The skeptical cardiologist received this reader comment recently:
So I went and got a Cardiac Calcium Score on my own since my cardiologist wouldn’t order one because he says they are basically voodoo.. Family History is awful for me.. I got my score of 320 and I’m 48 years old.. Doc looked at it and basically did the oh well.. so I switched docs and the other doc basically did the same thing.. I try so very hard to live a good lifestyle..I just don’t understand why docs wait so long to actually take a look at your heart.. I would have thought a score of 320 would have brought on more testing.. It did not..
It’s never too early to start thinking about your risk of cardiovascular disease. If heart disease runs in your family or you have any of the “risk-enhancing” factors listed above, consider a CAC, nontraditional lipid/biomarkers, or vascular screening to better determine where you stand and what you can do about it.
Here’s what I told this young man:
If your cardiologist tells you coronary calcium scores are voodoo I would strongly consider changing cardiologists.
A score of 320 at age 48 puts you in a very high risk category for stroke and heart attack over the next 10 years.
You need to find a physician who understands how to incorporate coronary calcium into his practice and will help you with lifestyle changes and medications to reduce that risk
Let’s analyze my points in detail and see if these off the cuff remarks are really justified
1, Changing cardiologists.
Recent studies and recent guideline recommendations (see here) all support utilization of CAC in this kind of patient. If you have a strong family history of premature heart disease or sudden death you want a cardiologist who is actively keeping up on the published literature in preventive cardiology, Such cardiologists are not dismissing CAC as “voodoo” they are incorporating it into their assessment of patient’s risk on a daily basis.
2. High risk of CAC score 320 at age 48
I plugged normal numbers for cholesterol and BP into the MESA risk calculator (see my discussion on how to use this here) for a 48 year old white male.
As you can see the high CAC score puts this patient at almost triple the 10 year risk of heart attack and stroke.
Immediate action is warranted to adjust lifestyle to reduce this risk! This high score will provide great motivation to the patient to stop smoking, exercise, lose excess weight, and modify diet.
Hidden risk factors such as lipoprotein(a), hs-CRP and LDL-P need to be assessed.
Drug treatment should be considered.
3. Find physician who will be more proactive in preventing heart disease
This may be the hardest part of all my recommendations. On your own you can get a CAC performed and advanced lipoprotein analysis.
However, finding progressive, enlightened, up-to-date preventive cardiologists can be a challenge.
We need a network of such cardiologists.
I frequently receive requests from readers or patients leaving St. Louis for recommendations on cardiologists.
If you are aware of such preventive cardiologists in your area email me or post in comments and I will keep a log and post on the website for reference.
The article, written by three prominent neurologists and dementia researchers at UC San Francisco, discusses the lack of science behind the $3.2 billion industry promoting unproven supplements for improved cognition and brain health.
Unproven supplements like Prevagen (made from jellyfish! and with a hard to pronounce crucial ingredient!) utilize a facade of “proven benefits” and succeed by promoting themselves as science-backed on radio, television and the internet.
The JAMA articles notes that this industry thrives due to the increasing prevalence of Alzheimer’s disease, and it’s lack of effective treatments.
Consumers, it goes on to say, who are intent on finding methods to prevent dementia need to know three things:
There is no known dietary supplement that prevents cognitive decline for dementia,.
Supplements do not undergo FDA testing for safety or review for effiacy.
Some supplements may cause harm. For example, Vitamine E-increases risk of hemorrhagic stroke and in high doses, increase risk of death.
The Facade of Science-Backed Research.
Companies like Quincy Bioscience, the maker of Prevagen, utilize sophisticated techniques that supply false scientific backing for brain health interventions.
The website for Prevagen states “prevagen improves memory” and “has been clinically shown to help with mild memory loss associated with aging.”
A tab promises to show the research behind this claim:
As the JAMA articled pointed out, these bogus brain supplement companies quote scientific articles which appear valid yet lack essential features such as “sufficient participant characterization, treatment randomization and fail to include limitations.” These bad papers are often published in predatory open access journals.
In the case of Prevagen, despite marketing which includes “The Science Behind Prevagen” there isn’t even a single study published in the peer-reviewed scientific literature, predatory or otherwise.
If you click on the “view the study” link you will be taken to a PDF of the “Madison Memory Study” which is a study sponsored by Quincy Bioscience, performed by an employee of Quincy Bioscience and published in house by Quincy Bioscience.
In the world of real science, this type of study is ignored and considered extremely preliminary until it is reproduced by a reputable unbiased scientific lab and published in a peer-reviewed journal. The chances for biased results are way too high to trust.
FTC Files Suit Against Quincy Bioscience
According to the Federal Trade Commission (FTC), which charged Quincy Bioscience with false and deceptive advertising in 2017, the initial version of this company study found that Prevagen was no more effective than a placebo at improving any of the nine cognitive skills, including memory, that the company measured.
“The marketing for Prevagen is a clear-cut fraud, from the label on the bottle to the ads airing across the country,” said New York Attorney General Eric Schneiderman. “It’s particularly unacceptable that this company has targeted vulnerable citizens like seniors in its advertising for a product that costs more than a week’s groceries, but provides none of the health benefits that it claims.”
“The marketers of Prevagen preyed on the fears of older consumers experiencing age-related memory loss,” said Jessica Rich, director of the FTC’s Bureau of Consumer Protection. “But one critical thing these marketers forgot is that their claims need to be backed up by real scientific evidence.”
The suit seeks to fine Quincy and force it to pay back consumers who bought the pills
Since then Quincy went back and “re-analyzed” their in-house data coming up with 3 parameters that improved and challenging the FTC in court. This process is called p-hacking and any significant findings gathered through this process are highly suspect.
This is an after-the-fact, unplanned exploration of the data to see if anything else of interest happened in the trial. Some might call it a fishing expedition. Scientists do this all the time, but with a big caveat: post hoc results are considered tentative, not conclusive. Before they’re accepted as valid outcomes, they need to be confirmed by additional studies.
That’s because random events happen all the time in scientific studies. Some of them may seem statistically significant, but they’re flukes and not the result of cause-and-effect. And the more post hoc analyses you do (like the more than 30 Quincy Bioscience did), the more likely you’ll encounter these chance results.
Scientists guard against accepting them as real by setting a high bar for statistical significance and by not accepting post hoc findings until they’ve been tested again.
Despite the total lack of proven efficacy and the lawsuit by the FTC the company continues to heavily market Prevagen and reap millions of dollars in profits from the gullible. Prevagen is sold at the pharmacies of the companies below which should immediately remove this snake oil if their aim is to help consumers.
For more in-depth analysis see below.
Jann Bellamy at Science-Based Medicine delves deeply into the case and cases against Prevagen in “Prevagen goes P-hacking.”
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
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).
It is cheap and well-tolerated.
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.
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.
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.
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.
The skeptical cardiologist has of late been obsessed with a Beatles song. It is the fifth song on the second side of the four mop tops seventh studio album and the third George Harrison contribution to Revolver, arguably the best record album of all time.
With a subscription to Apple Music I can listen to the entire Beatles catalogue now and one day I Want To Tell You (IWTTY) began playing. I hadn’t closely listened to this song before but at 25 seconds in someone begins playing very loudly two notes on a piano and keeps playing them for 8 seconds. The effect is strikingly dissonant but mesmerizing.
It turns out much has been written about this section of I Want To Tell you (along with anything else remotely related to The Fab Four.)
The two notes are F and E and they are being played by Paul McCartney emphasizing the flattened ninth (and highly dissonant) portion of the chord E 7 b9.
Tim Riley in his Beatles song by song analysis, “Tell Me Why” writes of IWTTY:
The guitar line is central, the backbone for the esoteric lyrics, and the piano’s annoying dissonant figure at the end of each verse disrupts its stability.
The piano conveys the frustration of the singer, and its single-note solo is the peace he wants to attain
I’ve also seen this section described as “creating a frustrated bitonal disonance ( G sharp 7 diminished against E7 or E7 flat 9)
Lacking formal music training, apart from in his sitar studies…later described the harsh-sounding E7♭9 as, variously, “an E and an F at the same time” and “an E7th with an F on top, played on the piano”.
Writing in Rolling Stone’s Harrison commemorative issue, in January 2002, Mikal Gilmore recognised his incorporation of dissonance on “I Want to Tell You” as having been “revolutionary in popular music” in 1966. Gilmore considered this innovation to be “perhaps more originally creative” than the avant-garde styling that Lennon and McCartney took from Karlheinz Stockhausen, Luciano Berio, Edgar Varese and Igor Stravinsky and incorporated into the Beatles’ work over the same period.
The Wikipedia entry goes on to say that the chord “became one of the most legendary in the entire Beatles catalogue.”
Harrison was deliberately using the chord’s dissonance to create an emotion.”The musical and emotional dissonance is then heightened by the use of E7♭9, a chord that Harrison said he happened upon while striving for a sound that adequately conveyed a sense of frustration.”
“speaking in 2001, Harrison said: “I’m really proud of that as I literally invented that chord.”
I thought it highly unlikely that George Harrison “invented” (literally or figuratively) the seventh flattened ninth chord but had no way of checking the accuracy of the Wikipedia quote (from Guitar World magazine.) or the context. Was Harrison that musically naive, was he joking or did he mean something else?
Later that day I sat at my Kawai baby grand piano and began playing songs from The Encylopedia of Jazz.
One of my favorites from this book is Satin Doll (written in 1953 by Duke Ellington and Billy Strayhorn) and as I was playing it I realized that it was loaded with flattened ninths. There’s a D7flat9 when the word Satin is sung. These chords make the song more complex and memorable.
Next I played my favorite song in this Jazz book i “Lullaby of Birdland” (music written by George Shearing in 1952) which features two 7flat9 chords (F# and B7) in the second measure (played with the words “that’s what I.”) Later on in the song we are treated to 7flat 9 in D and the chord that George Harrison claimed to have literally invented E7b9.
Here’s Ella Fitzgerald singing it with Duke Ellington
So a cursory review reveals that the chord was being utilized a lot in 1953 (and that I have a special attraction to its complexity.)
Perhaps Harrison can claim he was the first to appropriate the chord in rock and roll music? Alas, we know that an F#7b9 is prominent in the Beach Boys’ Caroline, No which was released in March, 1966, 3 months before the Beatles released IWTTY.
He may not have invented the chord or even been the first to use it in rock and roll but his use in IWTTY coupled with McCartney’s hammering on the F and E have made me forever cognizant of that song’s beauty.
For that plus his brilliant guitar work and songwriting during and after The Beatles I will be eternally grateful.
N.B. Dear Readers. If any of you have access to the Guitar World interview of 2001 (from Wikipedia-Garbarini, Vic (January 2001). “When We Was Fab”. Guitar World. p. 200) wherein Harrison is alleged to claim he invented the magical 7b9 please share it with me.
Also, please note there is a new button on my website which allows you to sign up for my weekly emal newsletter (which i promise will be mostly related to cardiology and not esoteric musical chords.)
The skeptical cardiologist saw a patient recently who had undergone stenting of a 95% blocked right coronary artery. Mr Jones had presented a year ago to our ER 2 days after he first began experiencing a light pressure-type discomfort in his left shoulder and scapular region. This pain persisted, waxing and waning, without a clear relationship to exertion or position or movement of his shoulder.
Upon arrival in the ER, his ECG was normal but his cardiac enzymes were slightly elevated (troponin peaking 0.92), thus he was diagnosed with a non-ST elevation myocardial infarction (MI).
He’s done great since the stent procedure fixed the coronary blockage that caused his infarct and chest pain, but during our office visit he related that since his hospitalization he had been feeling “logy.”
Being a lover of words, my ears perked up at this new-to-me adjective, and I asked him to describe what he meant by logy. For him, loginess was a feeling of fatigue or lacking energy.
Indeed, the online Merriam-Webster dictionary defines logy as sluggish or groggy. It is pronounced usually with a long o and a hard g.
The origin is unclear but has nothing to do with rum:
Based on surface resemblance, you might guess that “logy” (also sometimes spelled “loggy”) is related to “groggy,” but that’s not the case. “Groggy” ultimately comes from “Old Grog,” the nickname of an English admiral who was notorious for his cloak made of a fabric called grogram – and for adding water to his crew’s rum. The sailors called the rum mixture “grog” after the admiral. Because of the effect of grog, “groggy” came to mean “weak and unsteady on the feet or in action.” No one is really sure about the origin of “logy,” but experts speculate that it comes from the Dutch word log, meaning “heavy.” Its first recorded use in English, from an 1847 London newspaper, refers to a “loggy stroke” in rowing.
Fatigue is a common, nonspecific symptom that we all feel at times. It is more common as we age and it can be challenging for both patients and physicians to sort out when it needs to be further evaluated.
Occasionally, fatigue is the only symptom of a significant cardiac condition, but more frequently in the patient population I see it is either noncardiac (low thyroid, anemia, etc.) or iatrogenic.
When a patient tells me they are feeling fatigued I immediately scan their med list for potential logigenic drugs.
In this case, my patient had been started on a low dosage of the beta-blocker carvedilol (brand name Coreg) after his stent, and I suspected this was why he had felt logy for the past year.
In cardiology, we utilize beta-blockers in many situations-arrhythmias, heart failure, and heart attacks to name a few, and they are well-known to have fatigue as a common side effect. There was a really good chance that Mr. Jones’s loginess was due to the carvedilol.
It’s important to review all medications at each patient visit to check for side effects, interactions and benefits, and in the case of Mr. Jones’ carvedilol, loginess.
Do All Patients Post-Revascularization or Post-MI Need To Take Beta-Blockers
Beta-blockers (BBs) are frequently started in patients after a stenting procedure or coronary bypass surgery, and continued indefinitely. However, the evidence for their benefit in such patients with normal LV function long term is lacking.
If any post-revascularization population benefits from BBs, it is those, like Mr. Jones who have had a myocardial infarction (MI, heart attack) prior to the procedure, however the smaller the infarct, the less the benefits.
And with the widespread use of early stenting to treat MI, infarcts are much smaller and dysfunction of the left ventricle (LV) less likely.
In those patients with minimal damage and normal LV function, the benefits appear minimal. For this reason in the last 5 to 10 years I’ve been stopping BBs in this population if there are any significant side effects.
A 2015 meta-analysis of 10 observational acute MI studies including more than 40,000 patients showed that beta-blockers reduced the risk of all-cause death However, the benefit of these agents was not found in all subgroups and seemed confined to the patients with reduced LVEF, with low use of other secondary prevention drugs, or NSTEMI.
In a study of almost 180,000 patients post MI with normal LV systolic function in the UK between 2007 and 2013 there was no difference in mortality at one year in patients discharged with or without beta-blockers.
I’ll save readers the details, but the bottom line is that patients treated with optimal contemporary therapy for acute MI, whose LV function was not significantly impaired, did not benefit in any way from treatment with carvedilol, the beta-blocker my patient was taking.
It’s rare that we get such definitive evidence for a change in treatment that reverses what is in current guidelines. This has the potential to affect tens of thousands of patients and improve their quality of life. It should be trumpeted far and wide. The cynic in me suspects that if it were a study demonstrating the benefits of a new drug, physicians would be bombarded with the new information.
Helping Patients Feel Less Logy
We will be ordering an echocardiogram on Mr. Jones, and if his LV function is normal we will stop his carvedilol and see if he feels significantly better.
I feel like stopping a drug that is not beneficial and that is causing a lifetime of loginess is an incredibly important intervention a cardiologist can make. It’s not as life-saving as stenting for acute MI, but saving quality of life is something this non-invasive cardiologist can do every day for every patient.
N.B. The summary of the recent CAPITAL-RCT:
STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06).
While surveying his garden this morning the skeptical cardiologist felt the cockles of his heart warm when he viewed the budding plant below:
The plant I beheld was the glorious, mystical and medicinal foxglove or digitalis purpurea upon which I have waxed poetic innumerable times (see here and here and here.)
It is from the foxglove that William Withering made his potions to treat dropsy (the ancient term for heart failure) and since writing about my encounter with the foxglove in Wales I’ve been on a quest to get some in my garden.
This mission was accomplished when Quiet Village Landscaping installed the plants a month ago.
Now if I can keep them growing I’ll be able to enjoy the tall, showy spikes of tubular pink or purple flowers with speckled throats that should emerge in summer.
Foxglove and its medicinal derivative digitalis can be toxic to both humans and animals. Let’s hope that the five bunnies that were frolicking in my yard and eating my hosta earlier in the spring have the good sense to eschew chewing it.
The skeptical cardiologist was born in Wrexham, North Wales, not too far from the northern area in Wales known as Snowdonia, the ancestral lands of the great Princes of Wales.
I’ve been back to this wonderful area several times in the last dozen years, entranced by its beauty and connection with my ancestor, Prince Llewelyn the Great.
Most recently I stayed in Beddgelert, a small village nestled at the base of Mount Snowdon, which , according to (possibly tourism-inspired) legend, is named after the grave of Gelert, the faithful hound of Prince Llewelyn.
A brief hike along the gurgling Glaslyn river takes you to a stone monument with these words inscribed:
“In the 13th century Llewelyn, prince of North Wales, had a palace at Beddgelert. One day he went hunting without Gelert, ‘The Faithful Hound’, who was unaccountably absent. On Llewelyn’s return the truant, stained and smeared with blood, joyfully sprang to meet his master. The prince alarmed hastened to find his son, and saw the infant’s cot empty, the bedclothes and floor covered with blood. The frantic father plunged his sword into the hound’s side, thinking it had killed his heir. The dog’s dying yell was answered by a child’s cry. Llewelyn searched and discovered his boy unharmed, but nearby lay the body of a mighty wolf which Gelert had slain.
The prince filled with remorse is said never to have smiled again. He buried Gelert here”.
While lingering in the little stone wall enclosure within which a statue of the faithful Gelert stood I espied a plant that looked like digitalis purpurea, more commonly known as foxglove.
Moving closer, I realized that I had indeed come face to face with a wildly growing foxglove, the plant that William Withering had utilized to treat patients with dropsy in the late -1700s.
I was understandably ecstatic as I was on a sort of mission to observe foxglove in its native environs. I had expected to view the medicinal plant in Shropshire where William Withering was born and where he had encountered “the old woman of Shropshire” who first inspired him to use foxglove for dropsy.
This unexpected foxglove experience seemed like a serendipitous harbinger of wonderful Witheringesque experiences to come.
Sure enough as we left the fog-enshrouded mountains of Snowdonia and drove on the left side of narrow, winding Welsh roads toward Shropshire we spotted multiple large patches of wildly growing foxglove in a nearby meadow.
Although my children were eager to taste the foxglove and see if the inotropic properties of the digitalis within would make their hearts beat stronger and make them more powerful, I restrained them, for Withering’s writings and subsequent years of clinical experience with digitalis tell us that the therapeutic window is narrow and toxicity manifested by nausea and vomiting common.
The patients of the skeptical cardiologist have probably noted that over the last 10 years he has transitioned from wearing a tie to not wearing a tie and from always wearing a white coat to rarely wearing a white coat.
“My role models and mentors during my medical training taught me what I considered to be the proper appearance and demeanor of the professional physician.
The male doctor wore a dress shirt and a tie. The doctor wore a white coat over his/her regular clothes. The more senior the doctor was in the medical hierarchy the longer the white coat and the more impressive the words written on the coat.
Presumably, this professional appearance of the doctor increased the confidence that the patient had in the professionalism of the doctor.
Upon encountering a patient in the hospital room or office exam room, the doctor extends his right hand, greets the patient and smiles and shakes hands.
I wore a tie and a white coat and shook hands consistently during the first 20 years of my practice but gradually these markers of a good doctor have fallen under scrutiny.”
A major issue with all three of these, I pointed out , is transmission of bacteria and viruses.
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
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.
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.
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.
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
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:
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!
I am happy to report that I survived the incident and am not concerned at all that my longevity has been compromised.
My 2013 summary of eggs, dietary cholesterol and heart disease (see here) is still valid and I highly recommend patients and readers read that post plus my updates on eggs with newer data (see here and here) rather than information related to the new egg study.
Although CNN and other news outlets lead with an inflammatory headline suggesting that eating those 3 eggs increased my risk of heart disease the new egg study could not possibly prove causation because it was an observational study.
Nutritional epidemiology has come under considerable criticism in the last few years for churning out these weak observational studies .John Ionaddis has been particularly vocal about these limitations, writing:
A large majority of human nutrition research uses nonrandomized observational designs, but this has led to little reliable progress. This is mostly due to many epistemologic problems, the most important of which are as follows: difficulty detecting small (or even tiny) effect sizes reliably for nutritional risk factors and nutrition-related interventions; difficulty properly accounting for massive confounding among many nutrients, clinical outcomes, and other variables; difficulty measuring diet accurately; and suboptimal research reporting. Tiny effect sizes and massive confounding are largely unfixable problems that narrowly confine the scenarios in which nonrandomized observational research is useful
This egg study contains the usual flaws that render it inconclusive:
First, the study relies on data collected from a food frequency questionnaire. Have you ever sat down and tried to recall exactly what you ate in the previous week? How accurate do you think your estimate of specific food items would be?
Ed Archer has written about the inaccuracy of the food frequency questionairres extensively. Here’s a sample from one of his devastating critiques;
In lieu of measuring actual dietary intake, epidemiologists collected millions of unverified verbal and textual reports of memories of perceptions of dietary intake. Given that actual dietary intake and reported memories of perceptions of intake are not in the same ontological category, epidemiologists committed the logical fallacy of “Misplaced Concreteness.” This error was exacerbated when the anecdotal (self-reported) data were impermissibly transformed (i.e., pseudo-quantified) into proxy-estimates of nutrient and caloric consumption via the assignment of “reference” values from databases of questionable validity and comprehensiveness. These errors were further compounded when statistical analyses of diet-disease relations were performed using the pseudo-quantified anecdotal data. These fatal measurement, analytic, and inferential flaws were obscured when epidemiologists failed to cite decades of research demonstrating that the proxy-estimates they created were often physiologically implausible (i.e., meaningless) and had no verifiable quantitative relation to the actual nutrient or caloric consumption of participants.
In addition to unreliable initial data the subjects were followed up to 30 years without any update on their food consumption. Has your food consumption remained constant over the last 30 years? Mine hasn’t. I went from avoiding eggs to eating them ad lib and without concern for my cardiovascular health about 5 years ago after looking at the science related to dietary cholesterol.
It’s Hard To Get Around Confounding Variables
Observational studies like this one try to take into account as many factors as they can which might influence outcomes. Invariably, however, there are factors which are unaccounted for, indeed unknowable, which could be influencing the results.
Individuals who were avidly trying to follow a healthy lifestyle in 1985 likely had drummed into their heads the message when these questionnaires were filled out that they needed to limit egg consumption. These individuals were also likely following other healthy habits, including exercising more, smoking less, and eating more fruits and vegetables and less junk food.
Observational studies cannot account for all these confounding variables.
At science-media centre.org they do a fantastic job of having independent experts in the field present their evaluation of scientific studies which have been popularized in the media. For the JAMA egg study their analyses can be found here.
Prof Kevin McConway, Emeritus Professor of Applied Statistics, The Open University emphasized the problem with residual confounding :
That’s because, for instance, there will be many other differences between people that eat many eggs and people that eat few other than their egg consumption. These other differences might be what’s causing higher death rates in people who eat a lot of eggs, rather than anything to do with the eggs themselves. The researchers point out that this has been a particular problem in some previous studies, and that this may have been a reason for inconsistency in the results of those studies. They have made considerable efforts to allow statistically for other differences in the new study. But they, correctly, point out that their own study is still not immune from this problem (known as residual confounding), and that therefore it’s impossible to conclude from this new study that eating eggs, or consuming more cholesterol in the diet, is the cause of the differences in cardiovascular disease rates and overall death rates that they observed.
For observational epidemiological studies like this egg study which show increased risks that are only “modest” it is highly likely that the next such study will find something different.
Eggs Are Not Eaten In Isolation
Finally, It’s important to remember that eggs, like most foods, are rarely consumed without accompanying food. This accompaniment is often bacon in the US. Eggs are often cooked in oil or butter and unless you cook them yourself you are unlikely to know the nature of the oil.
Eggs are frequently components of recipes.
We have no idea how these factors play into the results of the egg study.
So, rather than drastically cutting egg consumption I propose that there be a drastic cut in the production of weak observational nutrition studies and a moratorium on inflammatory media coverage of meaningless nutritional studies.