quality”
Let me see here, Teavigo is natural but it is made by a “production process” with “constant product quality”.  Isn’t natural production process an oxymoron?
I have asked the Teavigo people to tell me their “production process” but so far I’ve gotten no response. Your guess is as good as mine as to what chemicals or other potentially damaging processes tea undergoes to reach the colorless and tasteless powder that is Teavigo.
 Green Tea Reality

The evidence supporting tea and green tea health benefits  is weak, coming from observational studies.  A recent review of all these observational studies (supported in part by the tea industry) concluded that

Although the evidence appears to be stronger for green tea than for black tea, which differ greatly in their flavonoid profiles, it is difficult to compare this evidence because the populations and their baseline risks of cardiovascular disease differ greatly between the individual studies on these 2 types of tea, and few studies of green tea provide evidence in non-Asian populations.

Whereas there is reasonable observational evidence that high tea consumption is associated with lower cardiovascular risk, the evidence for green tea being healthier is mostly marketing hype.

If you like green tea by all means drink it in whatever quantity you desire. It’s not bad for you. Weak observational data suggests it may reduce your stroke risk, especially if you are Asian.
On the other hand, if you like black tea or oolong tea you can feel very comfortable that it is not bad for you.  It might also reduce your risk of stroke.
There is nothing to suggest tea is healthier than coffee.
Don’t add sugar or titanium dioxide to your tea but feel free to add cream or full fat milk.
Don’t worry about caffeine unless it makes you jittery or brings on palpitations. Common sense should tell you what amount you can tolerate.
Please don’t buy or consume green tea extracts or Teavigo or any other nutraceutical.
The makers of these products are cynically preying on consumer desire for “natural” treatments, selling chemicals which have not been proven either safe or effective, and employing  misleading marketing and promotional material that implies “scientific” support that is either nonexistent or comes from very weak studies, often run by researchers employed by the industry.
 I guarantea this post was unbiased
-ACP

 

Doctor, My Cholesterol Levels Are Good. Why are You Starting a Statin?

I get this question frequently from patients.

It is a reasonable question. If statins are a treatment for abnormally high cholesterol levels why would we start them on a patient with normal or low levels.

ather_lowresThe answer is that we are not concerned with cholesterol levels. What we are concerned with is atherosclerotic cardiovascular disease (ASCVD) and its downstream consequences including heart attack and stroke.

Thus, the new guidelines recommend  calculating a patient’s 10 year risk of heart attack and stroke due to ASCVD ( see here for my discussion of smart phone app that makes this calculation) and if it is over 7.5% to consider starting a statin drug to reduce ASCVD risk.

Cholesterol is just one of many factors that effect the risk but we know that irrespective of cholesterol level, starting a statin will substantially lower the risk.

A patient  who has smoked   cigarettes lifelong  asked me this question recently.

When I plugged the patient’s excellent cholesterol values into the ASCVD app, the 10 year risk of heart attack or stroke was quite high, 14.9%. Bad cholesterol  (LDL) was 90, well below what is considered optimal. Good cholesterol (HDL) was 60, well above what is considered optimal.

Studies have demonstrated that even patients with cholesterol numbers this good benefit from statin therapy. Their risk of heart attack and stroke will be substantially reduced over time.

My patient has not yet had a heart attack or stroke and it is likely that despite engaging in the extremely damaging behavior of cigarette smoking , the genetically programmed excellent cholesterol values have somewhat protected from ASCVD.

However, a vascular screening study has demonstrated  that  early atherosclerotic plaque in both the patients carotids. The patient has ASCVD and it is only a matter of time if the patient keeps smoking before the patient  has a clinical event related to it.

I told my patient that if he/she stopped smoking cigarettes his/her estimated 10 year risk would drop to 9.7% and I would not recommend statin therapy.

We discussed methods to help quit and the patient indicated that the patient would start  using a nicotine patch and try to quit in the next few months.

Unfortunately, at follow up smoking was ongoing.

Thus, my recommendation to start statin therapy despite her excellent cholesterol values.

Other groups of patients besides cigarette smokers can have advanced or premature ASCVD with excellent or “normal” cholesterol values. Diabetics often have low bad cholesterol values associated with low good cholesterol and high triglycerides.

Sometimes, ASCVD develops prematurely even in patients who have a low 10 year risk based on standard risk factors. This is usually in patients with a strong family history of ASCVD who have an inherited atherogenic abnormality of lipid metabolism that is not manifested in the standard cholesterol parameters (see Dealing With the Cardiovascular Cards You’ve Been Dealt).

To identify these patients a search for subclinical atherosclerosis by vascular screening or coronary calcium scan is necessary. When advanced plaque is identified statin therapy is often warranted even with a low estimated 10 year risk and normal cholesterol values.

So some patients can have very high cholesterol values and I don’t recommend any therapy, some have low and I do. I’m much more focused on the presence or absence of ASCVD in my treatment decisions.

Ultimately we are not treating “high cholesterol” when we start cholesterol lowering therapy we are working to prevent or slow the progression of ASCVD,

-atherosclerosis is still my psychosis

-ACP

 

 

 

Stroke Risk Estimation in Atrial Fibrillation: Please Give Me Lip!

The best way we have of estimating a patient’s risk of stroke if they have atrial fibrillation (AF) is by the CHA2DS2-VASc scale.

Stroke Risk EstimationThis scale take the factors we know that increase the risk of stroke and assigns 1 or 2 points. The acronym comes from the first letter of the factors that are known to increase risk as listed to the left.

Most of the factors get 1 point, but prior stroke (S) and age>75 (A) get 2 points.

We then add up your points and use another chart (or app) to calculate the risk of stroke per year.

CHA2 stroke riskYour risk of stroke is very low if you have zero risk factor; it gets progressively higher as you reach the maximum number of 9.

Treatment with an oral anticoagulant (OAC),  either warfarin, or one of the four newer anticoagulant agents (NOACS), is recommended when the risk gets above 1-2% per year.

The higher the risk, the more the benefit of these blood thinners in preventing stroke.

In lower risk patients, the bleeding risk of OAC of 1% per year may outweigh the benefits conferred by stroke reduction.

Both European and American guidelines recommend using the CHA2DS2-VASc score for initial risk stratification. The European  guideline recommends OAC therapy for males with a CHA2DS2-VASc score ≥1 and for female patients with a score ≥2., whereas the American guideline recommends use of OAC if the CHA2DS2-VASc  score is ≥2 for men and women.

I’ve been using the CHA2DS2-VASc scale for several years in my AF patients. I try to review the patient’s risk of stroke and their risk of bleeding during every office visit, and decide whether they should be on or off an OAC.

Initially, it was helpful typing all those capital letters and number twos (although I never took the time to make the twos a subscript) because it helped remind me of the factors.

However, I now view this acronym as a big pain in the neck and I am sick of typing it into my electronic medical records. It is also, really hard to say. Do you say “chad -two-D-S-two-vasc?” That is six syllables! I could have told my patient that warfarin is rat poison during that time.

And, what is with the Sc? Sex category? Why not just an S?

An Easier Term For The Stroke Risk Estimator: The Lip Score

I would like to formally request that this be termed the Lip stroke risk score in honor of Dr. GregoryLip,Greg-Cropped-110x146 Y. H. Lip who developed it at the University of Birmingham (UK).

because (per his bio): 

“The CHA2DS2-VASc and HAS-BLED scores for assessing stroke and bleeding risk, respectively were first proposed and independently validated following his research, and are now incorporated into major international management guidelines.”

birminghamIf the Lip score should somehow be unacceptable, then let’s go with the Birmingham score (recognizing, of course, that this is Birmingham, England and not Birmingham, Alabama). After all, this is what the app I use terms itself and I can type Birmingham a lot faster than CHA2DS2-VASc (even without the subscripts).

The Lip Score will be a great advance in the world of stroke risk estimation for AF patients. It will make all of us doctors creating EMR notes much more efficient, shaving precious minutes off the work day. It will be easier to communicate to patients, medical students and other medical personnel.

Finally, it gives, credit where credit is due, to Dr. Lip, who, according to his bio: “In January 2014, was ranked by Expertscape as the world’s leading expert in the understanding and treatment of AF,”

(I have no knowledge of Expertscape but you can be sure I will be investigating them soon)

Giving Lip service to stroke and atrial fibrillation,

ACP

Nuts, Legumes, Drupes and Mortality

When I was a child in small town Oklahoma, I collapsed walking home from school one day after eating pecans. Apparently I had never encountered pecans in England where I grew up and I had a very severe, life-threatening  allergic reaction (anaphylaxis.)

My pediatrician was promptly called, drove over, picked me out of the street and (legend has it) with one hand on the steering wheel and the other jabbing me with epinephrine drove me to the local hospital (apparently ambulances were not invented at this time). There I spent several days in an oxygen tent recuperating.

Since then I had, until recently,  concluded (based on my own multiple food reactions and research) that I was allergic to “tree nuts.”

I would patiently explain to the uninitiated that I could eat almonds because they are in the peach family and I could eat peanuts because they are in the legume family: neither one of these, therefore, were true “tree nuts.”

To all whom I gave this seemingly erudite explanation I owe an apology for I have learned the earth-shattering truth that pecans are drupes! They are no more a nut than an almond is!

In fact, even walnuts are not nuts as hard as that is to believe.

Pecans, walnuts and almonds are all drupes.

Why, you may wonder, is any of this botanical folderol of any relevance to cardiology?

Nuts and Cardiovascular Death

For those paying attention to media reports on the latest food that will either kill you or make you live for ever you may already know the answer. This paper published in JAMA made big headlines.

Jane Brody of the New York Times wrote a piece extolling the virtues of nuts entitled “Nuts are a Nutritional Powerhouse”. Medical New Today wrote “Eating Nuts Linked to 20% Cut in Death Rates”.

It turns out, however, that most of what the 136,000 Chinese were eating and half of  the “nuts” the 85,000 low income Americans were eating in that JAMA study  were legumes: peanuts or peanut butter. The authors wrote:

“Our findings … raise the possibility that a diet including peanuts may offer some CVD (cardiovascular)  protection. We cannot, however, make etiologic inferences from these observational data, especially with the lack of a clear dose-response trend in many of the analyses. Nevertheless, the findings highlight a substantive public health impact of nut/peanut consumption in lowering CVD mortality, given the affordability of peanuts to individuals from all [socioeconomic status] backgrounds.”

These findings follow another large observational study published in 2013 which also found (in American doctors and nurses) an inverse relationship between nut consumption and mortality.

“compared with participants who did not eat nuts, those who consumed nuts seven or more times per week had a 20% lower death rate. Inverse associations were observed for most major causes of death, including heart disease, cancer, and respiratory diseases. Results were similar for peanuts and tree nuts, and the inverse association persisted across all subgroups.”

We also have a very good randomized trial (the PREDIMED study) that showed that  the Mediterranean diet plus supplementation with extra-virgin olive oil or mixed nuts performed much better than a control diet in reducing cardiovascular events.

Participants in the two Mediterranean-diet groups received either extra-virgin olive oil (approximately 1 liter per week) or 30 g of mixed nuts per day (15 g of walnuts, 7.5 g of hazelnuts, and 7.5 g of almonds) at no cost, and those in the control group received small nonfood gifts (I wonder what these were?)

After 5 years, those on the Med diet had about a 30% lower rate of heart attack, stroke or cardiovascular death.

Nuts versus Drupes versus Legumes

The evidence supporting “nut” consumption as a major part of a heart healthy diet is pretty overwhelming. But what is a nut and which nuts or nut-like foods qualify?

Let’s lay out the basic definitions:

Nut-Generally has a hard outer shell that stays tightly shut until cracked open revealing a single fruit inside. Examples are hazelnuts and acorns.

Drupe-Has a soft, fleshy exterior surrounding a hard nut. Classic drupes are peaches and plums with interior nuts so hard we won’t eat them. Examples are pecans, almonds, walnuts and coconuts.

Legume-generally has a pod with multiple fruit which splits open when ready. Examples are peas, carob, peanuts, soybeans and beans.

What Nuts Were Consumed in Studies Showing Benefits of Nuts?

Initially participants were given a questionnaire and asked

” how often they had consumed a serving of nuts (serving size, 28 g [1 oz]) during the preceding year: never or almost never, one to three times a month, once a week, two to four times a week, five or six times a week, once a day, two or three times a day, four to six times a day, or more than six times a day.”

After initial surveys, the questionnaires split out peanut consumption from “tree nut” consumption and whether you ate peanuts or nuts the benefits were similar.

Thus, for the most part, participants were left to their own devices to define what a nut is.  Since most people don’t know what a true nut is, they could have been eating anything from almonds (drupe related to peaches) to hazelnuts (true nut) to a pistachio “nut” (drupe) to a pine “nut” (nutlike gymnosperm seed).

Nutrient Content of Nuts

The nutrient components of these nuts varies widely but one consistency is a very high fat content. For this reason, in the dark days when fat was considered harmful, nuts were shunned.

However, in our more enlightened era we now know that fat does not cause heart disease or make you fat.

Please repeat after me “Fat does not cause heart disease or make you fat.”

A one ounce portion of pecans contains 20.4 grams of fat (11.6 arms monounsaturated and 6.1 polyunsaturated) so that 90% of its 204 calories come from fat.

Nuts, of course, also contain numerous other biologically active compounds that all interact and participate in the overall  beneficial effects that they have on cardiovascular disease and mortality.

They are a whole, real food which can be eaten intact without processing and these are the foods we now recognize provide the best choices in our diets, irrespective of fat or carbohydrate content.

They are also convenient, as they are easy to store and carry with you, providing a perfect snack.

If You Think It’s A Nut, It’s A Nut

IMG_3567

Hazelnut Death Experiment (Don’t try this at home!) A single hazelnut was partitioned into halves, quarters, slivers and little tiny bits. Progressively larger portions were consumed at 5 minute intervals. An Epipen (right) was available in case of anaphylaxis.

It turns out, that my attempts to put pecans and walnuts in to a specific family of nuts that increased my risk of dying if I consumed them were misguided.

I’m allergic to drupes.

In fact, I did an experiment recently and consumed a true nut (a hazelnut) and found I had no reaction.

I’m not allergic to nuts!!!

In the world of allergic reactions, thus,  there is no particular value to partitioning nuts from drupes from legumes.

Similarly, for heart healthy diets, it doesn’t matter if you are consuming a true nut or a drupe as long as you think of it as a nut.

Consume them without concern about the fat content and consume them daily and as along you are not allergic to them they will prolong your life.

Skeptically Yours,
-ACP

 

 

 

Why Does The TV Tell Me Xarelto is a BAD DRUG?

One of my patients called the office today concerned about a medication she was taking because she was “seeing about 4-5 commercials a day about how bad Xarelto is”.

She is the latest of many of my patients who have been inundated with ads like these which state in very strident tones that a drug is bad and that if “you or a loved one has had a serious bleeding problem” contact 1-800-BAD DRUG and see if you are eligible for compensation.

These drugs are not bad and the only reason these advertisements are being played is that tort lawyers sense an opportunity to make money.

To understand why they are flooding the TV market now I will have to give you some background on atrial fibrillation , stroke and the drugs available to reduce stroke risk.

Preventing Stroke Associated With Atrial Fibrillation

Patients with atrial fibrillation are at increased risk of stroke and since the 1950s the only drug available for doctors to reduce clot formation in the heart and susbsequent strokes was warfarin (brand name Coumadin). Warfarin is only effective and safe within a narrow window and its effects are strongly influenced by Vitamin K in the diet and most medications. Thus, frequent blood testing is needed, and close monitoring of diet and changes in medications. Even with this close monitoring, serious and sometimes fatal bleeding occurs frequently with warfarin.

Novel Anticoagulants

In recent years, three new drugs for reducing strokes in patients with atrial fibrillation which are much less influenced by diet and medications have gained approval from the FDA. These are generally referred to as “novel anticoagulants” reflecting their newness, different effects from warfarin or aspirin, and their blood thinning properties.  The first  (brand name Pradaxa) was released to much excitement and fanfare in October, 2010.  The press release for this approval read as follows:

PRADAXA, an oral direct thrombin inhibitor2 that was discovered and developed by Boehringer Ingelheim, is the first new oral anticoagulant approved in the U.S. in more than 50 years. As demonstrated in the RE-LY® trial, PRADAXA 150mg taken twice daily has been shown to significantly reduce stroke and systemic embolism by 35 percent beyond the reduction achieved with warfarin, the current standard of care for patients with non-valvular atrial fibrillation. PRADAXA 150mg taken twice daily significantly reduced both ischemic and hemorrhagic strokes compared to warfarin

Differences Between Warfarin and the Novel Anticoagulants

What was very clear from the study with Pradaxa  and stated very clearly in all publications and patient and doctor  information sources was that just like warfarin, patients could have severe bleeding complications, sometimes fatal. Overall serious bleeding complications were about the same (the rate of major bleeding in patients Pradaxa  in the RE-LY trial was 3.1% versus 3.4% in the warfarin group) but Pradaxa had about 50% more bleeding from the gastrointestinal tract and warfarin about 50% more bleeding into the brain.

Another big difference between the novel anticoagulants and warfarin is that we have antidotes (Vitamin K, fresh frozen plasma) that can reverse the anticoagulation state rapidly for warfarin but none for the newer drugs. This information also was made very clear to all doctors prescribing the medications in the package insert and educational talks. Despite this, in the major trials comparing these newer agents to warfarin, the newer agents were as safe or safer than warfarin.

The Pradaxa Bad Drug Ads

Beginning about a  year after Pradaxa was released advertisements paid for by law firms seeking “victims” of Pradaxa  identical to the ones we are now seeing for Xarelto began to appear.

The Pradaxa ads went away in mid 2014 when these lawsuits were settled and almost immediately the lawyers began paying for Xarelto ads. Xarelto was the second “novel anticoagulant) to be approved by the FDA and, similar to Pradaxa, was proven to as effective as warfarin in preventing strokes with a similar rate of serious bleeding complications.

As the Wall Street Journal noted (with the catchy title “The Clot Thickens” and opening line “Is a blood thinner causing lawyers to smell blood?”)

“Spending (on Xarelto ads)  jumped to $1.2 million in July from just $8,000 in June, according to The Silverstein Group Mass Tort Ad Watch, which noted the number of ads that ran in July exceeded 1,800. …

The spending increased shortly after Boehringer Ingelheim, which sells a rival blood thinner called Pradaxa, last May agreed to pay $650 million to settle about 4,000 lawsuits over claims the drug caused serious bleeding episodes. The settlement likely emboldened attorneys to turn their sights toward Xarelto which, like Pradaxa, is one of a relatively new batch of blood thinners.”

The third drug to be approved for preventing strokes in atrial fibrillation was Eliquis. Data from the large, randomized study comparing it to warfarin suggest that it is more effective at preventing stroke than warfarin and significantly less likely to have bleeding complications. However, I predict that within the year (especially if the Xarelto lawsuits also are settled by its manufacturer) we will start to see lots of TV ads telling us that Eliquis is a BAD DRUG.

It’s important to remember that all drugs have benefits and side effects. Seemingly harmless antibiotics can increase your risk of dying suddenly (see here), rupturing your achilles tendon or developing a life-threatening colitis.

Xarelto is not a BAD DRUG. When prescribed to appropriate patients with atrial fibrillation with  appropriate precautions it prevents strokes which are potentially life-threatening or disabling. All blood thinners are two-edged swords: they stop good clots and bad clots.

Ignore The Ads

Patients are better off ignoring both positive, direct to consumer, advertisements, promoting these newer anticoagulants and negative, greedy-lawyer sponsored advertisements, soliciting “victims”.

Hopefully when your doctor discusses the choices of blood thinners with you he will present to you a balanced discussion of the pros and cons both of whether or not to take  a blood thinner and whether to take the old standby warfarin or one of the newer agents. An interactive discussion should follow in which your particular issues and concerns factor into the final decision.