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Thoughts On Prolonged Bleeding Whilst Taking Baby Aspirin

I was hurriedly shaving the other day and felt a sharp stinging sensation in my philtrum.  Shortly thereafter, blood began pouring forth from the area and dribbling into my mouth.

I don’t typically name-check the area between the nose and the margin of the upper lip, but if one cuts the area (and wants to write about the experience), it is useful to have a single noun that describes it precisely.

This is not my philtrum but the graphic nicely demonstrates why the area is often called “cupid’s bow”. Courtesy of Wkipedia

The human philtrum is apparently vestigial; per Wikipedia

The philtrum (Latin: philtrum, Greek: φίλτρονphiltron, lit. “love charm”[2]), or medial cleft, is a vertical groove in the middle area of the upper lip, common to many mammals, extending in humans from the nasal septum to the tubercle of the upper lip. Together with a glandular rhinarium and slit-like nostrils, it is believed[by whom?] to constitute the primitive condition for mammals in general.

Although lacking function, it does cause a protrusion in the otherwise smooth facade of the face, and as a consequence, is at an increased risk for cuts.

Despite holding pressure on the cut for many minutes and daubing it with toilet paper, it continued to bleed. The bleeding continued on for much longer than I am use to, and after a while I realized that my bleeding was prolonged due to the aspirin I have been taking.

I’ve been following my own advice to those with documented significant atherosclerotic plaque, and have been taking 81mg aspirin daily. I began chewing daily my chewable aspirin after writing my post on the best form of baby aspirin to take. Prior to that it was only intermittently.

BARCing Up the Willow Tree

As a cardiologist I commonly hear patients complain about the nuisance of bruising and bleeding caused by the aspirin and other blood thinners I have prescribed them. Now I had joined their ranks.

Doctors mostly worry about major bleeding caused by aspirin; things like bleeding from the gastrointestinal (GI) tract, or into the head. A recent review found that baby aspirin doubles the risk of bleeding from the upper GI tract, and increases the risk of intracranial hemorrhage by a factor of 1.4.

There is relatively little concern about the type of minor bleeding I experienced. However, beginning in 2010, the Bleeding Academic Research Consortium (BARC) investigators came up with a more precise way of categorizing bleeding events, the BARC bleeding types.

By far, the most common bleeding on aspirin is the kind I had: Type 1 BARC.

Type 1: bleeding that is not actionable and does not cause the patient to seek unscheduled performance of studies, hospitalization, or treatment by a healthcare professional. Examples include, but are not limited to, bruising, hematoma, nosebleeds, or hemorrhoidal bleeding for which the patient does not seek medical attention. Type 1 bleeding may include episodes that lead to discontinuation of medications by the patient because of bleeding without visiting a healthcare provider.

Indeed, my Type 1 bleeding prompted me to skip my aspirin doses for the next few days.

Many patients do the same thing. Just this morning a patient told she had stopped taking her aspirin because she thought it was causing “little red spots” on her arms.

Does Prolonged Bleeding Mean You Are Taking Too Much Aspirin?

My philtrum persisted in bleeding, and as I felt the need to use my hands for something other than holding pressure, I put a band-aid on the area (actually a Nexcare), which temporarily stemmed the bleeding tide: I began pondering if I was taking too much aspirin.

Since aspirin is so widely used to prevent heart attacks and strokes caused by sticky platelets, why isn’t there a way to see how effective it is at making sticky platelets less sticky?  We have such methods for blood pressure meds (blood pressure levels) and cholesterol lowering drugs (cholesterol levels).

And for the older blood thinner warfarin, we have a blood test which helps us make sure the dosage of medication is keeping the blood thinning in a range that maximizes  effectiveness and minimizes bleeding risk.

It turns out there are lots of ways to measure how effective aspirin is in an individual, but no consensus on which particular method should be used, and authorities don’t recommend we make such measurements.

This article on platelet function tests lists 13 different platelet function tests, ranging from the mostly historical “bleeding time” to sophisticated tests of platelet aggregation.

The  Verify Now test (not available in the US) of platelet reactivity predicted in one study which patients would have BARC type I bleeding like mine.  The test did not predict major bleeding complications, things like GI bleeding and intracranial hemorrhage.

Those patients who had minor bleeding problems were more likely to be noncompliant, stopping their aspirin therapy.

I could easily visualize the following  scenario as the blood began pooling underneath my band-aid and progressing down my philtrum.

Let’s say I’ve just had a heart attack and had a drug-eluting stent placed in one of my coronary arteries. I’ve been started on aspirin and another anti-platelet drug. I cut myself and bleed excessively and prolongedly. I decide that the aspirin is the reason, and start skipping doses. The lower aspirin levels subsequently allow my platelets to become sticky again. As a result a clot forms in my coronary stent and a heart attack ensues.

Thus, prolonged bleeding from a cut, considered a minor side effect of aspirin therapy, could increase heart attack risk.

There is a clinically available test for aspirin effect called AspirinWorks.

The AspirinWorks Test Kit is an enzyme-linked immunoassay (ELISA) to determine levels of 11-dehydrothromboxane B2 (11dhTxB2) in human urine, which aids in the qualitative detection of aspirin effect in apparently healthy individuals post ingestion. Unlike platelet aggregation tests, which require freshly drawn blood that must be evaluated within at least four hours, the AspirinWorks Test is performed on a random urine sample that can easily be obtained in any doctor’s office.

AspirinWorks points out the putative benefits of testing for aspirin effect:

An increasing body of evidence in the medical literature overwhelmingly supports clinically significant variability in aspirin effect, which has been well-established in findings from trials, including the Heart Outcomes Prevention Evaluation (HOPE) Study and the CHARISMA trial published in Circulation (Journal) (2002 and 2008). These trials have demonstrated that:

  1. Increased levels of urinary 11dhTxB2 are associated with as much as a four fold increased risk for adverse cardiovascular events or death.
  2. Statin treatment is associated with lower concentrations of 11dhTxB2
  3. 11dhTxB2 is an independent, modifiable predictor of risk for stroke, heart attack and cardiac death (CHARISMA).

I have never ordered this test and am unaware of any other physicians ordering it on their patients.

Doctors don’t test for aspirin effect in individual patients because it is expensive and it won’t change our approach in most cases.
Taking  81 mg aspirin daily might be too high a dose to optimize the balance between bleeding and clotting in me.  If I took it every other day I might have less Type I BARC episodes. However, we don’t have any good evidence that adjusting the dosage based on aspirin effectiveness testing will improve my outcomes.
Thus, we bleeders on baby aspirin (the BOBA) of the world must find better ways of dealing with minor bleeding.
When I changed the band-aid on my philtrum several hours after the initial cut, I began actively bleeding again. This time I decided to apply ice to the area to vasoconstrict the arteries. This, plus more pressure and time, almost completely stopped the bleeding.
Another Nexcare was applied to the area, and when it was removed the next morning, the bleeding did not resume.
There are a variety of other measures that can be tried with varying degrees of success, as described here (deodorant, lip balm, listerine, Visine) and here (styptic pencils and powders, cayenne pepper, tea bag, sugar, alum-ironically this article mentions making a paste out of aspirin and applying it to the cut).
There also appears to be a thriving industry devoted to commercial  products for stopping bleeding from minor cuts outlined here.
Should We Worry About Minor Bleeding?
Ultimately, the seemingly excessive bleeding one experiences upon incidentally cutting oneself while taking aspirin is best viewed as a reassuring sign that the drug is doing its job: Your platelets are less sticky, less likely to cause bad clots that cause strokes and heart attacks.
Platelets don’t know bad from good clots, they just react indiscriminately.
The small amount of blood that exudes from superficial cuts can be scary but it can be controlled with fairly simple measures.
The little red dots my patient experiences, although unattractive, are benign.
Styptically Yours,
-ACP

AliveCor Mobile ECG : Ways To Minimize Low Voltage and Unclassified Recordings

Sometimes AliveCor’s Mobile ECG device yields unclassified interpretations of recordings. Understandably if you want to know whether your rhythm is normal or atrial fibrillation, the unclassified  classification can be very frustrating.

There are various caues of an unclassified tracing with different solutions.  Some unclassified recordings are due to a heart rate over 100 BPM or under 50 BPM and cannot be fixed. Similarly, some patients with ectopic beats like PVCS may consistently generate unclassified interpretations (see my discussion here).

Artifacts induced by poor recording techniques are common as a cause and almost always can be fixed.

These can be reduced by minimizing motion, extraneous noise, and maximizing contact with the electrodes.  Follow all the steps AliveCor lists here.

For me, the following step is crucial

  • If your fingers are dry, try moistening them with antibacterial wipes or a bit of lotion

And be aware the device needs to be near the microphone of your iPad or smartphone.

Low Voltage As Cause of Unclassified Kardia Recordings

Another cause of unclassified interpretations is a low voltage recording (which I initially discussed here.).

At the recent ACC meeting I asked Alivecor inventor and CEO David  Albert if he had any solutions to offer for those who obtain unclassified low voltage AliveCor tracings.

He told me that the cause is often a vertically oriented heart and that recording using the lead II technique can often solve the problem.

Lead II involves putting one electrode on your left knee and one your right fingers as described in this video:

Reader “J”  recently sent me a series of Kardia ECG recordings,  some of which were unclassified , some normal and one read as possible atrial fibrillation.

The unclassified and possible AF tracings looked like this:

 

They were very regular with a rate between 80 and 100 BPM but they totally lacked p waves. It was not clear to me what the rhythm was on these tracings.

Other tracings had lowish voltage but the p waves were  clearly visible  and Kardia easily classified them as normal

Lowish voltage with p waves (Type B)

 

Good QRS voltage with clear p waves ( Type B

 

Still others had improved QRS voltage with clear p waves and were also classified  appropriately as normal

 

After some back and forth emails we discovered that the ECG recordings with no p waves were always  made using the chest lead recording.   AliveCor-describes this as follows:

  • For an Anterior Precordial Lead, the device can be placed on the lower left side of the chest, just below the pectoral muscle. The bottom of the smartphone or tablet should be pointing towards the center of the body.

Mystery solved!

There is an abnormal cardiac rhythm that is regular between 80 and 100 BPM with no p waves and normal QRS called junctional tachycardia but in J’s case the absent p waves are related to the recording site.

Also, note that for this young woman the lead II voltage (Type B tracing) is much higher than the standard, lead I voltage (type A tracing).

Lead II With Pants On

After Dr. Albert told me of the advantages of Lead II I responded that it seemed somewhat awkward to take one’s pants off in order to make an ECG recording.

He immediately reached in his suit pocket and pulled out a pen-shaped device and began spraying a liquid on his left knee.

To my surprise he was able to make a perfect Lead II recording without taking his pants off!

Lessons learned from reader J and Dr. A:

  • Consider trying different leads if the standard Lead I (left hand, right hand) is consistently yielding unclassified ECG recordings
  • Try Lead II (left knee, right hand) to improve voltage and recording quality
  • You can record off your knee even with your pants on if you are prepared to spray liquids on your pants

Pantsonically Yours,

-ACP

Low-Fat Versus Low-Carb Diet: DIETFITS Show Both Can Work If They Are “Healthy”

In the ongoing nutritional war between adherents of low-fat and low-carb diets, the skeptical cardiologist has generally weighed in on the side of lower carbs for weight loss and cardiovascular health.

I’ve questioned the vilification of saturated fat and emphasized the dangers of added sugar. I’ve even dabbled in nutritional ketosis.

The science in  nutrition is gradually advancing and the DIETFITS study recently published in JAMA is a welcome addition.

DIETFITS is a  really well done study which provides important insights into three huge questions about optimal diet:

  1. Should we choose a low-fat or a  low-carb diet for  weight loss and cardiovascular health?
  2. Do baseline insulin dynamics predict who will respond to low-fat versus low-carb diet?
  3. Can we predict who will respond to low-fat versus low-carb by genetic testing?

The Details Of DIETFITS

Stanford investigators recruited 609 San Francisco area individuals between the ages of 18 to 50 years with BMI of 28 to 40  and randomized them to a “healthy” low-fat diet or a “healthy” low-carb diet.

During the first 8 weeks of the study, low-fat participants were instructed to reduce fat consumption to <20 gm/ day while the low carb participants were instructed to reduce digestible carbohydrate to <20 gms/day.

Then individuals were allowed to add back fats or carbs back to their diets in increments of 5 to 15 g/d per week until “they reached the lowest level of intake they believed could be maintained indefinitely.”  Importantly no explicit instructions for energy restriction were given.

The “healthy” instructions for both groups were as follows

  1. maximize vegetable intake
  2. minimize intake of added sugar, refined flours and trans-fats
  3. focus on whole foods that are minimally processed, nutrient dense and prepared at home whenever possible

Dietfits Outcomes-Diet And Weight

Major findings

  1. Total energy intake was reduced by 500-600 kcal/d for both groups
  2. The low-fat vs the low-carb intake at 12 months was 48% versus 30% for carbs, 29 vs 43% for fat and 21 vs 23% for protein.
  3. Mean 12 months weight change was -5.3 kg for low-fat vs 6-6.0 kg for low-carb which was not significantly different
  4. There was no difference between groups in body fat percentage or waist circumference
  5. Both diets improved lipid profiles and lowered blood pressure, insulin and glucose levels
  6. LDL (bad cholesterol) declined more in the low-fat group whereas HDL (good cholesterol) increased more and triglycerides declined more in the low-carb group.

Thus both diets were successful for weight loss and both improved risk markers for cardiovascular disease after a year.

DIETFITS- Can Genes and Insulin resistance Predict Best Diet?

Surprisingly, the study found no significant diet-genotype interaction and no diet-insulin secretion interaction with weight loss.

This means that they could not predict (as many believed based on earlier studies) who will benefit from a low carb diet based on either currently available genetic testing or a generally accepted measure of insulin resistance.

As the authors point out, these findings “highlight the importance of conducting large, appropriately powered trials such as DIETFITS for validating early exploratory analyses.”

DIETFITS-Perspectives

As you can imagine this study has led to quite an uproar and backlash from dedicated combatants in the macronutrient wars.

A reasoned summary and response from Andreas Eenfeldt, a low carb proponent can be found on his excellent low carb/keto Diet Doctor site here.

Eenfeldt concludes

If I’m allowed to speculate, the reason that we did not see any major additional benefit from low carb in this study is that the groups ended up so similar when it came to bad carbs. The low-fat group ended up eating fewer carbs too (!) and significantly less sugar, while the low-carb group ended with a somewhat weak low-carb diet, reporting 130 grams of carbs per day.

Eenfeldt emphasizes that low-fat diets never “win” these macronutrient dietary skirmishes:

On the whole, this study adds to the 57 earlier studies (RCTs) comparing low carb and low fat for weight loss.

From a standing of 29 wins for low carb, zero for low fat and 28 draws, we now have 29 wins for low carb and 29 draws. The wins for low fat stay at zero.

Larry Husten at Cardiobrief.org in his analysis of the study quotes a number of experts including Gary Taubes, the low carb pioneering journalist

Taubes speculates “that the weight loss may have been similar not because any diet works if you stick with it and cut calories (one possible interpretation) but because of what these diets had in common — avoid sugar, refined grains, processed foods. Whether the low-carb arm would have done even better had Gardner kept their carbohydrates low is something this study can’t say. (And Ornish [low-fat diet proponent] would probably say the same thing about fat consumption.)”

The low-fat or vegan disciples seem to have had a muted response to this study. I can’t find anything from John McDougal , Dean Ornish, Caldwell Esselstyn or Joel Fuhrman.

Readers feel free to leave comments which  link to relevant analysis from the low-fat proponents.

Dietfits-Perspective Of The Participants

Julia Volluz at Vox wrote a fascinating piece recently which involved interviewing some of the participants in this study.

She points out that although the average DIETFITS participant lost over 10 pounds, “Some people lost more than 60 pounds, and others gained more than 20 during the year.”

LOW_FAT_LOW_CARBS_DIETS1__1_

She obtained permission from the lead author, Christopher Gardner  and interviewed  “Dawn, Denis, Elizabeth*, and Todd — two low-fat dieters and two low-carb dieters — about their experiences of succeeding or faltering in trying to slim down”

LOW_FAT_LOW_CARBS_DIETS1

I highly recommend reading the entire article for details but Volluz concludes

And that leads us to one of the burning mysteries of diets: how to explain why some people fail where others succeed — or the extreme variation in responses. Right now, science doesn’t have compelling answers, but the unifying theme from the four study participants should be instructive: The particulars of their diets — how many carbs or how much fat they were eating — were almost afterthoughts. Instead, it was their jobs, life circumstances, and where they lived that nudged them toward better health or crashing.

DIETFITS-Importance of “Healthy” Diet

Most likely the success of both of these diets is due to the instruction that both groups received on following a “healthy” diet. This guidance is remarkably similar to what I advocate and is something that combatants in the diet wars ranging from paleo to vegan can agree on.

The JAMA paper only provides the description I listed above but Volluz adds that participants were instructed to:

… focus on whole, real foods that were mostly prepared at home when possible, and specifically included as many vegetables as possible, every day … choose lean grass-fed and pasture-raised animal foods as well as sustainable fish ... eliminate, as much as possible, processed food products, including those with added sugars, refined white flour products, or trans-fats … prepare as much of their own food as possible. …

Indeed, if you want to see a very detailed description of the instructional process for participants check out the very detailed description of the methods here.

Yours in Health,

-ACP

N.B. I was searching for a reasoned response to this study from the low fat camp and to my surprise came across this fascinating video featuring the lead author of the study, Christopher Gardner, on (no fat/vegan) John McDougal’s YouTube site. Gardner is clearly on the side of sustainable, local , ethical food consumption but to his credit, his research , publications and comments on DIETFITS don’t reveal this.

Can AliveCor’s Mobile ECG Device Combined With Its Kardia Pro Cloud-Based Platform Replace Standard Long Term Rhythm Monitors?

In March of 2017 AliveCor introduced Kardia Pro, a cloud-based software platform that allows physicians to monitor patients who use the Kardia mobile ECG device.

I have been utilizing the Kardia mobile ECG  device since 2013 with many of my atrial fibrillation (AF)  patients and have  found it be very useful as a personal intermittent long term cardiac monitor. (see here and here)

I signed up for the Kardia Pro service about 3 months ago and all of my patients who purchased Kardia devices prior to March of 2017 have been migrated automatically to Kardia Pro by AliveCor.

Now (post March 2017),  patients who acquire a Kardia device must sign up for the Kardia Pro service at $15 per month to connect with a  physician.

I think this is money well spent and I’ll demonstrate how the service works with a few examples.

Monitoring Patients With Atrial Fibrillation

 I saw a 68 year old man with persistent atrial fibrillation that was first diagnosed at the time of pneumonia in late 2017.

He underwent a cardioversion after recovering from the pneumonia but quickly reverted back to AF. His prior cardiologist offered him the option of repeat cardioversion and long term flecainide therapy for maintenance of normal sinus rhythm (NSR) but he declined.

When I saw him for the first time in the office  a  month ago I  listened to his heart and to my surprise, noted a regular rhythm: an AliveCor recording in the office confirmed he was in NSR. The patient had been unaware of when he was in or out of rhythm

We discussed methods for monitoring his rhythm at this point which include a 24 Holter monitor, a 7 to 14 day Long Term Monitor, a Cardiac Event Monitor and a Mobile Cardiac Outpatient Telemetry device. These devices are helpful and although expensive are often covered by insurance.  They require wearing electrodes or a patch continuously and the results are not immediately available.

I also offered him the option of monitoring his AF using a Kardia device with the recordings connected to me by Kardia Pro.

He purchased the device on his own for $99, downloaded the app for his smartphone and began making recordings.

I enrolled him in my Kardia Pro account and he received an email invitation with a code that he entered which connected his account with mine, allowing me to view all of his recordings as they were made.

When I log into my Kardia Pro account I can now view a graphic display of the recordings he has made with color coding of whether they were considered normal or abnormal by Kardia.

The patient overview page also displays BP information if the patient is utilizing certain Omron devices which work with Kardia.

kardia pro wc monthly

The display shows that after our office visit he maintained NSR for 3 days (green dots) and then intermittently had ECG recordings classified as AF (yellow dots) or unclassified (black).

The more he used the device and got feedback on when he was in or out of rhythm the more he was able to recognize symptoms that were caused by AF.

I can click on any of the dots and six second strips of the full recording are displayed.  In the example below I clicked on 2/27 which has both an unclassified recording (which is atrial flutter) and an AF recording

Clicking on the ECG strips brings up  the full 30 second recording on a page that also allows me to assign my formal  interpretation. In the example below I added atrial flutter as the diagnosis, changing it from Kardia’s unclassified (Kardia’s algorithm calls anything it cannot clearly identify as AF that is over 100 BPM as unclassified.)

The ECG can then be archived or exported for entry into an EHR.

The benefits of this patient being connected
to me are obvious: we now  have an instantaneous patient-controlled method for knowing what his cardiac rhythm is doing whether he is having symptoms or not.

This knowledge allows me to make more informed treatment decisions.

The Kardia Pro Dashboard

When I  log into kardia pro I see this screen.

dashboard karia pro It contains buttons for searching for a specific patient or adding a new patient. Adding new patients is a quick and simple process requiring input of patient demographics including  email and birthdate.

From the opening screen you can click on your triage tab. I have elected to have all non normal patient recorded ECGS go into the triage tab.

Other Examples

Another patient’s Kardia Pro page shows that he records an ECG nearly every day and most of the time Kardia documents NSR in the 60s. Overall, he has made 773 recordings and 677 of them were NSR, 28 unanalyzed (due to brevity) , 13 unclassified and 55 showing AF.

Monitoring Rate  Control  In Patients With AF and Reversion Post-Cardioversion

Another patient I saw for the first time recently has had long-standing persistent AF.  His previous cardiologist performed an electrical cardioversion a year ago but the patient reverted back to AF in 40 hours.   Before seeing me he had purchased a Kardia mobile ECG device and was using it  to monitor his heart rate.

After he accepted my email invitation to connect via Kardia Pro I was able to see his rhythm and rate daily. The Kardia Pro chart belowshows his daily heart rate while in atrial fibrillation. We utilized this to guide titration of his rate controlling medications.  Such precise remote monitoring of heart rate in AF (which is often difficult to accurately assess by standard heart rate devices) obviates the need for office visits for 12 lead ECGs or periodic Holter monitors.

I performed a  second cardioversion on him after which he made  daily recordings documenting maintenance of NSR. With this system we can determine exactly when AF returns, information which will be very helpful in determining future treatment options.

Kardia Pro Plus Kardia Mobile ECG Creates Personal Intermittent Long Term Rhythm Monitor

There are many potential applications of the Kardia ECG device beyond AF monitoring (assessing palpitations, PVCs, tachycardia, etc.) but they are all enhanced when the device is combined with a good cardiologist connected to the device by Kardia Pro.

I’ve gotten spoiled by the information I get from my AF patients who are on  Kardia Pro now. When they call the office with palpitations or a sense of being out of rhythm I can determine within a minute what their rhythm is wherever I am (excluding tropical beaches and mountain tops)  or wherever the patient is (for the most part.)

On the other hand patients who are not on Kardia Pro have to come into the office for  12-lead ECGs. When they call I feel like my diagnostic tools are limited. Such patients usually end up getting one of the standard Long Term Monitoring (LTM) Devices. If I am fortunate, after a  few days to weeks , the results of the LTM will be faxed to my office.

I am optimistic based on this early experience with Kardia Pro that ultimately this service in conjunction with the Kardia Mobile ECG device (or similar products) will replace many of the more expensive and inconvenient long term monitoring devices that cardiologists currently use.

Skeptically Yours,

-ACP

Should You Take An Antioxidant (Supplement or Vitamin) To Prevent Or Treat Heart Disease

Antioxidant-rich foods, vitamins and supplements are incessantly promoted to Americans as effective and safe means to stave off the chronic diseases of aging and even aging itself.

The simple concept that sells billions of dollars of these  products seems logical and seems to be supported by science: damaging and disease-causing  free radicals  are neutralized by super hero antioxidants.  All you have to do to benefit from these disease-fighting agents is identify foods with the highest level of antioxidants or take supplements with super antioxidant vitamins or chemicals.

To remain young  and free of heart disease, cancer and dementia, the glowing marketing material for antioxidant products proclaims,  eat this magical Italian fruit or drink this fruit juice or take this concentrated substance that we have carefully extracted from a super fruit.

Unfortunately, the early hopes that antioxidant therapy would reduce heart disease,in particular, and other chronic diseases of aging in general have been dashed by excellent scientific studies  performed in the 1990s.

For antioxidant vitamins, in particular, which continue to be heavily promoted for heart disease and cancer prevention, over the last 20 years a wealth of studies have accumulated which clearly demonstrate a lack of efficacy.

Despite data clearly showing no benefit in well done randomized trials (and in some cases evidence for harm) sales of antioxidant vitamins C, E and beta-carotene continue to thrive.

Why did scientists strongly believe in the idea that antioxidants in pure and concentrated form would prevent heart disease?

Antioxidants: Free Radical Scavengers

Laboratory and animal studies beginning in the 1950s suggested that excess free radicals generated by oxidative processes could be responsible for the chronic degenerative diseases of aging.

Oxygen, which is essential to animal life, undergoes processing in cells which creates unstable free radicals. Free radicals are short an electron and seek other molecules which can donate an electron and make them more stable. This process is termed oxidation.

The molecules produced by oxidation play an important role in a a number of biological processes such as the killing of bacteria and in cell signaling. These same unstable molecules, however,  have been implicated in a number of deleterious processes as they can participate in unwanted side reactions and create cell damage.

Thus, too many free radicals have been implicated as potentially causal in diseases ranging from cancer to cardiovascular disease to dementia.

Antioxidants can reduce damage from free radical reactions because they can donate electrons to neutralize free radicals or their offspring without forming another free radical.

This observation logically lead to the theory that large amounts of antioxidants taken as an oral supplement or within (either naturally or added artificially)  food and beverages can prevent the free radical damage presumably causing chronic disease  and aging.

Investigators early on identified three vitamins as the most important cellular antioxidants:

  • Vitamin E or  d-alpha tocopherol is a fat soluble vitamin.
  • Vitamin C or ascorbic acid. is a water soluble vitamin, deficiency of which leads to scurvy
  • Beta-carotene is a precursor to vitamin A (retinol)

Early Observational Studies Suggest  Taking An Antioxidant Prevents Heart Disease 

Based on laboratory, animal and human clinical trials many investigators by the early 1990s were convinced that oxidation of LDL cholesterol was the major cause of atherosclerosis and that antioxidant supplementation , in particular Vitamin E, could prevent the heart attacks and strokes caused by atherosclerosis.

The introduction to the landmark Nurses Health Study  summarizes the seemingly compelling evidence leading to these conclusions:

Rapidly growing evidence suggests that oxidation of low-density lipoprotein (LDL) plays an important part in atherosclerosis. As Steinberg et al. have found,1-3 oxidized LDL is taken up more readily than native LDL by macrophages to create foam cells. Also, oxidized LDL is chemotactic for circulating monocytes,4 and it inhibits the motility of tissue macrophages5. It may also be cytotoxic to endothelial cells6 and may increase vasoconstriction in arteries7. Oxidized LDL has been identified in atherosclerotic lesions,8-10 and elevated titers of circulating autoantibodies to epitopes of oxidized LDL are found in patients with atherosclerosis11. Lipid peroxide concentrations have been found to be higher in patients with atherosclerosis12. In addition, the susceptibility of LDL to oxidation was correlated with the severity of atherosclerosis13.

Vitamin E is a potent lipid-soluble antioxidant carried in LDL14,15. It inhibits the proliferation of smooth-muscle cells in vitro,16 and when added to plasma, it increases the resistance of LDL to oxidation17. LDL from volunteers given alpha-tocopherol supplements showed increased resistance to oxidation18

Starting in 1980  the Nurses Healthy Study began gathering information on diet and supplement use in 87,245 female nurses 34 to 59 years of age who were free of diagnosed cardiovascular disease and cancer. Information on diet was assessed every two years  and the participants were monitored for cardiovascular outcomes for 8 years.

High consumers of Vitamin E compared to lower consumers had a 34% lower risk of major coronary disease. Those who took Vitamin E for more than 2 years had a 41% reduction in risk which was significant after adjustment for age, smoking status, risk factors for coronary disease, and use of other antioxidant nutrients (including multivitamins).

After reading this study I and many of my colleagues began recommending that our patients take Vitamin E. These observational trials, however, could only show an association between antioxidants and disease, they didn’t prove causality.

Good Quality Randomized Trials Fail To Show Any Benefit of Antioxidants and Raise Concerns of Possible Danger

Given the strong evidence for antioxidants in reducing heart disease from the observational and laboratory studies the theory that antioxidant supplementation would reduce heart disease needed to be tested in randomized trials.

Fortunately, multiple well done randomized studies have tested whether supplementation with the major proposed antioxidants will reduce heart disease, cancer or mortality.

Sadly, the consensus assessment is that they are useless and in some cases antioxidant vitamin supplementation may increase risks.

The Physicians’ Health Study II is a great example:

Published in 2008, This study randomly assigned 14,641 physicians without heart disease to treatment with vitamin E 400 international units every other daily, vitamin C 500 mg daily, both, or neither; After  eight years, treatment with vitamin E  and Vitamin C either alone or in combination had no effect on major cardiovascular events or all-cause mortality.

Those participants taking Vitamin E had a significant 70% increased risk of hemorrhagic stroke compared to those taking placebo.

After this trial was published I took all my patients off Vitamin E.

Multiple good quality randomized controlled studies of Vitamin E, Vitamin C and beta-carotene in various combinations have also been done on patients who have established coronary heart disease and have shown no benefit in reducing cardiovascular events or mortality. This 2003 Lancet meta-analysis nicely summarizes the data.

These studies strongly called into question the theory that supplementation with antioxidants reduce chronic disease and by 2003 there was a broad consensus among serious scientists, cardiologists and nutritionists that Vitamin E and Vitamin C in various doses and in diverse populations had no benefit in reducing mortality, cardiovascular disease or cancer.

In fact, Vitamin E may increase hemorrhagic stroke and high-dose vitamin E supplementation (≥400 international units/day) may be associated with an increase in all-cause mortality

Studies with beta-carotene overall suggested an increase in overall mortality and one study has shown an increased risk of lung cancer in male smokers who received supplementation.

More recently, a 2012 BMJ meta-analysis   concluded that there was no benefit for any vitamin or antioxidant supplement in reducing cardiovascular risk or mortality.

 

Despite Scientific Studies Showing No Benefit, Antioxidant Sales Continue To Grow

You might conclude that based on high quality studies showing no benefits and potential harm that sales of antioxidants would taper off. Unfortunately, the opposite has occurred.

Nutraceuticals World reported that sales of antioxidant supplements are growing steadily, reaching all time highs.

Combining top antioxidant ingredient sales such as green tea, dark chocolate, superfruit juice and dietary supplements, Euromonitor estimated the combined global sales in these categories totaled $34 billion in 2010. According to Euromonitor, the top antioxidant markets are Japan, the U.S. and China, with sales growing steadily in all five ranked product areas in the past five years. Growth from 2005 to 2010 was 43% in current terms. As a point of comparison, the global organic packaged food and beverage market was only $27 billion.

The Sneakiness of the Nutraceutical Snake Oil Salesmen

The quacks and charlatans that make their living selling useless vitamins, minerals, supplement and nutraceuticals are masters at creating the appearance of a scientific basis for buying their snake oil.

Their promotional material always features references to scientific studies.  Almost invariably, these references do not prove any health benefit for the product being sold.

In cases like antioxidants where initial studies suggest a benefit and subsequent higher quality studies have shown no benefit, only the earlier studies will be quoted.

If relevant negatives studies for an antioxidant are referenced, the talented snake oil salesman will explain to his gullible audience that the lack of efficacy was because the wrong form of the antioxidant was utilized.

Fortunately, for you, the snake oil salesman has developed his own special formulation which is superior. Such formulations are typically described as containing additional ingredients that enhance efficacy. Often, the special formulation is described as somehow better at getting into the body or being absorbed.

None of these special formulations has any scientific support for treating or preventing any disease.

Dr. Mercola, A Master of Pseudoscientific Support For Selling Useless Vitamins

The most successful marketers of useless antioxidant supplements and vitamins convince their audience that they alone have the insight and wisdom to provide the consumer with the knowledge and products they need to be healthy.  To accomplish this, they must create mistrust of standard medical advice and prescription medications, often portraying doctors as ignorant of proper nutrition and hostile to allegedly superior “natural” or alternative cures.

Doctors, in this portrayal, are the enemy, pushing dangerous prescription medications along with unneeded procedures like coronary stents and bypass surgery because we are in the pay of the pharmaceutical and medical device industries.

Joseph Mercola, an osteopath, has created an alternative medicine internet empire by convincing millions to follow his advice and buy his useless supplements. He is arguably the master of alternative medicine misinformation. (See this article to fully understand how dangerous Mercola’s ideas are.)

Hoovers reports that Mercola makes 9.8 million dollars per year selling useless stuff and Alexa describes his website as the top “alternative medicine” website. Mercola sells so much snake oil it is mind-numbing.

Mercola (or more likely his marketing department)  has  an astonishingly long and  detailed  list of reasons why you should buy only his own special formulation of Vitamin E. None of them are supported by scientific references.

-His form is natural versus synthetic.

-Other natural forms of vitamin E come from soy which you should avoid because it is genetically engineered.

-You need all 8 forms of natural vitamin E and they must be balanced in the way that he deems most healthy. His form comes from sunflower seeds.

-Science has ignored the tocotrienol form of Vitamin E but has “started to wake up to the potential benefits.”

-Tocotrienols potentially “help support normal cholesterol levels., protect again  free radical damage and the normal effects of aging” and promote brain health.”

Mercola vitamin E

The average consumer reading this long and complicated discussion is likely to be impressed with the pseudoscientific language, the complicated chemical names, and  the appeal to a more natural approach and has no way of knowing that it is all unsubstantiated marketing hype.

The average consumer is not likely to see buried in small print at the bottom of the page the truth:

*These statements have not been evaluated by the Food and Drug Administration.

These products are not intended to diagnose, treat, cure, or prevent any disease.

Don’t Buy Antioxidant Supplements and Vitamins

What have we learned?

  1. Although early research suggested a role for antioxidant vitamins in preventing heart disease when high quality randomized controlled rials were performed they showed no benefit and in some cases increased risk.
  2. Despite this, antioxidant sales are booming.
  3. Supplement marketers are brilliant at confusing consumers with pseudoscience and sell billions of dollars of useless product.

There is minimal regulation of the nutraceutical/supplement industry. The snake oil purveyors get away with their lies and escape (for the most party) FDA scrutiny by admitting that their products don’t “treat, cure or prevent any disease.”

Rather than hiding this information, at a minimum, they should be forced to put it in large, bold letters at the beginning of every page on their website.

THESE PRODUCTS ARE NOT INTENDED TO TREAT, CURE OR PREVENT ANY DISEASE!

Please don’t buy them any more.

Uncleoxidantly Yours,

-ACP

 

What Can America Learn Now From Australian Gun Laws?

I wrote a post in December of 2016 which asked “What Can America Learn From Australian Gun Laws?”

Since then we’ve had more mass shootings in the US, most recently at least 17 have died in a high school in Florida, shot by a 19 year old with an AR-15 he purchased legally.

After the Las Vegas mass shooting I noticed that there was a call from the editors of most of the medical journals I follow for physicians to advocate for gun control.

These comments from an editorial in the Annals of Internal Medicine are typical:

Here’s a short list of how health care professionals can use our skills and voices to fight the threat that firearms present to health in the United States.
Educate yourself. Read the background materials and proposals for sensible firearm legislation from health care professional organizations. Make a phone call and write a letter to your local, state, and federal legislators to tell them how you feel about gun control. Now. Don’t wait. And do it again at regular intervals. Attend public meetings with these officials and speak up loudly as a health care professional. Demand answers, commitments, and follow-up. Go to rallies. Join, volunteer for, or donate to organizations fighting for sensible firearm legislation. Ask candidates for public office where they stand and vote for those with stances that mitigate firearm-related injury.
Meet with the leaders at your own institutions to discuss how to leverage your organization’s influence with local, state, and federal governments. Don’t let concerns for perceived political consequences get in the way of advocating for the well-being of your patients and the public. Let your community know where your institution stands and what you are doing. Tell the press.
Educate yourself about gun safety. Ask your patients if there are guns at home. How are they stored? Are there children or others at risk for harming themselves or others? Direct them to resources to decrease the risk for firearm injury, just as you already do for other health risks. Ask if your patients believe having guns at home makes them safer, despite evidence that they increase the risk for homicide, suicide, and accidents.
Don’t be silent. We don’t need more moments of silence to honor the memory of those who have been killed. We need to honor their memory by preventing a need for such moments. As health care professionals, we don’t throw up our hands in defeat because a disease seems to be incurable. We work to incrementally and continuously reduce its burden. That’s our job.

What follows is my original 2016 post.


In April of 1996, a 28-year old man murdered 35 people in Tasmania primarily utilizing a Colt AR-15 rifle (a lightweight, 5.56×45mm, magazine-fed, air-cooled semi-automatic rifle with a rotating bolt and a direct impingement gas-operation system.)

This event led to public outcry in Australia and  bipartisan passage of a comprehensive set of gun regulation laws (the National Firearms Agreement (NFA)).

In the 20 years since the law was put into place (1997-2016), there has not been a single fatal mass shooting in Australia.

In the 17 years prior to the NFA enactment 13 mass fatal shootings (defined as ≥5 victims, not including the perpetrator) occurred in Australia.

An analysis of this process was recently published in JAMA.

Australia’s 1996 NFA mandated:

  • the ban and buy-back of semiautomatic long guns.
  • licensing of all firearm owners and registration of firearms.
  • that  persons seeking firearm licenses  must document a “genuine need,” have no convictions for violent crimes within the past 5 years, have no restraining orders for violence, demonstrate good moral character, and pass a gun safety test.
  •  uniform standards for securing firearms to prevent theft or misuse, record-keeping for fire arms transfers, purchase permits, and minimum waiting periods of 28 days.
 I agree with the comments in an accompanying editorial written by Daniel Webster of the John Hopkins School of Public Health, Center for Gun Policy and Research(:gun-regulation.)

Research evidence should inform the way forward to advance the most effective policies to reduce violence. However, research alone will not be enough. Australian citizens, professional organizations, and academic researchers all played productive roles in developing and promoting evidence-informed policies and demanding that their lawmakers adopt measures to prevent the loss of life and terror of gun violence. Citizens in the United States should follow their lead.

-ACP

N.B. Of the 46 mass shooting since 2004, 14 featured assault rifles, including Newtown, Aurora, Orlando and San Bernardino. Apparently there are 10 million AR-15 type rifles in private hands in the USA and as Vox has pointed out

“the AR-15 is caught in a cycle. The more it’s used in high-profile mass shooting cases, the more people want to ban it. The more people want to ban it, the more AR-15s are sold. And the more AR-15s are sold, the harder it becomes to create a ban that would be able to stop the next tragedy.”

For more on assault-style rifles you can view this Washington Post video created after the Orlando shootings.
//www.washingtonpost.com/video/c/embed/28d02e8e-3118-11e6-ab9d-1da2b0f24f93

Sincerely,

-ACP

Which Kind of Baby Aspirin Should I Take To Prevent Heart Attack? Chewable Versus Enteric Coated Versus Regular

The skeptical cardiologist recently asked his Eternal Fiancée to grab a bottle of baby aspirin  while she was at the local Walgreen’s. Aspirin or acetyl salicylic acid (ASA) comes in either a 325 mg dose or in a low dose which can be between 75 to 100 mg and is often called “baby” aspirin.

However, since a link between aspirin use and a potentially lethal disease called Reye’s syndrome was identified in the 1980s, no authorities recommend aspirin in children or babies, and the low dose ASA (LDASA) is primarily marketed and used for prevention of cardiovascular disease.

Although Bayer and Dr. Oz would have us believe that all individuals over the age of 55 should be taking LDASA, as I pointed out here in 2014, the FDA no longer recommends it for prevention of cardiovascular disease.

The US Preventive Services Task Force, on the other hand, recognizes certain individuals without heart disease who benefit from LDASA:

The USPSTF recommends initiating low-dose aspirin use for the primary prevention of cardiovascular disease (CVD) and colorectal cancer (CRC) in adults aged 50 to 59 years who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years.
I’m 63  years old, so the USPTF recommendation for me to take LDASA is a little less enthusiastic:
The decision to initiate low-dose aspirin use for the primary prevention of CVD and CRC in adults aged 60 to 69 years who have a 10% or greater 10-year CVD risk should be an individual one. Persons who are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit. Persons who place a higher value on the potential benefits than the potential harms may choose to initiate low-dose aspirin.
Following my own advice (see here), I have started taking 81mg of aspirin regularly (well, when I remember) in order to prevent stroke and heart attack. I do have subclinical atherosclerosis with a plaque in my LAD, and I think the aspirin will make my platelets less sticky and less likely to form clots if my plaque ruptures, thereby reducing my chances of an acute heart attack.
I am willing to accept the increased risk of bleeding from the gastrointestinal tract and hemorrhagic stroke associated with LDASA use.

Previous to this I had been taking ASA from little sample bottles that Bayer sends to my office. These bottles are quite annoying as they are stuffed with cotton and contain very few pills making extrication of the tiny pills an exercise in futility (I am using this as an excuse for my lack of regularity in taking them).

There’s no reason to pay the premium for Bayer ASA despite the company’s advertising attempts to link inextricably their name with ASA.  Aspirin is aspirin, whether Bayer made it or Walgreens. In Bayer’s defense, their website has reasonable information on heart attacks and they appear to be giving aspirin away to people named Smith.

But what type of aspirin should you get? Enteric-coated, safety-coated, delayed release, chewable?

Chewable Aspirin

I asked the Eternal Fiancée to buy the cheapest baby aspirin possible.

She ended up buying a chewable formulation with orange flavoring, presumably aimed at children:

When I put one of these in my mouth I tasted the sickly sweet taste of an artificial sweetener. The ingredients are listed as: Dextrates, Ethyl Cellulose, FD&C Yellow 6 Aluminum Lake, Orange Flavor, Sodium Saccharin, Starch. Saccharine! Yikes!

The only reason to chew ASA is if you are having an acute heart attack.

In this situation, chew 4 of the LDASA or one regular 325 mg aspirin.  Chewing the aspirin makes the levels rise faster in your blood stream and can help dissolve the clot causing your heart attack more rapidly.

How do you know if you are having a heart attack? This is actually a very difficult question to answer with certainty. See here for a reasonable discussion.

Low Dose Aspirin: Enteric-Coated versus Non-coated

It is very difficult (perhaps impossible) to find low dose, non-chewable ASA that has not been “safety-coated” or “enteric-coated.” These formulations have become popular by promoting the idea that they are less likely to cause stomach pain or bleeding.

The concept is that the coating leads to delaying the aborption of the ASA until it reaches the small intestines where, presumably, it will do less damage. However, there is no good evidence to support lower bleeding risk with enteric-coasted (EC) ASA.

There is, on the other hand, very good evidence that therapeutic levels of aspirin in the bloodstream, and therefore the speed and efficacy of ASA in preventing heart attacks, is reduced by these “safety” formulations.

The most recent study showing this was published in 2017.

Volunteers were given either 325mg regular ASA or 325mg EC ASA and researchers looked at how each formulation effected platelet activity.  The onset of antiplatelet activity was determined by the rate and extent of inhibition of serum thromboxane B2(TXB2) generation.

The EC ASA took longer and was less effective at blocking platelet activity than plain ASA. Presumably, this translates into lower efficacy in preventing heart attacks and strokes.

Therefore,  if you feel like you are having a heart attack, chew ASA which is not enteric or safety-coated. Yes, you can chew a regular 325 mg ASA pill. Or you can chew 4 of the LDASA, preferably uncoated but still helpful if coated.

If it turns out you weren’t having a heart attack there is no down side to having chewed 325 mg ASA.

I just spent a fair amount of time trying to find non EC, non-chewable LDASA online and failed.

For the time being I will be swallowing daily the orange chewable LDASA and I will carry a bottle around in my satchel for emergency use.

Salicylically Yours,

-ACP

N.B. Aspirin is generally recommended in secondary prevention of cardiovascular disease, ie. for those who have had heart attacks, stents or bypass surgery . For a good review of the evidence for this see here.

Exercise As Medicine: Preventing Age-Related Decline in Cardiac Stiffness

As we age our hearts and arteries become stiffer. This cardiovascular stiffening plays a key role in hypertension, atrial fibrillation, and heart failure in older individuals (1).

Age-related cardiac stiffening is worse in those who are sedentary compared to those who exercise regularly (2).

Recent studies strongly suggest that regular exercise can prevent or minimize these age-related changes, thereby hopefully reducing the high rate of heart failure, hypertension and atrial fibrillation in the elderly.

In my post on fitness as a vital sign I briefly mentioned a fascinating study from 2014 which looked at 102 healthy seniors (age>64 years) and stratified them into 1 of 4 groups based on their lifelong histories of endurance exercise training.

Consider which of these 4 categories you fall into:

Sedentary subject-exercised no more than once per week during the prior 25 years.

Casual exercisers-engaged in 2-3 sessions per week

Committed exercisers-performed 4-5 sessions per week

Competitive “Masters level” athletes-trained 6-7 times per week

Exercise sessions were defined as periods of “dynamic activity lasting at least 30 minutes.”

The participants had sophisticated measures of their exercise capacity (max VO2), the size and mass of their left ventricles (cardiac MRI) and the stiffness of their left ventricles (invasive pressure/volume curves to calculate LV compliance and distensibility.)

This graph shows the key finding of the study: a markedly different pressure/volume curve in the sedentary and casual exercisers (blue and red dots) versus the committed or master exercisers. The two curves on the left correspond to a very stiff heart, similar to curves found in patients with heart failure.

The far right curve of competitive exercisers resembles that of a young heart.

The black triangle curve of the committed exerciser is in between these extremes

F5.large-3

The study concludes:

“low doses of casual, lifelong exercise do not prevent the decreased compliance and distensibility observed with healthy, sedentary aging. In contrast, 4 to 5 exercise sessions/week throughout adulthood prevent most of these age-related changes”

It would appear we need at least 4-5 30 minute exercise session per week to forestall the age-related stiffening of the heart and lower our chances of getting heart failure, hypertension and atrial fibrillation.

Since this was an observational study there is always a chance that lack of exercise is not the causes of poor cardiac stiffness.  It is conceivable that those of us with stiffer hearts tend to be more sedentary because of the poor cardiac function.

Can You Reverse The Age-Related Changes In Cardiac Stiffness?

If you have already reached middle age there is still hope for you as these same investigators recently published a study showing that cardiac stiffness can be improved with exercise. These findings imply that lack of exercise is the cause of worsening cardiac stiffness with aging.

This study identified 61 sedentary men in their mid-fifties and randomly assigned them to either 2 years of exercise training or attention control (a combination of yoga, balance, and strength training 3 times per week for 2 years) and measured their LV stiffness and max VO2 before and after intervention.

Max VO2 increased by 18% and LV stiffness declined from .072 to .051 in the exercise group but did not change in the control group.

The exercise training arm of this study involved a mixture of continuous moderate-intensity aerobic exercise combined with high intensity training. The high intensity portion of the program involved exercising at 90-95% of HR maximum for 4 minutes followed by a 3 minute active recovery period, repeated 4 times.

Over a period of 6 months under the guidance of exercise physiologists the participants had their exercise levels gradually increased. After 6 months they were training 5-6 hours per week, including 2 of the “high intensity interval” session and 1 long (>/= 1 hour) and one 30-minute base pace session each week.

By the sixth month, participants were training 5 to 6 hours per week, including 2 interval sessions, and 1 long (at least an hour) and one 30-minute base pace session each week.

How Much Exercise Do We Need To Minimize Cardiac Aging?

This chart from recent European guidelines on lifestyle for prevention of disease describes different intensities of aerobic exercise:

 

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These guidelines suggest that if you engage in vigorous exercise such as running or jogging, cycling fast or singles tennis, you only need to achieve 75 minutes per week. Moderate exercise such as walking or elliptical work-outs requires at least  150 minutes/week.

Based on these recent studies on exercise and cardiac stiffness and the bulk of scientific literature on the overall health benefits of exercise I would advise for all individuals with or without heart disease

-If you are sedentary, become a committed exerciser.

-Committed exercise means some form of dynamic exercise 4-5 times per week

-If you are already a committed exerciser at moderate intensity levels consider adding to your routine one or two sessions of high intensity interval exercise.

-High intensity exercise will require you to get your heart rate up to 90-95% of your maximum 

-Predicted maximal HR=220 -age.  For a 60 year old this equals 160 BPM. 90% of 160 equals 144 BPM. 

Compliantly Yours,

-ACP

 

 

 

 

Do You Need To Fast Before Your Cholesterol Test?

When the skeptical cardiologist trained in medicine and cardiology in the 1980s the standard protocol for obtaining a lipid profile (LDL and HDL cholesterol plus triglycerides) involved having the patient fast for >8 hours before the blood was drawn.

Beginning in 2009, however, various national organizations began recommending the use of nonfasting lipid profiles. In 2011 the American Heart Association endorsed the fasting lipid profile and shortly thereafter I began telling my patients they did not need to fast for these tests.

Old habits and ideas are hard to kill and to this day most of my patients think that fasting is a requirement. Lab personnel seem to be stuck in the past as well and I typically instruct my patients to lie if they are asked if they have eaten.

A recent JACC article makes powerful arguments for using non fasting lipid profiles.

Rather than go through it in detail I’m going to post the “central illustration” which summarizes the authors points in graphic form.

The nonfasting profile is “evidence-driven” and also is time-efficient, patient, laboratory and physician-friendly.

So to my patients I say “you don’t need to fast before seeing me or prior to any blood work I order on you.”

To other patients whose physicians are still requiring fasting before a lipid profile I recommend challenging your doctor’s rationale.

If that doesn’t work, print out a copy of the above infographic and politely ask them to read the associated paper.

Hungrily  Yours,

-ACP

 

AliveCor’s Kardia Band Is Now Available: Mobile ECG On Your Apple Watch

AliveCor has finally gotten approval from the FDA to release its Kardia Band in the United States.

The skeptical cardiologist is quite excited to get his hands (or wrist) on one and just gave AliveCor $199 to get it.

The device incorporates a mobile ECG sensor into a wrist band that works with either 42 or 38 mm Apple watches. I’ve written extensively about AliveCor’s previous mobile ECG product (here and here) which does a good job of recording a single lead ECG rhythm strip and identifying atrial fibrillation versus normal rhythm,

Hopefully, the Kardia Band will work as well as the earlier device in accurately detecting atrial fibrillation.

According to this brief video to make a recording you tap the watch screen then put your thumb on the sensor on the band.

The app can monitor your heart rate constantly and alerts you  to make a recording if it thinks you have an abnormal rhythm.

I was alerted to the release of Kardia by Larry Husten’s excellent Cardio Brief blog and in his post he indicates that the alert service , termed Smart Rhythm,  requires a subscription of $99 per year.:

AliveCor simultaneously announced the introduction of SmartRhythm, a program for the Apple Watch that monitors the watch’s heart rate and activity sensors and provides real-time alerts to users to capture an ECG with the Kardia Band. The program, according to an AliveCor spokesperson, “leverages sophisticated artificial intelligence to detect when a user’s heart rate and physical activity are out of sync, and prompts users to take an EKG in case it’s signaling possible abnormalities like AFib.”

The Kardia Band will sell for $199. This includes the ability to record unlimited ECGs and to email the readings to anyone. The SmartRhythm program will be part of the company’s KardiaGuard membership, which costs $99 a year. KardiaGuard stores ECG recordings in the cloud and provides monthly summary reports on ECGs and other readings taken.

AliveCor tells me my Kardia Band will be shipped in 1-2 days and I hope to be able to give my evaluation of it before Christmas.

Please note that I paid for the device myself in order to avoid any bias that could be introduced by receiving largesse from AliveCor.

Proarrhythmically Yours

-ACP

N.B. Larry Husten’s article includes some perspective and warnings from two cardiologist and can be read here.

Another article on the Kardia Band release suggests that the Smart Rhythm program at $99/ year is a requirement.

Perhaps, AliveCor’s David Albert can weigh in on whether the annual subscription is a requirement for making recordings or just allows the continuous monitoring aspect.

Unbiased, evidence-based discussion of the effects of diet, drugs, and procedures on heart disease

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