Category Archives: Atrial Fibrillation

Does Aspirin Have A Role In Stroke Prevention In Atrial Fibrillation Or Is It Time To Start Stopping It?

Old habits die hard in medicine.  For decades the skeptical cardiologist and his cardiology brethren and sistren have prescribed aspirin to prevent stroke in patients with atrial fibrillation.

For those patients with atrial fibrillation (AF)  who were considered low risk  it was felt that aspirin provided some benefit in preventing the clots that fly out of the heart (and land in arteries elsewhere in the body) at an acceptably low risk of bleeding. For higher risk patients more powerful and effective agents (oral anticoagulants) are usually recommended.

The American guidelines on AF (2014)  gave a IIB recommendation to aspirin. IIB is not a ringing endorsement having been described as “this is our suggestion, but you may want to think about it.”

  • For patients with nonvalvular AF and a CHA2DS2-VASc score of 1, no antithrombotic therapy or treatment with an oral anticoagulant (OAC) or aspirin may be considered. (Level of Evidence: C)* 

However, in the last 5 years the significant bleeding risks associated with taking low dose aspirin have become more widely appreciated.

Thus, in the 2016 European guidelines on the management of AF the authors state that  “the evidence supporting antiplatelet mono therapy (e.g. aspirin or clopidogrel) for stroke prevention in AF is very limited” and the bleeding rate” is similar to OAC”:

Aspirin and other antiplatelets have no role in stroke prevention (III A). The combination of anticoagulation with antiplatelets increases bleeding risk and is only justified in selected patients for a short period of time; for example, in patients with an acute coronary syndrome or stent, balancing the risk of bleeding, stroke and myocardial ischaemia (IIa B/C).

Stroke risk evaluation is based on the CHADS-VASc score. With a score ≥2 in male and ≥3 in female patients, anticoagulation for stroke prevention is clearly recommended, while in a score of 1 in males and 2 in females, anticoagulation should be considered. No antithrombotic therapy of any kind should be prescribed in patients with a CHADS-VASc score of 0 (males) or 1 (females).

Antiplatelet therapy increases bleeding risk, especially dual antiplatelet therapy (2.0% vs. 1.3% with antiplatelet monotherapy; P < 0.001), with bleeding rates that are similar to those on OAC. Thus, antiplatelet therapy cannot be recommended for stroke prevention in AF patients.

 The focused update (2019) on AF from America said nothing about aspirin alone for AF.

It’s not just European experts who feel this way.  At a 2016 Cardiovascular CME conference, American experts in the field were unanimous in their condemnation of aspirin use

“The European guidelines have done away with aspirin for stroke prevention in atrial fibrillation. It barely made it into our current US guidelines. I don’t think aspirin should be in there and I don’t think it will be there in the next guidelines. The role of aspirin will fall away,” said Bernard J. Gersh, MB, ChB, DPhil, Professor of Medicine at the Mayo Clinic in Rochester, Minnesota. “It’s not that aspirin is less effective than the oral anticoagulants, it’s that there’s no role for it. There are no good data to support aspirin in the prevention of stroke in atrial fibrillation.”

“The use of aspirin has probably been misguided, based upon a single trial which showed a profound effect and was probably just an anomaly,” said N.A. Mark Estes III, MD, Professor of Medicine and Director of the New England Cardiac Arrhythmia Center at Tufts University in Boston, and a past president of the Heart Rhythm Society

I would just take it off of your clinical armamentarium because the best available data indicate that it doesn’t prevent strokes. I’m certainly not using it in my patients. Increasingly in my patients with a CHA2DS2-VASc of 1, I’m discussing the risks and benefits of a novel oral anticoagulant,” said Dr. Estes.


Those are amazingly definitive statements. But, as I’ve learned  we can’t just except what the “experts” and the guidelines tell us we have to look at the original studies informing these decisions.

In 1991 the seminal study proving the benefits of warfarin in preventing stroke (Stroke Prevention in Atrial Fibrillation (SPAF) trial) was published.

It compared warfarin (measured by PT ratio) to placebo and aspirin 325 mg to placebo in preventing stroke in AF patients. Warfarin reduced stroke by 67% and aspirin by 42%. The risk of significant bleeding was similar at around 1.5% per year for all three arms.

Based on this and other AF trials (AFASAK, CAFA, SPINAF, EAFT, et al. ) when I gave talks or taught cardiology fellows in the 1990s my message (similar to this presentation) emphasized the superior benefits of warfarin compared to aspirin (especially when monitored by INR in a 2.0 to 3.0 range) in higher risk AF patients. Overall it was felt that aspirin (dosing varying from 100 to 325 mg) reduced stroke/embolism by 20-30% compared to placebo and would offer benefit to those patients at low risk or who could not tolerate warfarin.

Based on the 2014 American guidelines (and a focused update in 2019 which did not address this issue) I had not been actively taking my low risk patients off baby aspirin.

I was prompted to re-research this question and write this post because a 58 year old woman with paroxysmal AF and hypertension  called the office today asking if I wanted her to take a baby aspirin daily. She has a CHADS2VASC score of 2 (woman and hypertension) and falls into the category where we should have an in depth conversation about the risks and benefits of anticoagulant therapy.

I have that discussion with her each visit and thus far we’ve decided to hold off on starting an anticoagulant drug like Eliquis. She has promised to record her ECG daily (using her Kardia Mobile ECG device) and report any onset of AF. If AF recurs we will have another discussion about Eliquis.

I spent several hours pouring over the original  studies and more recent studies, reviews and meta-analyses and reached the following conclusions:

With the advent of the newer oral anticoagulants (NOACs) in the last decade which offer better stroke reduction and less bleeding than warfarin patient-physician  discussions should be about taking a NOAC or not. Aspirin should not be considered as a lower risk/effective alternative as its benefits are minimal and bleeding risks similar to NOACs.

I told my patient no on the daily baby aspirin and from now on I will recommend stopping aspirin (assuming no other reason to be on it) to all my low risk AF patients.

Antithrombotically Yours,

-ACP

N.B.

The components of the stroke risk score- CHA2DS2-VASc = Congestive Heart failure, hypertension, Age ≥75 (doubled), Diabetes, Stroke (doubled), Vascular disease, Age 65–74, and Sex (female);


For those interested in a discussion on why females get a point in the risk score but a different cut-off for OAC therapy this is from the ESC guidelines:

 Many risk factors contribute to the increased risk of stroke in patients with AF as expressed in the CHA2DS2-VASc score. The evidence for female sex as a risk factor has been assessed in many studies. Most studies support the finding that females with AF are at increased risk of stroke. One meta-analysis found a 1.31-fold (95% CI: 1.18–1.46) elevated risk of stroke in females with AF, with the risk appearing greatest for females ≥75 years of age (S4.1.1-35). Recent studies have suggested that female sex, in the absence of other AF risk factors (CHA2DS2-VASc score of 0 in males and 1 in females), carries a low stroke risk that is similar to males. The excess risk for females was especially evident among those with ≥2 non–sex-related stroke risk factors; thus, female sex is a risk modifier and is age dependent (S4.1.1-49). Adding female sex to the CHA2DS2-VASc score matters for age >65 years or ≥2 non–sex-related stroke risk factors


If you’re curious what constitutes a IIB recommendation it is described in the yellow box below  My best summary is still “not a ringing endorsement”.



If you want to see the ESC guideline recommendations in detail

An Early Look At AliveCor’s Amazing KardiaMobile 6L: Accurate 6 Lead ECG On Your Smartphone

The skeptical cardiologist has been evaluating a demo version of AliveCor’s new KardiaMobile 6L.

I have been a huge advocate of Kardia’s single lead ECG and use it with great success in dozens of my afib patients. I’ve written about how this personal ECG monitoring empowers patients and providers and is a crucial component of the enlightened medical management of afib.

In less than a month AliveCor plans to release its KardiaMobile 6L which will provide 6 ECG leads  using a smartphone based mobile ECG system that is similar to the Kardia single lead system.

AliveCor’s website proclaims “This is your heart x 6.”

 

 

 

I was fortunate enough to obtain a demo version of the 6L and have been evaluating it.

My  first impressions are that this is a remarkable step forward in the technology of personal ECG monitoring. I’m not sure if I would call it “your heart x 6” but I feel the ability to view six high quality leads compared to one is definitely going to add to the diagnostic capabilities of the Kardia device.

Kardia 6L Setup And Hardware

The 6L is similar in design and function to the single lead device.

I’m including this cool spinning video (from the AliveCor website) which makes it appear, slick, stylish and  futuristic

Once paired to the Kardia smartphone app (available for iOS or Android smartphones for free) it communicates with the smartphone  using BLE to create ECG tracings.

Like the single lead Kardia the 6L has two sensors on top for left and right hand contact. But in addition, there is a third on the bottom which can be put on a left knee or ankle.

The combination of these sensors and contact points yield the 6 classic frontal leads of a full 12 lead ECG: leads I, II, III, aVL, aVR, and aVF. This is accomplished, AliveCor points out “without messy gels and wires.

I found that using the device was simple and strait-forward and we  were able to get high quality tracings with minimal difficulty within a minute of starting the process in all the patients we tried it on.

The  Diagnostic Power Of Six Leads

Below is a tracing on a patient with known atrial fibrillation. The  algorithm correctly diagnoses it. With 6 different views of the electrical activity of the atrium I (and the Kardia algorithm)  have a better chance of determining if p waves are present, thereby presumably  increasing the accuracy of rhythm determination

Depending on the electrical vector of the left and right atria, the best lead to visualize p waves varies from patient to patient, thus having 6 to choose from should improve our ability to differentiate sinus rhythm from afib.

In the example below, the Kardia 6L very accurately registered the left axis deviation and left anterior fascicular block that we also noted on this patient’s 12 lead ECG. This 6L capability, determining the axis of the heart in the frontal plane,  will further add to the useful information Kardia provides.

 

For a good summary of axis determination and what abnormal axes tells us see here.

The History of ECG Leads

When I began my cardiology training the 12-lead ECG was  standard but it has not always been that way. I took this timeline figure from a nice review of the history of the ECG

 

 

Einthoven’s first 3 lead EKG  in 1901 was enormous.

Old string galvanometer electrocardiograph showing the big machine with the patient rinsing his extremities in the cylindrical electrodes filled with electrolyte solution.
 It is mind-boggling to consider that we can now record  6 ECG leads with a smartphone and a device the size of a stick of gum

For the first 30 years of the ECG era cardiologists only had 3 ECG leads to provide information on cardiac pathology.  Here’s a figure from a state of the art paper in 1924 on “coronary thrombosis” (which we now term a myocardial infarction) showing changes diagnostic of an “attack” and subsequent atrial fibrillation

In the 1930s  the 6 precordial leads were developed providing more information on electrical activity in the horizontal axis of the heart. The development of the augmented leads (aVr, aVL, aVF) in 1942  filled in the gaps of the frontal plane and the combination of all of these 12 leads was sanctified by the AHA in 1954.


I’ll write a more detailed analysis of the Kardia 6L after spending more time using it in patient care.

Specifically I’ll be analyzing (and looking for published data relative to):

-the relative accuracy of the 6L versus the single lead Kardia for afib determination (which, at this point would be the major reason for current Kardia users to upgrade.)

-the utility of the 6L for determination of cardiac axis and electrical intervals in comparison to the standard 12 lead ECG,  especially in patients on anti-arrhythmic drugs

For now, this latest output from the meticulous and thoughtful folks at AliveCor has knocked my socks off!

Stockingfreely Yours,

-ACP

N.B. If one uses the single lead kardia device in the traditional manner (left hand and right hand on the sensors) one is recording ECG lead I. However, if you put your right hand on the right sensor and touch the left sensor to your left leg you are now recording ECG lead II and if to the right leg, ECG lead III.

I describe this in detail here. For certain individuals the lead II recordings are much better than lead I and reduce the prevalence of “unclassified” recordings.

My feeling is that by automatically including the leg (and leads II and III) the 6L will intrinsically provide high voltage leads for review and analysis, thereby improving the ability to accurately classify rhythm.

And (totally unrelated to the 6L discussion) one can also record precordial ECG leads by putting the device on the chest thus theoretically completing the full 12 leads of the standard ECG.


Please also note that I have no financial or consulting ties to AliveCor.  I’m just a big fan of their products.

Catheter Ablation of Atrial Fibrillation: Will It Reduce Your Risk of Death, Serious Bleeding or Stroke?

The wide-spread public conception that catheter ablation cures atrial fibrillation and reduces one’s risk of stroke or dying has fueled a  $4.5 billion industry.  Until very recently there were no published randomized trials supporting this expensive and risky procedure.

The recently published landmark CABANA trial found that in patients with afib “the strategy of catheter ablation, compared with medical therapy, did not significantly reduce the primary composite end point of death, disabling stroke, serious bleeding, or cardiac arrest. ”

So there is no proven benefit of ablation on death, stroke, bleeding or cardiac arrest. This means that a medical management approach to management of afib is always an acceptable approach. Especially an enlightened medical approach.

In CABANA, women and those patients >75 years of age did worse with ablation as this chart shows.

What about complications? I mentioned that ablation was risky and this is because any time you put a catheter in someone’s heart you can create life-threatening problems. When you then heat up the tip of that catheter it is possible to burn/damage/destroy things that  are not your target.

As John Mandrola has pointed out at least ablation was not more dangerous than medical management:

A reassuring finding of CABANA was that ablation did not do worse than drugs. But one of the messages I heard from HRS was that CABANA showed that AF ablation is safe. This is a problem.

The complications in the ablation arm were more serious and more numerous than those in the drug arm. We will have to wait for the published paper for formal comparisons.  CABANA likely represents a best-case scenario because it allowed only experienced operators and centers to be part of the trial. Many people undergo ablation by less experienced operators.

Another important safety issue is the asymmetry of procedural complications. When you talk privately with ablation doctors, many, perhaps most, relay the story of a tragic death of an otherwise healthy middle-aged adult from an atrial-esophageal fistula.

Yes. A well-recognized and highly feared complication of ablation , atrial-esophageal fistula, causes rapid death due to exsanguination through a channel between the left atrium and the esophagus which develop due to destruction/burning of the normal esophageal/atrial tissue.

In this chart taken from the CABANA abstract presentation you can see the complications which do not include a highly feared atrial-esophageal fistula.

 

Can Catheter Ablation Improve Quality of Life?

Basically, after the CABANA trial we have no evidence that ablation will  improve hard outcomes in afib patients. However, there are numerous patients who feel they have greatly benefited from the procedure, experiencing years of afib free existence.

This benefit of ablation, of improving quality of life and making patients feel better is important.

The CABANA trial also looked at quality of life and in part II of this article I’ll examine that in detail.

Skeptically Yours,

-ACP


Update 6/12/2019 357 PM.

Twitter follower @mrice5025 was kind of enough to read the above closely enough to realize that the number of atrial esophageal fistulae was actually zero in the CABANA trial and I have corrected the text accordingly.

I have seen a case of this mostly fatal complication in a patient who had an ablation done at an outside hospital 5 weeks earlier and who rapidly died from it and I try to be very aware of its possibility as early diagnosis and surgery is the key to survival.

This review article gives an overview:

AF ablation carries a small risk of complications with the most serious being atrioesophageal fistula (AEF). Although the incidence is less than 0.1%, it is usually fatal Esophageal perforation or fistula was reported in 31 patients (0.016%) in the Global Survey of Esophageal and Gastric Injury in Atrial Fibrillation study. Symptom onset for esophageal perforation or fistula was reported on average 19.3 days after the ablation procedure but could appear as short as 6 days and as long as 59 days post ablation.Esophageal injury has been observed most frequently with percutaneous radiofrequency ablation, although it has also been reported with other energy sources including cryoablation,high-intensity focused ultrasound and even surgical ablation.

 


The featured image comes from this Cleveland Clinic video which has some great graphics and reasonable information (once you get by the annoying lady at the beginning who describes ablation as “an excellent minimally invasive” procedure.)

At my hospital, St. Luke’s, I have three outstanding electrophysiologists who do excellent ablations,, Jonas Cooper, Cary Fredman, and Mauricio Sanchez.

Enlightened Medical Management of Atrial Fibrillation: Part I. Amiodarone, Kardia And Cardioversions

The skeptical cardiologist is a firm believer in the benefit of maintaining normal rhythm in most patients who develop atrial fibrillation (AF, see here.)

Sometimes this can be accomplished by lifestyle changes (losing pounds and cutting back on alcohol , treating sleep apnea, etc.) but more often successful long term maintenance of normal rhythm (NSR) requires a judicious combination of medications and electrical cardioversions (ECV).

It is also greatly facilitated by a compliant and knowledgeable patient who is regularly self-monitoring with a personal ECG device.

My article on electrical cardioversion (see here)  was inspired by a patient (we’ll call her Sandy) who asked me  in April of 2016, “how many times can you shock the heart?”

In 2016 I performed her fifth cardioversion and last week I did her sixth.

Her story of AF is a common one which exemplifies how excellent medical management of AF can cure heart failure and mitral regurgitation and create decades of AF-free, happy and healthy existence.

A Tale Of Six Cardioversions

Sandy had her first episode of atrial fibrillation in 2001 and underwent a cardioversion at that time and as far as she knew had no AF problems for 14 years. I’ve seen numerous cases like this where following a cardioversion, patients maintain NSR for a long time without medications but I’ve also seen  many in whom AF came back in days to months.

In 2015 she saw her PCP for routine follow-up and AF with a rapid rate was detected.  She had been noticing shortness of breath on exertion and a cough at night but otherwise had no clue she was out of rhythm.

When I saw her in consultation she was in heart failure and her echocardiogram demonstrated a left ventricular  ejection fraction of 50% with severe mitral regurgitation.  She quickly went back into AF after an electrical cardioverson (ECV) and  reverted to AF again following a repeat ECV  after four days on amiodarone.

Since amiodarone can take months to reach effective levels in the heart we tried one more time to cardiovert after loading on higher dosage amiodarone for one month. This time she stayed in NSR

Following that cardioversion she has done extremely well. Her shortness of breath resolved and follow up echocardiograms have demonstrated resolution of her mitral regurgitation.

She had purchased a Kardia mobile ECG device for personal monitoring of her rhythm and we were able to monitor her rhythm using the KardiaPro dashboard. Recordings showed she was consistently maintaining NSR after her 2016 ECV

Image from my online KardiaPro Dashboard showing the date and HR of patient’s home ECG recordings leading up to the cardioversion and following it. The orange dots were Kardia diagnosed AF and following the cardioversion the green dots are NSR.

 

 

 

I’ve written extensively on the great value of KardiaPro used in conjunction with the Kardia mobile ECG device for monitoring patients pre and post cardioversion for atrial fibrillation.  Sandy  does a great job of making frequent Kardia ECG recordings, almost on a daily basis so even though she has no symptoms we are alerted to any AF within 24 hours of it happening.

Amiodarone-The Big Medical Gun For Stopping Atrial Fibrillation

The recurrence of AF Sandy had in 2016 occurred 8 months after I had lowered her amiodarone dosage to 100 mg daily.

Amiodarone is a unique drug in the AF toolkit.

It is the by far the most effective drug for maintaining sinus rhythm, an effect that makes it our most useful antiarrhythmic drug (AAD).

  1. It is cheap and well-tolerated.
  2. Uniquely among drugs that we use for controlling atrial fibrillation it takes a long time to build up in heart tissue and a long time to wear off.
  3. It is the safest antiarrhythmic drug from a cardiac standpoint. Unlike many of the other AADs we don’t have to worry about pro-arrhythmia (bringing out more dangerous rhythms such as ventricular tachycardia or ventricular fibrillation) with amio.
  4. Amiodarone, however, is not for all patients-it has significant long term side effects that necessitate constant vigilance by prescribing physicians including thyroid, liver and lung toxicity.

I monitor my patients on amiodarone with thyroid and liver blood tests every 4 months and a chest x-ray yearly and I try to utilize the minimal dosage that will keep them out of AF.

In Sandy’s case it was apparent that 100 mg was too little but with an increase back to 200 mg daily, the AF remained at bay.

In early 2017, Sandy read on Facebook that amio was a “poison” and after discussing risks and benefits we decided to lower the dosage to 200 mg alternating with 100 mg. It is common and appropriate for patients to be fearful of the potential long term and serious consequences of medications. For any patient taking amiodarone I always offer the option of stopping the drug with the understanding that there is a strong likelihood of recurrent AF within 3 months once the drug wears off.

In October, 2018 with Sandy continuing to show normal heart function and maintain SR as documented by her daily Kardia ECG tracings we decided to further lower the dosage to 100 mg daily.

Six months later she noted one day that her Kardia reading was showing a heart rate of 159 bpm and diagnosing atrial fibrillation. AF had recurred on the lower dosage of amiodarone.  She had no symptoms but based on prior experience we knew that soon she would go into heart failure.

Image from my online KardiaPro report on Sandy showing all green dots (NSR) until she went into AF (orange dots). Upon discharge from the hospital the daily Kardia recordings now show NSR (green dots).

Thus, her amiodarone was increased and a sixth cardioversion was performed. We could find no trigger for this episode (unless the  bloody mary she consumed at a  Mother’s Day Brunch 2 days prior was the culprit.)

Medical Management With Antiarrhythmics Versus Ablation

Many patients seek a “cure” for atrial fibrillation. They hear from friends and neighbors or the interweb of ablation or surgical procedures that promise this.  Stopafib.org, for example,  promotes these types of procedures saying “Catheter ablation and surgical maze procedures cure atrial fibrillation”

In my experience the majority of patients receiving ablation or surgical procedures (Maze procedure and its variants) ultimately end up having recurrent episodes of atrial fibrillation. Guidelines do not suggest that anticoagulants can be stopped in such patients. Often, they end up on AADs.

I’ve prepared a whole post on ablation for AF but the bottom line is that there is no evidence that ablation lowers the AF patient’s risk of dying, stroke, or bleeding. My post will dig deeper into the risks and benefits of ablation.

There is no cure for AF, surgical, catheter-based or medical.

In the right hands most patients can do very well with medical management combined with occasional cardioversion.

Who posseses the right hands?

In my opinion, most AF patients are best served by a cardiologist who has a special interest in atrial fibrillation and takes the time to read extensively and keep up with the latest developments and guideline recommendations in the area. This does not need to a be an electrophysiologist (EP doctor-one who specializes in the electrical abnormalities of the heart and performs ablations, pacemakers and defibrillators.)

I have a ton of respect for the EP doctors I work with and send patients to but I think that when it comes to doing invasive, risky procedures the decision should be based on a referral/recommendation from a cardiologist who is not doing the procedure.

In many areas of cardiology we are moving toward an interdisciplinary team of diagnosticians, interventionalists, surgeons and non-cardiac specialists to make decisions on performance of high-risk and high-cost but high-benefit procedures like valve repair and replacement, closure of PFOs and implantation of left atrial appendage closure devices.

It makes sense that decisions to perform high-risk , high-cost atrial fibrillation procedures also be determined by a multi-disciplinary team with members who don’t do the procedure.

This is a rule of thumb that can also be applied to many surgical procedures as well.  For example, the decision to proceed to surgical treatment of carotid artery blockages (carotid endarterectomy) is typically  made by the vascular surgeons who perform the procedure. In my opinion this decision should be made by a neurologist with expertise in neurovascular disease combined with a good cardiologist who has kept up with the latest studies on the risks and benefits of carotid surgery and is fully briefed on the latest guideline recommendations.

Unbenightedly Yours,

-ACP

A Guide To Using Apple Watch and Kardia ECG devices-What They Can and Can’t Do

Many patients (and perhaps physicians) are confused as to how best to utilize personal ECG devices. I received this question illustrating such confusion from a reader recently:

I first came across your website a year ago during persistent angina attacks, and returning now due to increasing episodes of symptoms akin to Afib. I bought a Kardia 2 yrs ago for the angina episodes, and looking to buy the Apple Series 4 for the Afib, as I want to try a wearable for more constant monitoring. What I would greatly appreciate if you had a basic guide for both the Kardia & Apple devices, specifically when and how to best employ them for unstable angina and detecting undiagnosed Afib. As in, what can I as a patient provide to you as a doctor for diagnosis in advance of a formal visit. I’m a US Iraq vet medically retired in the UK, and most of my concerns get dismissed out of hand as “anxiety”, not sure why they thought a stent would cure my anxiety though  

Personal, Wearable ECG Devices Won’t Diagnose Angina (or Heart Attacks)

First. please understand that none of these devices have any significant role in the management of angina. Angina, which is chest/arm/jaw discomfort due to a poor blood supply to the heart muscle cannot be reliably diagnosed by the single lead ECG recording provided by the Apple Watch, the Kardia Band or the Kardia mobile ECG device. Even a medical-grade 12 lead ECG doesn’t reliably diagnose angina and we rely on a constellation of factors from the patient’s history to advanced testing to determine how best to manage and diagnose angina.

Second, as you are having episodes “akin to Afib”, all of these devices can be helpful in determining what your cardiac rhythm is at the time of the episodes if they last long enough for you to make an ECG recording.

The single lead ECG recording you can make from the Apple Watch, the Kardia Band and from the Kardia mobile device can very reliably tell us what the cardiac rhythm was when you were feeling symptoms.

The algorithms of these devices do a good job of determining if the rhythm Is atrial fibrillation. Also, if the rhythm is totally normal they are good at determining normality.

However, sometimes extra or premature beats confuse the algorithms resulting in an unclassified tracing and (rarely) an inaccurate declaration of afib

These tracings can be reviewed by a competent cardiologist to sort out what the rhythm really is.

In all of these cases, having an actual recording of the cardiac rhythm at the time of symptoms is immensely helpful to your doctor or cardiologist in determining what is causing your problems.

My recommendation, therefore, would be to make several recordings at the time of your symptoms. Print them out and carefully label the print-out with exactly what you were feeling when it was recorded and present these to the doctor who will be reviewing your case.

As I’ve mentioned in previous posts (see here), my patients’ use of Kardia with the KardiaPro online service has in many cases taken the place of expensive and inconvenient long term monitoring devices.

Case Example-Diagnosing Rare And Brief Attacks Of Atrial Fibrillation

I recently saw a patient who I think perfectly demonstrates how useful these devices can be for clarifying what is causing intermittent episodes of palpitations-irregular, pounding, or racing heart beats.

She was lying on a sofa one day when she suddenly noted her heart “pumping fast” and with irregularity. The symptoms last for about an hour. She had noticed this occurred about once a year occurring out of the blue.

Her PCP ordered a long term monitor, a stress test and an echocardiogram.

The monitor showed some brief episodes of what I would term atrial tachycardia but not atrial fibrillation but the patient did not experience one of her once per year hour long episodes of racing heart during the recording. Thus, we had not yet solved the mystery of the prolonged bouts of racing heart.

She was referred to me for evaluation and I recommended she purchase an Alivecor device and sign up for the KardiaPro service which allows me to view all of her recordings online. The combination of the device plus one year of the KardiaPro service costs $120.

She purchased the device and made some occasional recordings when she felt fine and we documented that these were identified as normal by Kardia. For months nothing else happened.

Then one day in April she had her typical prolonged symptom of a racing heart and she made the recording below (She was actually away from home but had the Kardia device with her.)

When she called the office I logged into my KardiaPro account and pulled up her recordings and lo and behold the Kardia device was correct and she was in atrial fibrillation at a rate of 113 BPM.

With the puzzle of her palpitations solved we could now address proper treatment.

Continuous Monitoring for Abnormal Rhythms

Finally, let’s discuss the wearables ability to serve as a monitor and alert a patient when they are in an abnormal rhythm but free of any symptoms.

My reader’s intent was to acquire a device for “constant monitoring”:

I’m looking to buy the Apple Series 4 for the Afib, as I want to try a wearable for more constant monitoring.

This capability is theoretically available with Apple Watch 4’s ECG and with the Kardia Band (using SmartRhythm) which works with Apple Watch Series 1-3.

However, I have not been impressed with Apple Watch’s accuracy in this area (see here and here) and would not at this point rely solely on any device to reliably alert patients to silent or asymptomatic atrial fibrillation.

In theory, all wearables that track heart rate and alert the wearer if the resting heart rates goes above 100 BPM have the capability of detecting atrial fibrillation. If you receive an alert of high HR from a non ECG-capable wearable you can then record an ECG with the Kardia mobile ECG to see if it really is atrial fibrillation.

At 99$, the Kardia is the most cost-effective way of confirming atrial fibrillation for consumers.

I hope this post adds some clarity to the often confusing field of personal and wearable ECG devices.

Electroanatomically Yours,

-ACP

Can The Apple Watch Or Kardia ECG Monitor Detect Heart Attacks?

The skeptical cardiologist recently received this email from a reader:

With the new Apple Watch that’s out now, people have suggested my husband (who had a heart attack at 36) should get it since it could detect a heart attack. But I keep remembering what you said – that these devices can’t detect heart attacks and that Afib isn’t related to a heart attack most of the time – is that still the case? I don’t really know how to explain to people that it can’t do this, since absolutely everyone believes it does.

The answer is a resounding and unequivocal NO!

If we are using the term heart attack to mean what doctors call a myocardial infarction (MI) there should be no expectation that any wearable or consumer ECG product can reliably diagnose a heart attack.

The Apple Watch even in its latest incarnation and with the ECG feature and with rhythm monitoring activated is incapable of detecting a myocardial infarction.

Similarly, although the AliveCor Kardia ECG monitor is superb at diagnosing rhythm abnormalities it is not capable of detecting an MI

To make this even clearer note that when you record an ECG on the Apple Watch it intermittently flashes the following warning:

 

Note: “Apple Watch never checks for heart attacks”

How did such this idea take root in the consciousness of so many Americans?

Perhaps this article in 9-5 Mac had something to do with it

The article begins
Scott Killian never imagined his Apple Watch might save his life, but that’s exactly what happened a few weeks ago when he had a heart attack in the middle of the night. Killian recently shared his personal experience with 9to5Mac, and the details of his story are absolutely amazing.
In reality,  the man received an alarm that his resting heart rate was high at night. Apparently he also was experiencing chest pain and went to an ER where a cardiac enzyme was elevated.  Subsequently he underwent testing that revealed advanced coronary artery disease and he had a bypass operation. 
Even if we assume all the details of this story are accurate it is absolutely not a case of Apple Watch diagnosing an MI.
 
A high resting heart rate is not neccessarily an indicator of an MI and most MIs are not characterized by high heart rates.  We have had the technology with wearables to monitor resting heart rate for some time and no one has ever suggested this can be used to detect MI.
 
The rate of false alarms is so high and the rate of failure to diagnose MI so low that this is a useless measure and should not provide any patient reassurance.
 
The writer of this story and the editors at 9-5 Mac should be ashamed of this misinformation.
 
Several other news sources have needlessly muddied the water on this question including Healthline and Fox News:
 
 
 
 
 
 
 
The Fox News article entitled “Could The Apple Watch Series 4 save you from a heart attack” quotes a non-physician who suggests that AW can detect early signs of a heart attack:
 

In clear cut cases the Apple Watch could make the difference between life and death,” says Roger Kay, president of Endpoint Technologies Associates. Because you wear the Apple Watch at all times, it can detect an early sign of a stroke or a heart attack, and that early indication is critical, he says.

And the Healthline article on the new Apple Watch also incorrectly implies it can diagnose MI:

The device, which was unveiled last week, has an electrocardiogram (ECG) app that can detect often overlooked heart abnormalities that could lead to a heart attack.

And if you are felled by a heart problem, the fall detector built into the Apple Watch Series 4 could alert medical professionals that you need help

Fox News and Healthline should modify their published articles to correct the misinformation they have previously provided.

And it is still true that  although both Apple Watch and Kardia can diagnose atrial fibrillation the vast majority of the time acute heart attacks are not associated with atrial fibrillation.

Readers, please spread the word far and wide to friends and family-Apple Watch cannot detect heart attacks!

Skeptically Yours,

-ACP

Apple Heart Study: Despite The Ballyhoo, No Benefits Demonstrated, Harms Not Measured

The results of the Apple Heart Study, were presented this morning at the American College of Cardiology Scientific Sessions amid intense media scrutiny. The AHS is a “prospective, single arm pragmatic study” which had the primary objective of measuring the proportion of participants with an irregular pulse detected by the Apple Watch who turn out to have atrial fibrillation on subsequent ambulatory ECG patch monitoring.

 

I and over 400,000 other Apple Watch owners participated in the AH study by downloading the Apple Heart Study app and self-verifying our eligibility. 

My assessment is that we have learned little to nothing from the AHS that we didn’t already know. I’m also concerned that many patients suffered anxiety or unnecessary testing after being referred to urgent care centers, emergency departments, cardiologists or primary care providers and the results of these inappropriate referrals may never be determined.

Here is the study in a nutshell:

  1. Participants enrolled by submitting  information using the iPhone Heart Study app and none of their isubmitted nformation was verified.
  2. An irregular pulse notification was issued to 0.5% of participants who were then  contacted and asked to participate in a Telehealth visit with a doctor (who we will call Dr. Appleseed)
  3. Only 945 of the 2161 who received a pulse notification participated in the first study visit.
  4. Interestingly, Dr. Appleseed was empowered to send participants to the ER if they had symptoms (chest pain, shortness of breath, fainting/losing consciousness) It is not clear how many were sent to the ER and what their outcomes were but this flow diagram shows that 20 were excluded from further testing due to “emergent symptoms.”

  5. Another 174 participants were excluded after finding out at the first visit that they had a history of afib or aflutter and 90 due to current anticoagulant use (both of these factors were exclusion criteria which gives us an idea of how accurate the information was at the time of participant entry.)
  6. After all these exclusions only 658 ECG monitor patches were shipped to the participants of which only 450 were returned and analyzed.
  7. This means of the original 2161 participants who were notified of pulse irregularity, the study only reports data on 450 or 21%. Such a low rate of participation makes any conclusions from the study suspect.
  8. Of the 450 ECG patches analyzed only 34% were classified as having afib. Only 25% of this afib lasted longer than 24 hours.
  9. After the patch data was analyzed, patients had a second Telehealth visit with Dr. Appleseed who reviewed the findings with the patient. Per the initial published description of the methods of the AHS (see here) Dr. Appleseed  would tell the participant to head to the ER if certain abnormalities were found on the ECG.

Per the study description (apple heart study), Dr. Appleseed recommended a visit to the PCP for “AF or any other arrhythmia” detected by the patch:”

“If AF or any other arrhythmias have been detected in reviewing the ambulatory ECG monitor data, or if there are other non-urgent symptom identified by the study physician during the video visit that may need further clinical evaluation, the Study Telehealth Provider directs the participant to his or her primary health care provider”

At this point it seems likely that a lot of participants were instructed to go see their PCPs. Because as someone who looks at a lot of 2 week ambulatory ECG recordings I know that is the rare recording that does not show “other arrhythmias.”

Even more distressing is the call that participants would have received based on “the initial technical read:” I’m presuming this “technical read” was by a technician and not by a cardiologist. In my experience, many initial reads from long term monitors are inaccurate.

“If the initial technical read identifies abnormalities that require urgent attention (ventricular tachycardia or ventricular fibrillation, high-degree heart block, long pauses, or sustained and very rapid ventricular rates), then the participant is contacted immediately and directed to local emergency care or advised how to seek local emergency care.”

I wonder how many  ERs had AHS participants show up saying they had been told they had a life-threatening arrhythmia? How much down stream testing with possible invasive, life-threatening procedures such as cardiac catheterization were performed in response to these notifications?

Overall, these findings add nothing to previous studies using wearable PPG technology and they certainly don’t leave me with any confidence that the  Apple Watch is accurately automatically detecting atrial fibrillation.

Was more harm than good done by the Apple Heart Study?

We will never know. The strength of this study, the large number of easily recruited participants is also its Achilles heel. We don’t know that any information about the participants is correct and we don’t have any validated follow up of the outcomes. In particular, I’m concerned that we don’t know what happened to all of these individuals who were sent to various health care providers thinking there might be something seriously wrong. 

Perhaps Apple and Stanford need to review the first dictum of medicine: Primum Non Nocere, First Do No Harm.

Tachogramophobically Yours,

-ACP

Apple Watch Fails To Notify Patient Of 3 Hour Episode Of Rapid Atrial Fibrillation

Apple claims that its Apple Watch can detect atrial fibrillation (AF) and appropriately notify the wearer when it suspects AF.

This claim comes with many caveats on their website:

Apparently it needs to record 5 instances of irregular heart beat characteristic of atrial fibrillation over at least 65 minutes before making the notification.

This feature utilizes the watch’s optical heart sensors, is available  in Apple Watch Series 1 or later and has nothing to do with the Apple Watch 4 ECG recording capability which I described in detail in my prior post.

Failure To Detect AF

A patient of mine with known persistent AF informed me yesterday that she had gone into AF and remained in it for nearly 3 hours with heart rates over 100 beats per minute and had received no notification. She confirmed the atrial fibrillation with both AW4 recordings and AliveCor Kardia recordings while she was in it.

The watch faithfully recorded sustained heart rates up to 140 BPM but never alerted her of this even though the rate was consistently over her high heart rate trigger of 100 BPM.

The patient had set up the watch appropriately to receive notifications of an irregular rhythm.

Reviewing her tracings from both the AW4 and the Kardia this was easily diagnosed AF with a rapid ventricular response.

What does Apple tell us about the accuracy of the Apple Watch AF notification algorithm? All we know is the unpublished , non peer-reviewed data they themselves collected and presented to the FDA.

From this link on their website Apple says:

In a study of 226 participants aged 22 years or older who had received an AFib notification while wearing Apple Watch and subsequently wore an electrocardiogram (ECG) patch for approximately 1 week, 41.6% (94/226) had AFib detected by ECG patch. During concurrent wear of Apple Watch and an ECG patch, 57/226 participants received an AFib notification. Of those, 78.9% (45/57) showed concordant AFib on the ECG patch and 98.2 % (56/57) showed AFib and other clinically relevant arrhythmias. These results demonstrate that, while in the majority of cases the notification will accurately represent the presence of AFib, in some instances, a notification may indicate the presence of an arrhythmia other than AFib. No serious device adverse effects were observed

This tells us that about 80% of notifications are likely to be Afib whereas 20% will not be Afib. It is unclear what the “other clinically relevant arrhythmias”  might be. If I had to guess I would suspect PVCS or PACS which are usually benign.

If 20% of the estimated 10 million Apple Watch wearers are getting false positive notifications of afib that means 2 million calls to doctor or visits to ERs that are not justified.  This could be a huge waste of resources.

Thus the specificity of the AF notification is 80%. The other important parameter is the sensivitiy. Of the cases of AF that last >65 minutes how many are detected by the app?

Apple doesn’t seem to have any data on that but this obvious case of rapid AF lasting for 3 hours does not give me much confidence in their AF detection algorithms.

They do have a lot of CYA statements indicating you should not rely on this for detection of AF:

It is not intended to provide a notification on every episode of irregular rhythm suggestive of AFib and the absence of a notification is not intended to indicate no disease process is present; rather the feature is intended to opportunistically surface a notification of possible AFib when sufficient data are available for analysis. These data are only captured when the user is still. Along with the user’s risk factors, the feature can be used to supplement the decision for AFib screening. The feature is not intended to replace traditional methods of diagnosis or treatment.

My patient took her iPhone and Apple Watch into her local Apple store to find out why her AF was not detected. She was told by an Apple employee that the Watch does not detect AF but will only notify her if her heart rate is extremely low or high. I had asked her to record what they told her about the problem.

As I’ve written previously (see here) the Apple Watch comes with excessive hype and minimal proof of its accuracy. I’m sure we are going to hear lots of stories about AF being detected by the Watch but we need some published, peer-reviewed data and we need to be very circumspect before embracing it as a reliable AF monitor.

Skeptically Yours,

-ACP

Putting The Apple Watch 4 ECG To The Test In Atrial Fibrillation: An Informal Comparison To Kardia

My first patient this morning, a delightful tech-savvy septagenarian with persistent atrial fibrillation told me she had been monitoring her rhythm for the last few days using her Apple Watch 4’s built in ECG device.

Previously she had been using what I consider the Gold Standard for personal ECG monitoring- AliveCor’s Kardia Mobile ECG   and I monitored her recordings through our Kardia Pro connection.

I had been eagerly awaiting Apple’s roll out since I purchased the AW4 in September (see here) and between patients this morning I down-loaded and installed the required iPhone and Watch upgrades and began making AW4 recordings.

Through the day I tried the AW4 and the Kardia on patients in my office.

Apple Watch 4 ECG Is Easy and Straightforward

The AW4 ECG recording process is very easy and straightforward. Upon opening the watch app you are prompted to open the health app on your iPhone to allow connection to the Watch ECG information. After this, to initiate a recording simply open the Watch ECG app and hold your finger on the crown.

Immediately a red ECG tracing begins along with a 30 second countdown.

Helpful advice to pass the time appears below the timer:

“Try Not to move your arms.”

and

“Apple Watch never checks for heart attacks.”

When finished you will see what I and my patient (who mostly stays in sinus rhythm with the aid of flecainide) saw-a declaration of normality:

Later in the day I had a few patients with permanent  atrial fibrillation put on my watch.

This seventy-something farmer from Bowling Green, Missouri was easily able to make a very good ECG recording with minimal instruction

The AW4 nailed the diagnosis as atrial fibrillation.

We also recorded a Kardia device ECG on him and with a little more instruction the device also diagnosed atrial fibrillation

After you’ve made an AW4 recording you can view the PDF of the ECG in the Health app on your iPhone where all of your ECGs are stored. The PDF can be exported to email (to your doctor) or other apps.

ECG of the Bowling Green farmer. I am not in afib.

Apple Watch Often “Inconclusive”

The AW4 could not diagnose another patient with permanent atrial fibrillation and judged the recording “inconclusive”

The Kardia device and algorithm despite a fairly noisy tracing was able to correctly diagnose atrial fibrillation in this same patient.

I put the AW4 on Sandy, our outstanding echo tech at Winghaven who is known to have a left bundle branch block but remains in normal rhythm and obtained this inconclusive report .

Kardia, on the other hand got the diagnosis correctly:

One Bizarre Tracing by the AW4

In another patient , an 87 year old lady with a totally normal recording by the Kardia device, the AW4 yielded a bizarre tracing which resembled ventricular tachycardia:

Despite adjustments to her finger position and watch position, I could not obtain a reasonble tracing with the AW4.

The Kardia tracing is fine, no artifact whatsoever.

What can we conclude after today’s adventures with the Apple Watch ECG?

This is an amazingly easy, convenient and straightforward method for recording a single channel ECG.

I love the idea that I can record an ECG whereverI am with minimal fuss. Since I wear my AW4 almost all the time I don’t have to think about bringing a device with me (although for a while I had the Kardia attached to iPhone case that ultimately became cumbersome.)

Based on my limited sample size today, however, the AW4 has a high rate of being uncertain about diagnoses. Only 2/3 cases of permanent atrial fibrillation were identified (compared to 3/3 for the Kardia) and only 4/6 cases of sinus rhythm were identified.

If those numbers hold up with larger numbers, the AW4 is inferior to the Kardia ECG device.

I’d rather see the AW4 declare inconclusive than to declare atrial fibrillation when it’s not present but this lack of certainty detracts from its value.

What caused the bizarre artifact and inconclusive AW4 tracing in my patient is unclear. If anybody has an answer, let me know.

We definitely need more data and more studies on the overall sensitivity and specificity of the AW4 and hopefully these will be rapidly forthcoming.

For most of my patients the advantages of the AW4 (assuming they don’t already have one) will be outweighed by its much greater cost and we will continue to primarily utilize the Kardia device which will also allow me to view all of their recordings instantaneously in the cloud.

Conclusively Yours,

-ACP

Note. The original version of this post had the wrong ECG tracing for the first “inconclusive” AW4 recording of a patient with permanent atrial fibrillation. H/t to discerning reader Vignesh for pointing this out months after the initial posting.

Has REDUCE-IT Resurrected Fish OIl Supplements (And Saved Amarin)?

The answers are no and yes.

There is still no reason to take over the counter fish oil supplements.

In fact, a study published Saturday found that fish oil supplementation (1 g per day as a fish-oil capsule containing 840 mg of n−3 fatty acids, including 460 mg of eicosapentaenoic acid [EPA] and 380 mg of docosahexaenoic acid [DHA]

did not result in a lower incidence than placebo of the primary end points of major cardiovascular events (a composite of myocardial infarction, stroke, or death from cardiovascular causes) and invasive cancer of any type.

However, another study  published Saturday (REDUCE-IT) and presented at the annual American Heart Association Scientific Sessions to great fanfare found that an ethyl-ester formulation (icosapent ethyl) of eicosapentanoic acid (EPA, one of the two main marine n-3 fish oils)  reduced major cardiovascular events by 25% in comparison to placebo.

When I wrote about Icosapent ethyl (brand name Vascepa) in a previous blog post in 2015 there was no data supporting its use:

A fish oil preparation, VASCEPA,  available only by prescription, was approved by the FDA in 2012.

Like the first prescription fish oil available in the US, Lovaza, VASCEPA is only approved by the FDA for treatment of very high triglycerides(>500 mg/dl).

This is a very small market compared to the millions of individuals taking fish oil thinking that  it is preventing heart disease.

The company that makes Vascepa (Amrin;$AMRN)would also like to have physicians prescribe it to their patients who have mildly or moderatelyelevated triglycerides between 200 and 500 which some estimate as up to 1/3 of the population.

The company has a study that shows that Vascepa lowers triglycerides in patients with such mildly to moderately elevated triglycerides but the FDA did not approve it for that indication.

Given the huge numbers of patients with trigs slightly above normal, before approving an expensive new drug, the FDA thought, it would be nice to know that the drug is actually helping prevent heart attacks and strokes or prolonging life.

After all, we don’t really care about high triglycerides unless they are causing problems and we don’t care about lowering them unless we can show we are reducing the frequency of those problems.

Data do not exist to say that lowering triglycerides in the mild to moderate range  by any drug lowers heart attack risk.

In the past if a company promoted their drug for off-label usage they could be fined by the FDA but Amarin went to court and obtained the right to promote Vascepa to physicians for triglycerides between 200 and 500.

Consequently, you may find your doctor prescribing this drug to you. If you do, I suggest you ask him if he recently had a free lunch or dinner provided by Amarin, has stock in the company (Vascepa is the sole drug made by Amarin and its stock price fluctuates wildly depending on sales and news about Vascepa) or gives talks for Amarin.

If he answers no to all of the above then, hopefully, your triglycerides are over 500.

And although elevated triglycerides confer an elevated CV risk nearly all prior trials evaluating different kinds  of triglyceride-lowering therapies, including extended-release niacin, fibrates, cholesteryl ester transfer protein inhibitors, and omega-3 fatty acids have failed to show reductions in cardiovascular events

REDUCE-IT, Amarin trumpeted widely in September (before the actual data was published)  now provides impressive proof that it prevents cardiovascular disease. Has the skeptical cardiologist changed his mind about fish oil?

Vascepa Is Not Natural Fish Oil

Although Amarin’s marking material states “VASCEPA is obtained naturally from wild deep-water Pacific Ocean fish” the active ingredient is an ethyl ester form of eicosapentoic acid (EPA) which has been industrially processed and distilled and separated out from the other main omega-3 fatty acid in fish oil (DHA or docosohexanoieic acid).

Natural fish oil contains a balance of EPA and DHA combined with triacylglycerols (TAGS).

So even if the REDUCE-IT trial results can be believed they do not support the routine consumption of  over the counter fish oil supplements for prevention of cardiovascular disease.

Does REDUCE-IT  Prove The Benefit of Purified High Dose EPA?

REDUCE-IT was a large (8179 patients) randomized, double-blind placebo controlled trial

Eligible patients had a fasting triglyceride level of 150 to 499 mg per deciliter  and a low-density lipoprotein (LDL) cholesterol level of 41 to 100 mg per deciliter  and had been receiving a stable dose of a statin for at least 4 weeks. In 2013 the protocol was changed and required a triglyceride level>200 mg/dl.

Participants were randomized to icosapent ethyl (2 g twice daily with food [total daily dose, 4 g]) or a placebo that contained mineral oil to mimic the color and consistency of icosapent ethyl and were followed for a median of 4.9 years. A primary end-point event occurred in 17.2% of the patients in the icosapent ethyl group, as compared with 22.0% of the patients in the placebo group.

More importantly, the hard end-points of CV death, nonfatal stroke and heart attack were also significantly lower in the Vascepa arm compared to the “placebo” arm.

These results are almost unbelievably good and they are far better than one would have predicted given only a 17% reduction in triglycerides.

This makes me strongly consider prescribing Vascepa (something I heretofore have never done) to my higher risk patients with triglycerides over 200 after we’ve addressed lifestyle and dietary contributors.

Perhaps the high dose of EPA (4 grams versus the 1 gram utilized in most trials) is beneficial in stabilizing cell membranes, reducing inflammation and thrombotic events as experimental data has suggested.

Lingering Concerns About The Study

Despite these great results I have some concerns:

  1. The placebo contained mineral oil which may not have been neutral in its effects. In fact, the placebo arm had a significant rise in the LDL cholesterol.
  2. Enrolled patients were predominantly male and white. No benefit was seen in women.
  3. Higher rates of serious bleeding were noted in patients taking Vascepa
  4. Atrial fibrillation developed significantly more often in Vascepa patients (3.1%) versus the mineral oil patients (2.1%)

Finally, the trial was sponsored by Amarin Pharma. This is an aggressive company that I don’t trust.  The steering committee consisted of academic physicians (see the Supplementary Appendix), and representatives of the sponsor developed the protocol,  and were responsible for the conduct and oversight of the study, as well as the interpretation of the data. The sponsor was responsible for the collection and management of the data. All the data analyses were performed by the sponsor,

After i wrote my negative piece on Vascepa in 2015 a number of Amarin investors attacked me because Vascepa is the only product Amarin has and any news on the drug dramatically influences its stock price. Here is the price of Amarin stock in the last year.

The dramatic uptick in September corresponds to the company’s announcement of the topline results of REDUCE-IT. Since the actual results have been published and analyzed the stock has dropped 20%.

High Dose Purified and Esterified EPA-Yay or Nay?

I would love to see another trial of high dose EPA that wasn’t totally under the control of Amarin and such trials are in the pipeline.

Until then, I’ll consider prescribing Amarin’s pills to appropriate patients* who can afford it and who appear to have significant residual risk after statin therapy*.

But, I will continue to tell my patients to stop paying money for useless OTC fish oil supplements.

Megaskeptically Yours,-

ACP

N.B.* Appropriate patients will fit the entry criteria for REDUCE-IT described below.

Patients could be enrolled if they were 45 years of age or older and had established cardiovascular disease or were 50 years of age or older and had diabetes mellitus and at least one additional risk factor. Eligible patients had a fasting triglyceride level of 150 to 499 mg per deciliter (1.69 to 5.63 mmol per liter) and a low-density lipoprotein (LDL) cholesterol level of 41 to 100 mg per deciliter (1.06 to 2.59 mmol per liter) and had been receiving a stable dose of a statin for at least 4 weeks;

So either secondary prevention (prior heart attack or stroke) or primary prevention in patients with diabetes and another risk factor.