Tag Archives: AF

Should You Participate In The Apple Watch Heartline Study?

Apple and Johnson and Johnson are collaborating on an interesting research study which aims to analyze the impact of an app-based heart health program with Apple Watch on the early detection  of atrial fibrillation (AFib), and the reduction of stroke risk.

I tried to participate in this study but didn’t meet the entry requirements which are as follows:

  • Be age 65 or older
  • Be a resident of the United States for the duration of the study
  • Use an iPhone 6s or later, with iOS 12.2 or later (Learn more)
  • Have Original Medicare, sometimes called Traditional Medicare (Learn more)

Because I’m still working I have private health insurance and didn’t qualify.

According to the Heartline website:

The Heartline Study is a pragmatic, randomized, controlled, virtual research study, from Johnson & Johnson, in collaboration with Apple. The primary objective is to analyze the impact of features on Apple Watch, combined with a heart health engagement program, on early detection of atrial fibrillation and clinical outcomes such as stroke. In addition, the study seeks to determine the impact of a heart health engagement program paired with a medication adherence intervention among those participants receiving an oral anticoagulant therapy who have been previously diagnosed with AFib. The data will also be used to find novel markers to identify, predict, or evaluate other health conditions.

The study website indicates some participants may get to borrow an Apple Watch 5:

Some participants may be asked to obtain an Apple Watch Series 5 or later. These participants will be offered two options to obtain a watch: purchase a watch, or get one on loan for the duration of the study and return it when your participation in the study ends. Johnson & Johnson and Apple are committed to ensuring that participation in the study is not limited based on financial need. Not all participants will be asked to obtain a watch, so make sure to follow the instructions in the app.

Information for Healthcare Providers who are trying to decide whether their patients should participate Is here.

Here is the study in graphic form

 

Screen Shot 2020-03-01 at 8.23.01 AM There is an extensive FAQ section on the Healthline website which reveals the following companies roles:

Janssen Scientific Affairs, LLC, an affiliate of Johnson & Johnson, is the sponsor of the Heartline Study. Apple is supporting the study technology and design of the app. Evidation Health provides the technology and study operations that enable the Heartline app and study experience for participants. Best Buy operates the Apple Watch distribution program for eligible study participants.

 

The ostensible motive for Apple and J  and J is to improve outcomes in patients with afib.  Obviously Janssen will sell more of its blood thinner Xarelto if more cases of afib are identified.

Participants will be sharing lots of private information with Apple and Evidation.

Despite these concerns I would likely have participated if I qualified and I will recommend that interested patients consider participating in Heartline.

Skeptically Yours,

-ACP

AliveCor’s Kardia Mobile ECG Accurately Identifies Atrial Fibrillation >120 BPM

The skeptical cardiologist revealed recently that the  Apple Watch (AW) ECG app is incapable of identifying atrial fibrillation (AF) if the heart rate is greater than 120 beats per minute. It labels these recordings as “inconclusive”.

Since it is common for AF to present at rates >120 BPM, AW ECG will fail to notify many (if not most) of its users that they are in AF.

AliveCor’s Kardia mobile ECG device (both the single lead and the six lead), on the other hand, has no problems identifying AF >120 BPM. I have found that the Kardia ECG was highly accurate in patients with rapid AF from using the device in hundreds of my patients since 2013.

After writing about the AW AF flaw I opened my KardiaPro dashboard which connects to the online ECG recordings each of my patients has made.

Two of my patients with paroxysmal AF had gone into AF in the last 2  days and made recordings.

Both of them had rates > 120 BPM. In both cases, Kardia had easily made the diagnosis. AW would have declared these “inconclusive.”

Patients should be aware of this AW AF flaw. The absence of a declaration of possible AF on the AW ECG should not reassure anyone of the absence of AF.

AW users should have their high rate recordings reviewed by a cardiologist.

Alternatively, they could purchase a Kardia device and utilize it for heart rates over 120 BPM.

Tachyagnostically Yours,

-ACP

Eight Lifestyle Changes All Patients Should Make To Reduce The Recurrence Of Atrial Fibrillation

Previously, the skeptical cardiologist answered the question “Why Did I Go Into Atrial fibrillation?

An equally important question is “how can I reduce the chances that I have more spells of atrial fibrillation (AF)?”

I spend a fair amount of time discussing with my AF patients what lifestyle changes they can make in this regard. I’ve discovered, however, that many AF patients I am seeing for a second opinion seem unaware of the changes they can make to minimize AF recurrence.

Herein I give you the eight most important changes you can make to minimize both the onset and the recurrence of AF.

  1. Eliminate or substantially reduce alcohol.
  2. Lose weight if you are obese.
  3. Stop smoking. Stopping is associated with a 36% lower risk of AF.
  4. Get your blood pressure under good control.
  5. Get regular aerobic exercise. At least 150 minutes of moderate cardio exercise weekly.
  6. Eat A Healthy Diet. Don’t Eat Crap (as Younger Next Year says). In general, because obesity is such a big factor  in AF, I am fine with whatever diet plan has you at a BMI <28. Healthy diets controlling weight avoid ultra-processed foods, sugar-sweetened beverages, and minimize white rice, pasta, pastries, and potatoes. These diets include lots of fresh vegetables, nuts, olive oil, and fish. Full fat yogurt and cheese are fine in moderation. Eat real food, mostly plants, not too much as Michael Pollan has famously said.
  7. Get high-quality sleep. This means treating any sleep apnea properly in addition to standard advice for getting a good night’s sleep. The risk of AF is four times higher in patients with obstructive sleep apnea (OSA) independent of other confounding variables
  8. Reduce stress. Easier said than done I know. Everything from meditation to Yoga to retiring or cutting back at work to psychotherapy can be tried in this category. Go with whatever works for you. Knowing when you are in or out of AF by utilizing personal ECG monitoring devices may help reduce stress, especially if used under physician supervision.

Let’s dig a little deeper into some specific recent evidence on three which have a huge impact: alcohol, exercise, and obesity.

Alcohol and Atrial Fibrillation

In March, I wrote about the alcohol AF trial recently published in NEJM:

The Alcohol-AF Trial. Binge alcohol consumption (holiday heart) can trigger atrial fibrillation (AF) and observational studies show a higher incidence of AF with higher amounts of alcohol consumption.

This trial was the first-ever randomized controlled trial of alcohol abstinence in moderate drinkers with paroxysmal AF (minimum 2 episodes in the last 6 months) or persistent AF requiring cardioversion.

Participants consumed >/= 10 standard drinks per week and were randomized to abstinence or usual consumption.

Participants underwent comprehensive rhythm monitoring with implantable loop recorders or existing pacemakers and twice-daily AliveCor monitoring for 6 months.

Abstinence prolonged AF-free survival by 37% (118 vs 86 days) and lowered the AF burden from 8.2% to 5.6%

AF related hospitalizations occurred in 9% of abstinence patients versus 20% of controls

Participants in the abstinence arm also experienced improved symptom severity, weight loss and BP control.

This trial gives me precise numbers to present to my AF patients to show them how important eliminating alcohol consumption is if they want to have fewer AF episodes. The study further emphasizes lifestyle changes (including weight loss, exercise, and stress-reduction) can dramatically reduce the incidence of atrial fibrillation.

Obesity and Atrial Fibrillation

We have known for some time of a strong association between obesity and atrial fibrillation. We also know we can make sheep go into atrial fibrillation by making them obese and creating a diseased, fat-infiltrated left atrium.

More recently we have solid evidence that sustained weight reduction can significantly reduce the recurrence of AF.

The Australian LEGACY study took 355 AF AF patients with BMI>27 and offered them a weight management program:

Weight loss was categorized as group 1 (≥ 10%), group 2 (3% to 9%), and group 3 (<3%). Weight trend and/or fluctuation was determined by yearly follow-up. Endpoints included impact on the AF severity scale and 7-day ambulatory monitoring.

Weight loss ≥ 10% resulted in a 6-fold  greater probability of no AF recurrences compared with the other 2 groups. High weight fluctuation doubled the risk of AF recurrence.

Of course, all these factors are interrelated. Exercise, diet, stress, alcohol consumption, and sleep quality all impact weight control and obesity. Patients with AF should be working on all 8 levers for optimal benefit.

Given the LEGACY study findings, if you have AF and are obese, you should be using all lifestyle factors at your disposal to get your body weight down >10%. Do this in a slow and steady fashion with lifestyle changes that are sustainable for the rest of your life. You want to lose that weight and keep it off.

Exercise And AF

The most compelling evidence for the independent role of exercise in reducing AF comes from a Norwegian study of 51 patients with AF who were randomized either to aerobic interval training (AIT) or to their regular exercise habits. The patients randomized to AIT engaged in four 4-minute bouts of high-intensity (85 to 95% peak heart rate) aerobic exercise interspersed with 3 minutes of recovery.

There was a significant reduction in AF burden (measured by implanted loop recorders) in the exercise group, with the mean time in AF dropping from 8.1% to 4.8%, with no significant change in the control group. Patients in the exercise group experienced fewer and less severe symptoms whereas the non-exercising, control group had no change. In comparison with controls, patients randomly assigned to exercise also increased their peak oxygen consumption (Vo2peak), cardiac function, and quality of life, while improving body mass index and blood lipids

Screen Shot 2020-02-02 at 12.19.44 PM
Atrial fibrillation (AF) burden in patients with AF during the study. Mean time in AF was measured by an implanted loop recorder (n=36) before, during, and after 12 weeks of aerobic interval training (exercise) or usual care (control). Patients without AF during the study period are excluded. Mean changes from baseline to follow up were −6.2±8.9 percentage points (pp), P=0.02 for exercise; 4.8±12.5 pp, P=0.09 for control; and 11.0±3.9 pp, P=0.007 between groups. Error bars show the 95% confidence interval.

An accompanying editorial provides this graphic on the benefits of exercise training in AF

 

For all you readers without AF you can minimize your chances of developing AF by following these lifestyle recommendations.

Afibrillatorily Yours,

-ACP

N.B. A PDF summary of the 8 factors is available here (Lifestyle changes Afib)

N.B.2 For those wishing to mimic the Norwegian AIT protocol here is the complete description:

Endurance training was performed as walking or running on a treadmill 3 times a week for 12 weeks. Each session started with a 10-minute warmup at 60% to 70% of maximal heart rate obtained at exercise testing (HRpeak), followed by four 4-minute intervals at 85% to 95% of HRpeak with 3 minutes of active recovery at 60% to 70% of HRpeakbetween intervals, ending with a 5-minute cooldown period. During AF, patients exercised at the same treadmill speed and inclination as in the previous sessions in sinus rhythm, with the Borg scale of 6 to 20 as an aid to control intensity. When familiar with the training regimen, patients were allowed to perform 1 exercise per week at home, where exercise intensity was documented with a heart rate monitor (RS300X, Polar Electro, Kempele, Finland).

 

 

 

 

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

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

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

Kardia’s Fascinating SmartRhythm For Apple Watch Is Very Cool: Will It Allow Personal Atrial Fibrillation Detection?

The KardiaBand for Apple Watch from AliveCor has delivered on  its  unique promise of a medical grade single lead ECG recording made by placing your thumb on your wristwatch band.

The ECG recordings are equivalent in quality to those made by their previously available KardiaMobile (see my prior post here.) After more experience with the Band I think the ease of recording is superior to KardiaMobile and the ability to discriminate atrial fibrillation from normal sinus rhythm is similar to KardiaMobile.

By combining either a KardiaBand or a KardiaMobile device with Kardia’s SmartRhythm monitoring system for Apple Watch we now have the promise of personal monitoring to detect atrial fibrillation.

What is SmartRhythm?

SmartRhythm is AliveCor’s term for its system for monitoring your heart rate and activity levels in order to identify when your rhythm is abnormal.

The system “takes your heart rate and activity data gathered from the Apple Watch and evaluates it using a deep neural network to predict your heart rate pattern.”

The heart rate is obtained from the Apple Watch PPG sensor every 5 seconds.  If it differs from what is predicted SmartRhythm notifies you to record an ECG.

If you’d like to learn more detail about the development of SmartRhythm and how it functions, AliveCor has an excellent informational piece here.

You can choose to have the Kardia SmartRhythm display come up whenever your Apple Watch awakens. It’s got information on your heart rate and activity over the preceding several hours

SmartRhythm display. The light blue vertical bars representing heart rate range during an interval. The continuous lines above and below the vertical bars show the boundaries of heart rate predicted by the neural network based on your measured activity from the Watch accelerometer. . Upper left corner is yellow triangle indicating that the system detected potential abnormal rhythm and recommended a recording. The dot on the right is an ECG recording. The vertical bars at the very bottom represent steps taken during an interval

The AliveCor FAQ on SmartRhythm stresses that a notification does not always mean an abnormal rhythm. Clearly false positives can and will occur. The first day I wore my KardiaBand I had several of these.

Causes for false positives include exercise that Apple Watch couldn’t detect, stress or anxiety-in other words, situations where your heart rate is higher than predicted by how much activity you are doing.

The long term record of your SmartRhythm recordings resides on your iPhone . Here’s my record for the last week

Note that Kardia , in addition to tracking your heart rate, also shows you by the green, yellow and orange dots, the times that ECG recordings were made.

Green dots indicate recordings classified as normal and yellow as “unclassified.” In my case most of the unclassified recordings were due to heart rate >100 BPM associated with exercise.

There is one orange dot indicating that Kardia felt the ECG showed “possible atrial fibrillation.”

This happened when I took my Apple Watch off my wrist and put it on one of my patients who has permanent atrial fibrillation. I had him push on the KardiaBand sensor to make an ECG recording and it was correctly identified as atrial fibrillation.

Thus far I have had no notifications of “possible atrial fibrillation” while I have been wearing my watch thus the false positive rate appears acceptably low.

How Does SmartRhythm Perform During Exercise?

I checked out SmartRhythm’s ability to predict normal and abnormal  heart patterns by wearing it during a session on my indoor bike trainer. The device did a good job of tracking both my heart rate and activity during the workout.  You can view the most recent data by viewing your Apple Watch screen during the workout as below

Or for more detailed information you can view the complete history on your iPhone as below

The system accurately tracked my heart rate and activity (although AliveCor lists stationary bike as an activity that may result in false positives). During a session of weights after the aerobic workout despite erratic heart rates and arm movements it did not notify me of an abnormality. I also did 100 jumping jacks (which involves wildly flailing my arms) and the heart rate remained within the predicted boundaries.

What is more remarkable is that I was able while cycling at peak activity to make a  very good quality ECG recording by taking my right hand off the handle bar and pushing my thumb down on the KardiaBand sensor on my left wrist.

This recording clearly  displays p waves and is sinus tachycardia. It’s unclassified by Kardia because the rate is >100 BPM.

Afib Patient Experience

One of my patients last week, a 70 year old woman with paroxysmal atrial fibrillation, had already set up SmartRhythm monitoring on her Apple Watch.

The Apple Watch face of my patient with the Kardia icon bottom right. Note also that she has a Starbucks reward available

I have this patient like many of my afibbers utilizing KardiaMobile to check an ECG when  they think they are in afib.

However, she, like many of my afib patients, is totally unaware when her heart is out of rhythm. Such asymptomatic patients are alerted to the fact that they are in afib by detection of a rapid heart rate (from a heart rate tracking wearable or BP monitor) or an irregular heart beat (from BP monitor or by someone checking the pulse) or by a random recording of an ECG.

She’s started using SmartRhythm in the hopes that it will provide a reliable and early warning of when she goes into atrial fibrillation.

We discussed the possibility of stopping the flecainide she takes to maintain normal rhythm to test the accuracy of the SmartRhythm system for detecting atrial fibrillation in her but decided not to. She’s on an oral anticoagulant and therefore protected from stroke so development of atrial fibrillation will not be dangerous for her.

I eagerly await the first real world, real patient reports of SmartRhythm’s performance in atrial fibrillation detection.

If there are any afibbers out there who have had an episode of atrial fibrillation detected by  SmartRhythm please let me know the details.

We need such anecdotes along with controlled trials to determine how useful SmartRhythm will be as a personal wearable system for detection of afib.

Fastidiously Yours,

-ACP

N.B. I’ve copied a nice section from AliveCor’s website which describes in detail the difference between measuring heart rate from the PPG sensor that all wearable devices use versus measuring the electrical activity of the heart with an ECG.

To understand how Kardia for Apple Watch works, let’s start by talking about your heart, how the Apple Watch and other wearable devices can measure your heart rate, and how an ECG is different from the information you get from a heart rate sensor alone.

Your heart is a pump. With each beat of your heart, blood is pumped through your arteries and causes them to expand. In the time between beats, your arteries relax again. On the underside of the Apple Watch is a sensor, called a photoplethysmogram (PPG), that uses green and infrared LEDs to shine light onto your skin, and detects the small changes in the amount of light reflected back as your arteries expand and relax with each beat of your heart. Using this sensor, the Apple Watch can tell how fast your heart is beating, and how your heart rate changes over time.

But, your heart rate does not tell everything there is to know about your heart. The PPG sensor on the Apple Watch can only see what happens after each heartbeat, as blood is pumped around your body. It can’t tell you anything about what is making your heart beat, or about what happens inside your heart during each beat. An ECG is very different, and tells you a lot more!

Three hearts showing a P-Wave, QRS-Complex, and a T-Wave

An ECG measures the electrical activity in your heart muscles. It detects the small pulse of electricity from the sinoatrial node (the body’s natural pacemaker, which normally initiates each heartbeat) and the large electrical impulses produced as the lower chambers of the heart (the ventricles) contract and relax. By looking at an ECG, a doctor can discern a wealth of information about the health and activity of your heart muscle, much more than you can tell from your heart rate alone. ECGs are the required gold standard for diagnosis of arrhythmias and many cardiac abnormalities, and can even be used to see evidence of acute heart attacks and even events that have occurred in the past.

Research has shown that taking frequent ECGs increases the likelihood of detecting certain arrhythmias, and decreases the mean time to diagnosis.

Why Did I Go Into Atrial Fibrillation?

The skeptical cardiologist is asked this  question or  variations of it (such as  what caused me to go out of rhythm?) on a daily basis.

Most patients would like to have a reason for why their atria suddenly decided to fibrillate.  It’s understandable. If they could identify the reason perhaps they could stop it from happening again.

There are two variations on this question:

For the patient who has just been diagnosed with afib the question is really “what is the underlying reason for me developing this condition?”

For the patient who has had afib for a while and it comes and goes seemingly randomly the question is “what caused the afib at this time? i.e. what triggers my episodes?”

For most patients, there is no straighforward and simple answer to either one of these questions

The Underlying Cause of Atrial Fibrillation

My stock response to this first question goes like this:

“Atrial fibrillation is associated with getting older and having high blood pressure. 10 % of individual >/= 80 years have atrial fibrillation. 90% of patients with afib have hypertension.

Aging and hypertension may increase scarring or damage in the left atrium or pulmonary veins that drain into the left atrium setting up abnormal electrical signals.

There are some specific things that cause afib and we will be doing a complete history and physical and some testing to check for the most common. We’ll check you for thyroid or electrolyte abnormalities and we will do an echocardiogram to look for any structural problems with your heart.

If we do find a treatable cause such as hyperthyroidism or a cardiac valve problem we will fix that and the afib may go away, however chances are we won’t find a specific reason why you developed atrial fibrillation.

Finally, and possibly most importantly, let’s take a close look at your lifestyle. Are you overweight? If so, losing 10% of your body weight will substantially lower your risk of recurrent atrial fibrillation. Let’s get you exercising regularly and eating a healthy diet, Make sure your sleep is optimized and your stress minimized.”

If you’d like a more sophisticated look into what causes afib take a look at this graphic from a recent paper.

Current theory has it that factors that we know are associated with atrial fibrillation  including obesity, hypertension and sleep apnea cause atrial structural abnormalities or remodeling which then create various atrial electrical abnormalities.

 

Exhaustive List of Causes

If you’d like an exhaustive list of factors associated with atrial fibrillation, you can memorize the acronym P.I.R.A.T.E.S. which is sometimes used by medical students to remember the causes of atrial fibrillation which include:

  • Pulmonary disease (COPD, PE)/Phaeochromocytoma
  • Ischemia (ACS)
  • Rheumatic heart disease (mitral stenosis)
  • Anemia (high output failure/tachycardia)/Atrial myxoma/Acid-base disturbance
  • Thyrotoxicosis (tachycardia)
  • Ethanol/Endocarditis/Electrolyte disturbance (hypokalaemia, hypomagnesaemia)/Elevated BP
  • Sepsis/Sick Sinus Syndrome/Sympathomimetics (Drugs)

And here’s a cute  mnemonic from the Family Practice Notebook using ATRIAL FIB itself (although you have to use the ph of pheochromocytoma to make the f of fib)

  1. Alcohol Abuse
  2. Thyroid Disease
  3. Rheumatic Heart Disease
  4. Ischemic Heart Disease
  5. Atrial Myxoma
  6. Lung (Pulmonary Embolism, Emphysema)
  7. Pheochromocytoma
  8. Idiopathic
  9. Blood Pressure (Hypertension)

Both of these mnemonics are a little outdated. For example, rheumatic mitral stenosis is quite rare as a cause of afib in the US but  degenerative and functional mitral regurgitation is a common cause.

Ischemic heart disease (aka coronary heart disease) isn’t felt to cause atrial fibrillation unless it results in a myocardial infarction and subsequent heart failure. Way too many cardiac catheterizations are performed on patients who present with atrial fibrillation by doctors who don’t know this.

Congenital heart defects (not mentioned in either mnemonic) especially atrial septal defects often are associated with afib

There may be case reports of pheochromocytoma (a catecholamine-secreting neuroendocrine tumor) causing afib but they are few and far between.

Finally, genetics clearly play a role in the younger patient with afib without any known risk factors. One of my patients and his twin brother both developed symptomatic afib in their 40s.

In The Chronic Afibber What Triggers An Episode?

Alas, for most afibbers we won’t identify specific reasons why you go in and out of afib although there are some triggers you should definitely avoid such as excessive alcohol.

Some of the “causes” listed in the mnemonic are acute triggers of afib episodes.

For example low potassium or magnesium (typically induced by diuretics, diarrhea or vomiting) can bring on episodes .(See my discussion on potassium and PVCS here-much of it is relevant to afib.)

And I  have definitely seen patients go  into atrial fibrillation who have acute pulmonary problems such as pneumonia, pulmonary embolism or exacerbation of COPD.  In these cases, it is felt that the lung process raises pressure in the pulmonary arteries thereby  putting strain on the right heart leading to higher right atrial pressures.

Sleep apnea is associated with afib and I have had a few cases where after identifying that a patient’s  afib always began during sleep we were able to substantially lower episodes by treatment of sleep apnea.

Pericarditis with inflammation adjacent to the left atrium not uncommonly causes  afib. This is the likely mechanism for the afib that occurs frequently after cardiac surgery. Since pericarditis may never recur (especially in the cardiac surgery patient) we think the risk of afib recurring is low in these patients.

Anything that raises stress and stimulates the sympathomimetic nervous system can be a trigger. For example, a young and otherwise healthy patient of mine went into afib after encountering a car in flames along the side of the road. We found that beta-blockers (which block the sympathetic nervous system) helped prevent her episodes.

Some patients have odd but reproducible triggers. One of my patients routinely went into afib when he ate ice cream. I had a simple , very effective treatment plan for him.

Caffeine and Chocolate

Many afibbers have been told to avoid caffeine but a recent study of 34,000 women found that there was no increased risk of afib with increasing caffeine content and no sign that any of the individual contributors to caffeine in the diet (coffee, tea, cola, and chocolate) were more likely to cause afib.

Higher chocolate consumption, in fact, has recently been linked to a lower rate of afib. An observational  study of 55 thousand Danish men and women found that those who consumed 2 to 6 servings per week of 1 oz (30 grams) of chocolate had a 20% lower rate of clinically apparent afib.

Alcohol and Atrial Fibrillation

Binge drinking has long been known to cause acute atrial fibrillation.

However, it appears that even light to moderate chronic alcohol consumption increases the risk of going into atrial fibrillation.

This graphic from an excellent recent review of the topic gives the potential mechanisms:

The review concludes that although light to moderate alcohol consumption lowers your risk of dying, any alcohol consumption increases your risk of afib.

This graph shows the relationship between dying from heart disease (red line) and risk of going into afib (blue line) and amount of alcohol consumed.

Looking at the 15 drinks per week point on the x-axis (about 2 drinks per day) we see that your CV mortality is reduced by 20% whereas your risk of afib has increased by 20%.

A better point on the x-axis is 7 (1 drink per day) which has a 25% lower CV mortality but only a 10% higher risk of afib.

Whatever caused you to go into afib the good news is that with lifestyle changes and the care of a good cardiologist chances are excellent that you can live a normal, happy, healthy , long and active life.

Etiologically Yours,

ACP

 

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

The skeptical cardiologist has been testing the comparative accuracy of two hand-held mobile ECG devices in his office over the last month. I’ve written extensively about my experience with the AliveCor/Kardia (ACK) device here and here. Most recently I described my experience with the Afib Alert (AA) device here.

Over several days I had my office patients utilize both devices to record their cardiac rhythm and I compared the device diagnosis to the patient’s true cardiac rhythm.

Normal/Normal

In 14 patients both devices correctly identified normal sinus rhythm. AFA does this by displaying a green check mark , ACK by displaying the actual recording on a smartphone screen along with the word Normal.

The AFA ECG can subsequently uploaded via USB connection to a PC and reviewed in PDF format. The ACK PDF can be viewed instantaneously and saved or emailed as PDF.

 

Normal by AFA/Unreadable or Unclassified by AliveCor

In 5 patients in normal rhythm (NSR) , AFA correctly identified the rhythm but ACK was either unreadable (3) or unclassified (2). In the not infrequent case of a poor ACK tracing I will spend extra time adjusting the patient’s hand position on the electrodes or stabilizing the hands. With AFA this is rarely necessary.

In this 70 year old man the AFA device recording was very good and the device immediately identified the rhythm as normal.

Chaput AFA SR

ACK recording was good quality but its algorithm could not classify the rhythm.

GC Unclassified

A 68 year old man who had had bypass surgery and aortic valve replacement had a very good quality AFA recording with correct classification as NSRChaput AFA SR

AliveCor/Kardia recordings on the same patient despite considerable and prolonged efforts to improve the recording were poor and were classified as “unreadable”

Scott AC unreadable
Alivecor tracing shows wildly varying baseline with poor definition of p wave

 

False Positives

There were 3 cases were AFA diagnosed atrial fibrillation (AF) and the rhythm was not AF. These are considered false positives and can lead to unncessary concern when the device is being used by patients at home. In 2 of these ACK was unreadable or unclassified and in one ACK also diagnosed AF.

A 90 year old woman with right bundle branch block (RBBBin NSR was classified by AFA as being in AF.

VA AFA read as AF
Slight irregularity of rhythm combined with a wider than normal QRS from right bundle branch block and poor recording of p waves likely caused AFA to call this afib

VA unclassified RBBB
AliveCor tracing calls this unclassified. The algorithm does not attempt to classify patients like this with widened QRS complexes due to bundle branch block.

The ACK algorithm is clearly more conservative than AA. The ACK manual states:

If you have been diagnosed with a condition that affects the shape of your EKG (e.g., intraventricular conduction delay, left or right bundle branch block,Wolff-Parkinson-White Syndrome, etc.), experience a large number of premature ventricular or atrial contractions (PVC and PAC), are experiencing an arrhythmia, or took a poor quality recording it is unlikely that you will be notified that your EKG is normal.

 

One man’s rhythm confounded both AFA and AC. This gentleman has had atrial flutter in the past and records at home his rhythm daily using his own AliveCor device which he uses in conjunction with an iPad.IMG_8399.jpg

During our office visits we review the recordings he has made. He was quite bothered by the fact that he had several that were identified by Alivecor as AF but in fact were normal.

Screen Shot 2017-05-06 at 11.48.47 AM
These are recordings Lawrence made at home that i can pull up on my computer. He makes a daily recording which he repeats if he is diagnosed with atrial fibrillation. In the two cases above of AF a repeat measurement was read as normal. Of the two cases which were unclassified , one was normal with APCs and the other was actually atrial flutter

A recording he made on May 2nd at 845 pm was read as unclassified but with a heart rate of 149 BPM. The rhythm is actually atrial flutter with 2:1 block.

Screen Shot 2017-05-06 at 11.47.37 AM

Sure enough, when I recorded his rhythm with ACK although NSR (with APCS) it was read as unclassified

Screen Shot 2017-05-06 at 11.49.49 AM

AFA classified Lawrence’s rhythm as AF when it was in fact normal sinus with APCs.

AFA Mcgill AF

 

 

One patient a 50 year old woman who has a chronic sinus tachycardia and typically has a heart rate in the 130s, both devices failed.

We could have anticipated that AC would make her unclassified due to a HR over 100 worse than unclassified the tracing obtained on her by AC (on the right)was terrible and unreadable until the last few seconds. On the other hand the AFA tracing was rock solid throughout and clearly shows p waves and a regular tachycardia. For unclear reasons, however the AFA device diagnosed this as AF.

 

 

Accuracy in Patients In Atrial Fibrillation

In 2/4 patients with AF, both devices correctly classified the rhythm..

In one patient AFA correctly diagnosed AF whereas ACK called it unclassified.

This patient was in afib with HR over 100. AFA correctly identified it whereas ACK called in unclassified. The AC was noisy in the beginning but towards the end one can clearly diagnose AFScreen Shot 2017-05-06 at 8.39.06 AMScreen Shot 2017-05-06 at 8.11.53 AM

In one 90 year old man AFA could not make the diagnosis (yellow)

Screen Shot 2017-05-06 at 11.35.40 AM

ACK correctly identified the rhythm as AF

Screen Shot 2017-05-06 at 11.37.51 AM

One patient who I had recently cardioverted from AF was the only false positive ACK. AliveCor tracing is poor quality and was called AF whereas AFA correctly identified NSR>

Screen Shot 2017-05-06 at 8.42.46 AMScreen Shot 2017-05-06 at 8.42.26 AM

 

 

Overall Accuracy

The sensitivity of both devices for detecting atrial fibrillation was 75%.

The specificity of AFA was 86% and that of ACK was 88%.

ACK was unreadable or unclassified 5/26 times or 19% of the time.

 

The sensitivity and specificity I’m reporting is less than reported in other studies but I think it represents more real world experience with these types of devices.

Summary

In a head to head comparison of AFA and ACK mobile ECG devices I found

-Recordings using AfibAlert are usually superior in quality to AliveCor tracings with a minimum of need for adjustment of hand position and instruction.

-This superiority of ease of use and quality mean almost all AfibAlert tracings are interpreted whereas 19% of AliveCor tracings are either unclassified or unreadable.

-Sensitivity is similar. Both devices are highly likely to properly detect and identify atrial fibrillation when it occurs.

-AliveCor specificity is superior to AfibAlert. This means less cases that are not AF will be classified as AF by AliveCor compared to AfibAlert. This is due to a more conservative algorithm in AliveCor which rejects wide QRS complexes, frequent extra-systoles.

Both companies are actively tweaking their algorithms and software to improve real world accuracy and improve user experience but what I report reflects what a patient at home or a physician in office can reasonably expect from these devices right now.

-ACP

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

I’m writing this brief post as a warning to any individuals who have purchased the  smartphone app AF Detect (screen shot below from Apple app store.) It is not a reliable detector of atrial fibrillation (AF).

screen-shot-2017-02-19-at-11-25-56-am

 

A patient of mine with AF recently  purchased this app unbeknownst to me. He  relied on its faulty information which  reassured hm he was not in AF when in fact he was in AF. Such misinformation has the potential to lead to dangerous delays in diagnosis.

There are multiple reviews on the Apple and Google app sites which confirm the total lack of reliability of this app to diagnose AF with screen-shot-2017-02-19-at-9-18-10-ammultiple instances of both failure to detect known AF and inappropriate diagnosis of AF when rhythm was not AF.

In the description of the app the company says the app will “transform you rmobile device into a personal heart rate monitor and atrial fibrillation detector”.

However after purchasing the app and before using it you see this disclaimer which img_8348states it is not to be used for any medical diagnosis.

 

 

 

 

 

 

I will be performing a more detailed analysis of this app’s performance in the future and contacting the FDA about the danger such inaccurate medical testing confers on victims.

In the meantime if you have any experience with this app or other apps claiming to detect AF reliably using detection of the pulse from finger application to the camera lens please share them with me (via email  DRP@theskepticalcardiologist.com or via comments below.)

-ACP