The skeptical cardiologist stopped wearing his initial wearable piece of technology (a Garmin device that constantly prompted him to move, described here), within 6 months of purchasing it; it just wasn’t worth the effort of charging and putting on the the wrist.
I am not alone in finding FitBit type devices not worth wearing after awhile. ConscienHealth points out that sales and stock price of FitBit are down significantly. Part of this is competition, part saturation of the market, but part must be due to individuals going through a process similar to mine.
The great promise that wearable fitness/sleep/activity tracking devices would make us healthier has not been fulfilled.
A recent study showed that among obese young adults, the addition of a wearable technology device to a standard behavioral intervention resulted in less weight loss over 24 months.
Taking the Apple Watch Plunge
However, knowing I was a fan of all things Apple, the eternal fiancee bought me a Series 1 Apple Watch, which I have come to love. This love has little to do with how the device tracks my steps or my sleep or my pulse or my movement.
Let me count the ways I do love my Apple Watch…
I can answer my phone without touching my phone or
having it near me or even knowing where my phone is.
Since I’m constantly misplacing the damn thing, this is a surprisingly helpful feature. There is also the really cool aspect of walking around and having a telephone conversation using my watch.
During a busy day of seeing patients in the office I typically will receive multiple calls from the ER or other doctors I have to talk to immediately. Now, I can rapidly screen my calls with a tilt of my wrist and excuse myself to take the call. If I’ve been trying to get ahold of Dr. X to discuss a mutual patient, and he calls while I’m doing a transesophageal echocardiogram, I can have someone touch my watch instead of reaching into my pants for my iPhone, or searching in my office for it, or missing the call altogether.
I’m missing much less important calls these days.
And although previously I would take calls while driving, the watch makes this process much simpler and therefore much safer.
2. Receiving and responding to text messages does not require accessing my iPhone.
This doesn’t seem like that big of a deal, but again, the ability to rapidly scan incoming texts with just a tilt of the wrist greatly facilitates expeditious screening and processing.
The Apple Watch allows response via either audio recording (translated seamlessly and quickly to text) or pre-set standard responses or emojis.
3. “Hey Siri” function simplifies and makes hands-free and iPhone-free many useful tasks. For example:
To set a timer for my (heart-healthy) boiled eggs, I say “Hey Siri, set timer for 11 minutes.” Normally in this situation I avoid setting the timer because I’m too busy to grab my phone, open it, and find the timer app (I know I could use Siri on my phone, but that requires more effort).
If I suddenly remember I need to call someone while driving, the “Hey Siri” function allows making the call without taking my hands off the steering wheel.
If a brilliant idea for a blog post occurs to me while driving or walking through the hospital corridors, “Hey Siri” can take a note with ease.
4. Checking the time is a lot easier (I know, all watches do this, but I’ve haven’t worn a watch for about 20 years).
5. If I misplace my iPhone (this happens roughly once per hour when I am at home), I can “ping” it by pushing a button on my Apple Watch: follow the ping and “voila!” I have found my iPhone. Most of the time it is lying under a piece of paper or article of clothing within a few feet of where I’m working, but sometimes it is in an obscure corner for obscure reasons.
Here’s a true story which illustrates my tremendous absent-mindeness and the value of the “ping.”
I left my office Friday evening and after stepping outside I realized I did not have my iPhone in its usual location, the left front pocket of my pants. I searched the pockets in my pants and in the jacket I was wearing to no avail. I began heading back to my office believing that I had left it on my desk but then realized that I might have put it in my satchel. Not in my satchel. A bright idea then occurred to me: ping the iPhone to see if it was in the satchel, but hidden.
Sure enough I heard the iPhone ping. But it was not in the satchel; it was (for obscure reasons) in my shirt pocket (a place that apparently makes it undetectable to me).
6. Information on local weather is immediately available. I have configured my watch “dial” to show me the local temperature. Right now with a flick of my wrist I can see that it’s 17 degrees outside and I’m going to have to dress warmly. I’ve also configured my watch dial to tell me when sunrise/sunset is and what my heart rate is.
These last two things, although immensely interesting, are not that helpful.
Oh, excuse me, my watch timer is telling me my eggs are done.
P.S. I’m still in the process of evaluating the work-out/sleep/move/mindfulness features of Apple Watch and hope to write about it in the near future.
Feel free to share the things you love or hate about your Apple Watch below.
I’ve been evaluating the ability of a mobile hand-held ECG device called AfibAlert to detect atrial fibrillation for the last few weeks.
I found that the device made very reliable and consistent recordings of cardiac rhythm and did a reasonably good job of detecting atrial fibrillation (afib).
The device came in a plastic case with a USB cable for uploading recordings and two metal bracelets which attach to electrodes and provide an alternative recording method.
The device itself is about 6 by 3 by 1 inch.
Recordings are made by placing your thumbs on the silver/siver chloride electrodes
After a few seconds the display in the center will give heart rate and after 45 seconds the
device will make a decision about your rhythm:
If it diagnoses normal sinus rhythm a green check appears and if it diagnoses afib a red telephone appears.
If it is confused you get yellow circular arrows.
As the maker of the device explains:
Lohman Technologies’ patented algorithm analyzes the patient’s heartbeat and the appropriate icon illuminates to show what action is needed. AfibAlert’s® algorithm was validated against 51,000+ ECG strips from the MIT-BIH Atrial Fibrillation Database with known diagnosis. The Afib monitor’s results were excellent, with 94.6% accuracy in detecting the presence of arrhythmias. Each recording produces a 45-second diagnostic quality ECG rhythm strip
The device I tested does not allow you to immediately see the ECG tracing. The recordings are uploaded to a PC via USB cable and then can be viewed as a PDF document.
I made 17 recordings on patients in my office one day. The age range was 50 to 93 years and most patients were able to rapidly and easily grasp the device with thumbs appropriately positioned to make interpretable recordings.
Only 2/17 came back. yellow. In both cases, I repeated the recording and the device was able to make the correct diagnosis. Twice I got the yellow signal on an elderly, partially blind patient who had trouble keeping his thumb on the electrode.
In 15 cases of normal sinus rhythm the device correctly identified NSR.
In one case of atrial fibrillation the device correctly identified atrial fibrillation.
In one case of SR with
APCs the device
incorrectly identified afib
Overall the device correctly classified 88% of the tracings. This was superior to the device I normally utilize ( AliveCor/Kardia mobile ECG) in head to head comparison (I’ll present this comparison in a subsequent post).
My bullet points on the AfibAlert device:
-5 stars for Ease of Recording
-5 stars for Quality of recording
In all cases that uploaded, the recordings were very clear and free of artifact. The device did not upload yellow signal events and I presume more artifact is present in these recordings.
-2 stars for Convenience.
I found the software and uploading to be very awkward and slow. The company indicates new software soon to be released along with the ability to interface directly with iPads or smartphones that hopefully will improve this factor.
The inability to instantaneously view the ECG tracings means I cannot use it in my office to screen patients for arrhythmias. However, if a patient is solely using it to determine if afib is present or absent, this information is available right away.
-3 stars for Accuracy.
It does a reasonable job of identifying the patient who is in normal rhythm versus one in atrial fibrillation.
However, like AliveCor and other devices which strictly look at the variability of the pulse, it can be easily fooled by premature beats, especially when they are frequent, and inappropriately classify these as afib resulting in false positives.
In addition, when afib rates are very slow and thus much less variable it is likely AfibAlert will incorrectly classify them as normal thus resulting in false negatives.
False Negatives and False Positives
False negatives result in delayed diagnosis of afib. Patients will be falsely reassured that their rhythm is normal when it is not.
False positives result in needless anxiety and testing/treatment.
If afib monitoring devices are to be successful they have to have a very low frequency of both types of inaccuracy.
The solution to inaccuracy of interpretation, of course, is to have a cardiologist over-read the tracings.
AfibAlert recordings are available online for review by your personal physician after being uploaded. This requires your physician to have an account with AfibAlert. There is no capability for having the recordings over read by an online cardiologist for a charge.
As far as I can tell the device is only available for purchase in the US and only on the AfibAlert website.
Interestingly, you cannot purchase AfibAlert without a prescription from a physician.
Why this is mandated for AfibAlert and not AliveCor is a mystery to me.
The skeptical cardiologist is fascinated by the cardiac drug digoxin and the plant from which it is derived, the foxglove.
I wrote about “foxglove equipoise” in a previous post, touching on the contributions of William Withering in the 1700s, to understanding the toxicity and therapeutic benefits of the foxglove, and more recent concerns that digoxin increases mortality in patients with heart failure.
At the American College of Cardiology Scientific Sessions in Washington, D.C. yesterday, a paper showing higher mortality for patients on digoxin may be the final nail in the foxglove coffin.
Despite lack of evidence for its safety in the treatment of atrial fibrillation from randomized trials, digoxin is used in 30% of patients with atrial fibrillation (AF) worldwide, and current AF guidelines recommend it for rate control in patients with AF (with and without heart failure).
The investigators used data from the ARISTOTLE study of apixiban versus warfarin for their analysis.
They looked at mortality in patients taking or not taking digoxin at baseline, using a Cox model with propensity weighting, which included demographic features as well as biomarkers and digoxin levels at baseline. Major findings:
-In patients already taking digoxin, mortality was not higher in digoxin users, however, the risk of death was related to dig levels: for every 0.5 ng/ml increase in dig level, the risk of death rose by 19 percent and if dig level was >1.2 ng/ml the death rate increased by 56 percent.
–Patients not taking digoxin before the trial who began taking it over the course of the study had a 78 percent increase in the risk of death from any cause and a four-fold increased risk of sudden death after starting digoxin use. Most sudden deaths occurred within six months after digoxin was started.
–Risk of death with initiation of digoxin was increased in patients with and without heart failure.
The use of foxglove to treat dropsy is a fascinating and instructive chapter in the history of medicine.
This study added to prior systematic reviews suggests that it is time to end the use of digitalis and close the chapter.
William Withering might turn over in his grave but at least we won’t be sending afib patients to join him prematurely!
The skeptical cardiologist has been in Washington, DC attending the Scientific Sessions of the American College of Cardiology for the last three days in an attempt to upgrade his cardiology knowledge and obtain CMEs for all the various areas he needs CME (echo/nuclear/CT/vascular).
I’ve written some posts for SERMO, a physician social media site, on interesting presentations from the meeting.
I’m a big advocate of coronary artery calcium (CAC) scans for helping make decisions on individual patients with intemediate risk for CAD. Several speakers at this year’s American College of Cardiology Meetings presented convincing data supporting this approach, providing more information to get patients off the fence about taking statins.
However, CAC apparently would be a useless test in the Tsimane (pronounced chee-MAH-nay) people according to a study presented at the ACC meeting and published simultaneously in The Lancet.
Researchers performed CT scans on 700 of these “forager-horticulturalist” people, indigenous to the Bolivian Amazon Rainforest and found very little calcium suggesting that they have an amazingly low rate of atherosclerosis compared to we who have to live in the industrialized world.
Obviously CT scanners are not portable so the Tsimane traveled by river and jeep from the Amazon rainforest to Trinidad, a city in Bolivia and the nearest city with a CT scanner. It took tribe members one to two days to reach the nearest market town by river, and then another six hours driving to reach Trinidad.
85% of the Tsimane people studied had CAC scores of 0. In those over age 75 years, 65% had CAC scores of 0, and just four individuals in their 80s had moderately elevated CAC (> 100). The incidence of CAC > 100 in the entire Tsimane population was 3%, which is about one tenth the prevalence in a matched industrialized population. In addition, incidences of obesity, hypertension, high glucose concentrations, and cigarette smoking were rare overall.
The Tsimane live a subsistence lifestyle that includes hunting, gathering, fishing, and farming. They don’t eat at McDonalds and the men spend almost 7 hours pers day on physical labor. Their diet consists mostly of unprocessed fiber-rich carbohydrates with rice, plantain, manioc, corn, wild nuts, and fruit composing their staples. Fat consumption is 9% of calories versus 23% in the U.S.
Supporters of plant-based diets, of course, seized on these data to support the unsubstantiated claim that meat and dairy consumption is the main cause of atherosclerosis in western civilization.
Hillard Kaplan, one of the authors and a Professor of anthropology at the University of New Mexico said:
“Their lifestyle suggests that a diet low in saturated fats and high in non-processed fibre-rich carbohydrates, along with wild game and fish, not smoking and being active throughout the day could help prevent hardening in the arteries of the heart. The loss of subsistence diets and lifestyles could be classed as a new risk factor for vascular aging and we believe that components of this way of life could benefit contemporary sedentary populations.”
However, the real cause of the low levels of coronary artery calcification in the Tsimane remains a mystery because this kind of observational study cannot establish causality. Perhaps it is the 17,000 steps a day that they walk engaging in foraging and horticulturalism. Could it be due to the absence of processed food and added sugar? The Tsimane have high levels of parasitic infections: perhaps that is protecting them.
Of two things I am certain:
-The Tsimane don’t need statins.
-I prefer my lifestyle to munching on manioc and foraging all day.
As I sit here writing, I perceive a scintillating band of zig-zags in the shape of a reverse C on the left side of my visual field. I sense the scintillating reverse C with either, or both eyes closed, and I first noted it when the letters in the New Yorker article I was reading became obscured by the C. Attempts to focus on the crescent are futile: it moves as I move my eyes or head. Within its body are vague browns, blacks and whites, and overall it is reminiscent of an Egyptian or Art Deco piece of art.
I have a friend in Brooklyn, a flaneur, and one in Florida, a raconteur; I have now become a migraineur: one who suffers from migraine headaches or, in my case, the visual or tactile hallucinations known as migraine aura that precede the headaches.
I go to my bookshelf and find Oliver Sacks’ book “Migraine: Understanding a Common Disorder, which I purchased long ago when I was not a migraineur (primarily to complete my collection of Sacks’ unique and brilliant writing). On page 62, figure 2b, I find a drawing which closely approximates what I’m “seeing.”
I had asked Siri to start the timer on my Apple watch when I first noticed the visual disturbance, and now note that at 16 minutes 32 seconds, my vision was back to normal. At 25 minutes 16 seconds, I experienced a very subtle ache in my left frontal region which persisted for 5 minutes.
I have observed patients with severe migraine headaches: suffering from nausea, intense pain, photosensitivity and requiring dark and sleep and powerful analgesics to cause remission. I am fortunate because my after-aura headaches, if any, are minimal and brief.
The first time I experienced the visual hallucination was five years ago. I was not blogging then, but made a detailed note of the experience, complete with paranoid rumination on brain testing and side effects of MRIs. What follows is the transcript with the comments of the present day skeptical cardiologist in green or red.
“I had a crazy day Thursday. I gave a talk to the echo lab from 7 to 8 AM and then rushed over to the hospital to see the most urgent of the 9 inpatients I had. I had seen 4 patients by the time I got paged to see my first patient in the office. I headed over there and saw 6 patients . Then I hurried back to the hospital to grab the EKGs I was supposed to read that day. I was a little stressed because I needed to read these and try to see more of my inpatients before heading over to the outpatient testing facility which I had to be at by 1230 to supervise stress testing. I sat down in my hospital office and started reading the EKGs. After I had read a few, I became aware of a defect on the left side of my vision. It felt like when you have looked at a bright light and it leaves a residual on your retina.
At first I thought it was due to the fact that i was reading the EKGs with only the desk lamp on my left on. I turned on the overhead light and it didn’t help. I then realized that I had a hockey puck shaped defect in my left visual field in both eyes. When the defect covered key portions of the EKG, I couldn’t read it. It was filled with a jagged, prism like filling. Otherwise I felt fine. My first thought was that I was having a scintillating scotoma and that this was a migraine aura. Other things seemed much less likely-TIA for example. I called Dr S, my favorite neurologist, on his cell phone and told him what was going on. He suggested I visit him in his office right then. His office was in 400 East which would necessitate a right turn from my office. Instead, I took a left turn down to the West office building, took the elevator up to the fourth floor and finally realized my mistake when all I could find were office numbers that ended in W. (At the time young Dr. P felt this disorientation was related to the aura but perhaps it was due to distraction) By the time I reached his office twenty minutes after the visual symptoms started, they had resolved.
Dr. S did a neuro exam and history, and concluded that I most likely had a migraine aura but thought that I should get an MRI to be certain there was no structural brain disease. After I left his office I began feeling slightly nauseated with a slight headache. Over the next two hours the headache became a moderate frontal headache associated with a sense of fatigue.
I got the MRI yesterday and Dr. S thinks it is normal, although the radiologist read it as showing small subcortical defects which could be consistent with “chronic migraine, small vessel disease, or demyelinating process.”
I almost didn’t get the MRI. This is one of the classic situations in medicine where the history and physical alone makes the diagnosis with near certainty (young Dr. P is correct, see what Choosing Wisely says here), but because a very small number of cases might have something more serious (a brain tumor or vascular lesion in this case ), (perhaps also fueled by medical legal concerns and patient’s love of fancy tests) an expensive imaging test is ordered.
If you took 1000 people with my symptoms and the normal neuro exam with low atherosclerotic risk factors, and did brain MRIs on them, the vast majority of findings would be incidental, probably false positives (I believe young Dr. P made up this statistic but the national migraine center in the UK says :
“The main problem with MRI scans is ‘looking for a shilling and finding a sixpence,’ in finding abnormalities that are unrelated to headache, entirely by chance. The risk of a minor abnormality of no medical significance is 1 in 4. The risk of a chance abnormality that might need treatment is about 1 in 40. Once these ‘incidentalomas’ have been found, the patient may then find it difficult to obtain insurance (for example travel) and there is often a temptation to repeat the scan time and time again to check that the ‘incidentaloma’ is not changing..)
False positives lead to unnecessary anxiety in patients and in some cases unnecessary testing (Dr. S told me that he sees tons of patients who have had normal MRIs with readings similar to mine who are convinced they have MS) (MS=multiple sclerosis, a demyelinating process. Although my MRI was read as having abnormalities possibly due to a “demyelinating process” I must not have had one because 6 years later I have had no other symptoms)) and in some cases unnecessary additional testing.
As I was lying in the MRI gantry listening to the “ratatat “of the scanner, I wondered if we really know the consequences of rearranging the molecules of brain tissue with giant magnetic fields.
Dr. S had ordered the MRI with gadolinium. I recalled seeing adds from law firms seeking “victims” of MRI scans (one man was awarded 5 million dollars after developing nephrogenic systemic fibrosis after one dose of gadolinium (NSF). I knew that gadolinium had been linked to some really serious disorders. The tech had said nothing to me about adverse effects of the “dye” she would be using. My nose began itching like crazy, then my left eyelid. I couldn’t scratch until I emerged from the scanner. After the initial images were done and I was brought out of the scanner, I scratched my face like crazy and asked the tech if there were any side effects from gadolinium.
“Why yes, she said, you can have severe allergic reactions,” but we’ve only had a couple.” Also, she said, there is some disorder… she couldn’t remember the name or what it did but knew that it was only a problem if you had kidney failure or had diabetes and were over the age of 60.
As I was lying in the scanner after receiving the gadolinium, I began trying to estimate what risk I would be willing to assume in this situation. The disease you can get if you have severely impaired kidney function and receive gadolinium is nephrogenic systemic fibrosis.
Would I accept a 1 in 1/1000 chance of NSF in exchange for diagnosing something other than migraine 1/1000 times? I couldn’t and can’t easily and logically make that call. I have no idea how patients can make these decisions.
Migraine experiences have served as a major source of artistic inspiration in both past and contemporary painters, sculptors, film-makers and other visual artists. Check some of their work out at migraine aura foundation.
The skeptical cardiologist has had several of his readers submit stories and tracings of AliveCor Mobile ECG recordings which yield unclassified or unreadable recordings. In some cases this is due to excess noise but a lot of these tracings suffer from low voltage: the height of the tracing is very small.
John, a skepcard reader, is typical.
Recently, he noted his heart was racing and made an AliveCor recording which came back interpreted by the app as normal
Three hours later he made a second recording which has drastically lower voltage: the only deflections visible are tiny QRS complexes, the p waves have disappeared. I think this is also normal sinus rhythm but because p waves can’t be seen this came back uninterpretable and if there were any irregularity AliveCor would have called it atrial fibrillation:
John has a theory on the cause of some of his low voltage recordings which I shall reveal in a subsequent post after testing it.
In the meantime, if any readers have suggestions as to causes of low voltage recordings or have noted similar issues please comment below or send recordings and observations to DRP@theskepticalcardiologist.com.
The skeptical cardiologist was shocked to hear from a patient last week that she would have to pay considerably more for generic rosuvastatin (GR) than Crestor, its brand name equivalent.
Crestor is the most potent statin we have at lowering LDL (bad) cholesterol, raising HDL (good) cholesterol, and preventing strokes and heart attacks. It is also the best tolerated statin in my experience; I use it frequently at low or intermittent dosages in patients who have developed muscle aches on other statins.
In comparison to atorvastatin (Lipitor, the most widely prescribed statin), Crestor is less likely to interact with other medications and (very important for a surprising number of my patients), you can consume grapefruit when taking it.
When a generic (rosuvastatin calcium) of Crestor became available last year I rejoiced, believing that the high cost of Crestor would now drop to the levels we have typically seen with other generic statins.
For example, when Lipitor (atorvastatin, the statin market leader for 20 years) went generic, patients no longer worried about its cost.
Initially it seemed GR was much more affordable for my patients than Crestor, however recently, I have had many of them report a rise in its cost.
Why Would The Generic Cost More Than Crestor?
The reasons for brand name versus generic pricing are many and complex, and they yield insight into the legal machinations that Big Pharma engages in to maintain high patient pharmaceutical costs.
This NY Times piece from July, 2016 reveals how hard AstraZeneca fought to protect its exclusivity in selling Crestor and to prevent generics from entering the market. AstraZeneca’s last tactic involved a lawsuit claiming that their patent was protected by the orphan drug act. They lost and were heavily criticized:
“This case is not about the medical needs of a small population of pediatric patients with a rare disease,” the F.D.A. and Justice Department said in a brief filed in the lawsuit. “It is about AstraZeneca’s profit-driven desire to substantially extend its virtual monopoly on one of the world’s most popular medicines.”
There are other factors that slow the drop in generic prices. Consumer Reports, writing on the anticipated release of GR in May quoted an expert thusly:
“While some pharmacies drop the price as generics enter the market, others will hold it near the brand-name price as long as possible.” They get away with it, he says, because many customers who have health insurance pay a set co-pay regardless of the retail price. But those consumers who pay the entire cost of the drug themselves because they don’t have insurance or have a high deductible may not see the substantial savings that should come with generic availability.”
What an individual pays for drugs varies wildly depending on their insurance coverage. These costs are extremely hard for a physician to anticipate and rarely reflect the actual cost of drugs. Thus, in America, patients as consumers are often isolated from the true costs of pharmaceuticals to society.
I did not pay anything for the 25 pills, however the paperwork states a cost of $220 if I had to buy this outside of a health insurance plan. Do you know if the health insurance company is being charged the $220, or do they negotiate a lower cost with the manufacturer?
I don’t have that answer, but would love to know it. This kind of information is hard to get at.
Send Me Your Observations On The Cost of Generic Rosuvastatin
I would like to get input from my patients and readers on their experience regarding the cost of GR to them and/or their insurance company.
I’d also appreciate input from those in the pharmaceutical or insurance portion of this equation (I know I have at least one patient who is in the pharmaceutical industry).
Finally, if any of you have experience with purchasing GR online from international pharmacies, please share it below. For example, this site claimed in May, 2016:
In a previous post, the skeptical cardiologist pontificated on the causes and evaluation of the most common cause of palpitations: premature ventricular contractions or PVCs.
The vast majority of these common extra beats turn out to be benign (meaning not causing death, heart attack or stroke), and most patients with sufficient reassurance of this benignity (often accompanied by significant caffeine reduction), do well. These people usually continue to notice the beats either randomly, or with stress, but they recognize exactly what is going on and are able to say to themselves “there go my benign PVCs again,” and aren’t worried or bothered.
A small percentage of patients that I diagnose with palpitations due to benign PVCs continue to have symptoms.
Part of my initial evaluation involves checking potassium, magnesium, kidney function, and thyroid levels.
Potassium Supplementation For PVCs
Low potassium levels (hypookalemia) have been clearly associated with an increase in ventricular ectopy. Patients who take diuretics like hydrochlorothiazide (HCTZ, often used for high blood pressure) or furosemide (Lasix, often used for leg swelling or heart failure), are at high risk for hypokalemia with potassium levels less than 3.5 meQ/L.
Hypokalemia can also develop if you are vomiting, having diarrhea, or sweating excessively. There are lots of other infrequent causes including excess licorice consumption. The body regulates potassium levels closely, due to its importance in the electrical activities involved in cardiac, muscular and neurological function.
The normal range of potassium (K) is considered to be 3.5 to 5 meq/L , however, I have found that PVCs are more frequent when the potassium is less than 4.
Most of my symptomatic PVC patients with potassium less than 4 find significant improvement with potassium supplementation. I usually give them a prescription for potassium chloride (KCl) 10-20 meq daily to accomplish raising the level to >4.
An alternative to potassium supplements is ramping up how much potassium you consume in your diet. Most patients I talk to about low K immediately assume they should eat more bananas, but lots of fresh fruit and vegetables contain as much or more K than bananas.
The charts to the right show that a medium tomato contains as much K as a medium banana with a third of the calories. Avocados are a great source of K and contain lots of healthy fat. Yogurt (and I recommend full fat yogurt, of course) is a great source as well.
If you have kidney disease you are much more likely to develop hyperkalemia, or high K, and you want to avoid these high K foods. Potassium infusions are used as part of a “lethal injection” in executions because extreme hyperkalemia causes the heart to stop beating. (In fact, Arkansas is hurrying to execute 8 men between April 17 and 27 utilizing KCl. According to deathpenaltyinformation.org: “The hurried schedule appears to be an attempt to use the state’s current supply of eight doses of midazolam, which will expire at the end of April. Arkansas does not currently have a supply of potassium chloride, the killing drug specified in its execution protocol, but believes it can obtain supplies of that drug prior to the scheduled execution dates”)
Lifestyle, Stress and PVCs
It’s probably time I revealed that I have PVCs. I feel them as a sense that something has shifted inside my chest briefly, like my breath has been interrupted, like my heart has hiccoughed. If I didn’t know about PVCs and hadn’t made the diagnosis very quickly by hooking myself up to an ECG monitor in my office, I know I would have become very anxious about it.
I know exactly what causes them: stress and anxiety. And this is the case for many patients. Stress activates our sympathetic nervous system, causing the release of hormones from the adrenal gland that prepare us for “fight or flight.” These hormones stimulate the heart to beat faster and harder and often trigger PVCs.
I rarely get PVCs these days, as the major source of stress in my personal life has gone away. This is also a typical story my patient’s relate: troubling palpitations seem to melt away when they retire or change to less stressful occupations, or as they recover from depression/anxiety/grief related to death of loved ones, divorce or illness.
You can’t always control external stresses, but several factors in your lifestyle are key to managing how those stresses activate your sympathetic nervous system and trigger troubling PVCs.
Dr. Mandrola lists as Steps 5-8 (Steps 1-4 are reassurance) for PVC treatment his “four legs of the table of health”:
: good food, good exercise, good sleep and good attitude. Cutting back on caffeine and alcohol, looking critically at the dose of exercise, going to bed on time, and smiling are all great strategies for PVCs.
Of these four table legs, I consider regular aerobic exercise the most important, and modifiable factor for PVC reduction. Aerobic exercise improves mood and increases the parasympathetic (the calming component of the autonomic nervous system) activity, while lowering the output of the sympathetic nervous system.
The three factors that I find essential to handling the demanding and stressful job of being a cardiologist: restful sleep, regular, aerobic exercise and lots of love from my eternal fiancee (who also has occasional PVCs!)
Beyond sleep and exercise there is a plethora of techniques that purport to help individuals deal with stress: yoga, meditation, and progressive muscular relaxation, among them.
Apps touting methods for relaxation abound these days. My new Apple Watch is constantly advising me to engage in a breathing exercise for a minute at a time. I don’t find any of these techniques helpful for me (I haven’t found a good way to shut my brain down without falling asleep), but they may work for you.
Magnesium, Snake Oil and PVCs
Patients will find that the internet is rife with stories of how this supplement or vitamin or herb dramatically cures PVCs. You can be assured that a sales pitch accompanies these claims and that the snake oil being promoted has not been proven effective or safe. Because symptomatic PVCs like most benign, common and troubling conditions (lower back pain, fatigue, and nonspecific GI troubles come to mind), are closely related to mood and wax and wain spontaneously; the placebo effect proves powerful. In such conditions, snake oil and charlatans thrive.
Magnesium is enthusiastically hyped on the internet for all manner of cardiovascular problems including PVCs. Even Dr. Mandrola, who I respect quite a lot as an EP doc who promotes lifestyle change and who is definitely not a quack, lists his step 10 for PVCs (apologetically) as follows:
Step 10 (a): Please don’t beat me up on this one. Some patients report benefit from magnesium supplementation. I have found it helpful in my case of atrial premature beats. Let me repeat, I am not promoting supplements. Healthy patients with benign arrhythmia might try taking magnesium, especially at night. Don’t take magnesium if you have kidney disease. And if you take too much, watch out for diarrhea.
Most of the internet’s top quacks, however, greedily market and glowingly swear by magnesium. A Google search for magnesium cardiovascular disease yields 833,000 entries and the first page is a Who’s Who of quackery, including Dr Mercola (strong candidate for America’s greatest quack), Dr. Sinatra (see here, currently in the semifinals for America’s greatest quack cardiologist), NaturalNews and Life Extension (see here). This totally unsupported and dangerous blather from the Weston Price Foundation is often repeated and is typical:
(magnesium) Deficiency is related to atherosclerosis, hypertension, strokes and heart attacks. Deficiency symptoms include insomnia, muscle cramps, kidney stones, osteoporosis, fear, anxiety, and confusion. Low magnesium levels are found in more than 25 percent of people with diabetes. But magnesium shines brightest in cardiovascular health. It alone can fulfill the role of many common cardiac medications: magnesium inhibits blood clots (like aspirin), thins the blood (like Coumadin), blocks calcium uptake (like calcium channel-blocking durgs such as Procardia) and relaxes blood vessels (like ACE inhibitors such as Vasotec) (Pelton, 2001).
Magnesium levels are very important to monitor in hospitalized and critically ill patients, especially those receiving diuretics and medications that can effect cardiac electrical activity.
However, for individuals with normal diets and palpitations due to PVCs, there is scant evidence that it plays a significant role in cardiovascular health.
The MAGICA study looked at supplementation with both magnesium and potassium (in the active treatment group, daily oral dosing consisted of 2 mg of magnesium-dl-hydrogenaspartate (6 mmol magnesium) and 2 mg of potassium-dl-hydrogenaspartate (12 mmol potassium) daily. The dose was chosen to increase the recommended minimal daily dietary intake of magnesium (12 to 15 mmol) and potassium (20 to 30 mmol) by ∼50% in addition to usual diet ) in 307 patients with more than 720 PVCs per hour and normal baseline K and Mg levels.
The patients receiving magnesium/potassium supplements showed a decrease of 17% in frequency of PVCs but no improvement in symptoms.
A 2012 study in a Brazilian journal evaluated magnesium pidolate (MgP) in 60 patients with both PVCs and premature atrial contractions (PACs). The dose of MgP was 3.0 g/day for 30 days, equivalent to 260 mg of Mg elemental.
93% of patients receiving MgP experienced improved symptoms compared to only 13% of patients recieiving placebo. Both PVC and PAC frequency was reduced in those receiving MGP, whereas they increased by 50% in those receiving placebo.
This small study has never been reproduced, and the main results table makes little sense. It would not have been published in a reputable American cardiology journal and cannot be relied on to support magnesium for most patients with benign PVCs or PACs.
Drug or Ablation Treatment of PVCs: Usually Not Needed
A small percentage of my patients require treatment with beta-blockers which reduces the effects of the sympathetic nervous system on the heart. Very rarely, I will use anti-arrhythmic drugs. And every once in a while, very frequent PVCs resulting in cardiomyopathy require an ablation.
However, the vast majority of patients with benign PVCs, in my experience, feel drastically better with a simple non-pharmacological approach consisting of 4 factors:
Reassurance that the PVCS are benign
Caffeine (or other stimulant) reduction
Lifestyle adjustment with regular aerobic exercise
As part of the Health Nuts Project, the skeptical cardiologist has been evaluating walnuts, hazelnuts and almonds which he plans to put in packets and distribute to patients and readers.
Previously, we discovered that most raw almonds from the US have been fumigated with a chemical called propylene oxide and that roasting almonds creates potentially carcinogenic chemicals.
Consequently, after considerable searching, I purchased raw organic almonds from a company called NutsinBulk. These turn out to be from Spain (where pasteurization of almonds is not required) and are quite tasty.
As I was munching on one of these almonds I suddenly noticed an incredibly bitter taste causing me to spit the chewed almond out. My first thought was that this almond had gone “bad” in some way. Perhaps a mold had crept into it. Looking at the pieces I had spit out, however, I could see no discoloration or other visible difference from the “normal” almonds.
Subsequent experimentation has revealed that about one in ten of these almonds is incredibly bitter and there is no way to predict this from the external appearance of the almond.
The Source of Bitter Almonds
The sweet almond that we are used to eating in the US is produced from one type of almond tree (Prunus amygdalus var. dulcis) and does not contain poisonous chemicals. However, the bitter almond that I encountered comes from a different type of almond tree (Prunus amygdalus var. amara).
Prunus amara trees were likely the original almond trees but over time the sweet almond trees have been selected for and now dominate. According to the LA Times and Paul Schrade, who provides bitter almonds to restaurants:
Until recent decades, most Mediterranean almond orchards were grown from seed, and the shuffling of genes resulted in a mix of bitter almond trees among the sweet. Growers liked to keep a few bitter trees around because they helped to pollinize the sweet varieties. The inclusion of bitter nuts gave snackers occasional unpleasant surprises, but they deepened the flavor of marzipan, almond milk and glazes for cakes. In Italy, bitter almond paste was traditionally used to make crisp amaretti cookies, and bitter almond extract flavored amaretto liqueur. In Greece, bitter almonds are used in soumada, a sweet syrup. (apparently cooking or adding alcohol eliminates the toxic cyanide)
There’s little large-scale cultivation of bitter almonds left in Spain and Italy, mostly just scattered trees remain, but it is still possible to buy raw bitter almonds at European specialty markets. Morocco and Iran now lead in commercial production of bitter almonds.
A recessive gene causes bitter almond trees to produce in their shoots, leaves and kernels a toxic compound called amygdalin, which serves as a chemical defense against being eaten. When amygdalin is moistened, it splits into edible benzaldehyde, which provides an intense almond aroma and flavor, and deadly hydrocyanic acid, a fast-acting inhibitor of the respiratory system.
The lethal dose of raw bitter almonds depends on the size of the nuts, their concentration of amygdalin and the consumer’s sensitivity. But scientists estimate that a 150-pound adult might die from eating between 10 and 70 raw nuts, and a child from ingesting just a few.
YIKES!!!When I read this I was shocked. Could it be that consuming 10 of these raw biter almonds would kill me.? How could I distribute these potentially lethal edibles to my patients?
Amygdalin (Laetrile) , Alternative Cancer Therapy and Quackery
In addition to bitter almonds, significant amounts of amygdalin are found in the stone fruit kernels of apricots, peaches and plums. A synthetic form of amygdalin called Laetrile achieved great notoriety in the 1980s as a cancer treatment. Although research had shown the chemical to be ineffective, it was embraced by “alternative” healers who claimed it was a “natural” cure for cancer which was being suppressed by a conspiracy between the US FDA, big pharma, and the the medical community.
Steve McQueen, suffering from pleural mesothelioma sought the care of a delisted American holistic orthodontist practicing in Mexico, William Kelley. The NY Times reported:
In July 1980, McQueen secretly traveled to Rosarita Beach, Mexico, to be treated by Mexican and American doctors using Dr. Kelley’s regimen. He received not only pancreatic enzymes but 50 daily vitamins and minerals, massages, prayer sessions, psychotherapy, coffee enemas and injections of a cell preparation made from sheep and cattle fetuses. McQueen was also given laetrile, a controversial alternative treatment made from apricot pits.
Although we hear little about Laetrile these days, like most snake oil it is still promoted by alternative medicine. For example, The notorious quack Dr. Mercola still promotes the idea that laetrile is a safe and effective treatment of cancer on his web site with a post that has been viewed over 700,000 times.
You Can Die From Eating Bitter Almonds
Certainly, there is considerable evidence that Laetrile can be toxic or lethal but bitter almonds can also cause lethal cyanide poisoning. A case report describes a woman with colon cancer who turned down potentially curative surgery/chemotherapy and turned to alternative treatments including Laetrile. A helpful friend gave her a bag of bitter almonds for their “medicinal properties”, whereupon the woman consumed a slurry composed of 12 ground up almonds with water. Within 30 minutes she developed severe cyanide poisoning with vomiting, abdominal pain, pulmonary edema, severe lactic acidosis and loss of consciousness.
Analysis of the bitter almonds showed they contained on average 6.2 mg of cyanide per almond. It is estimated that a lethal dosage of cyanide is 50 mg or 0.5 mg per kg body weight, thus the calculation that 10 almonds could kill someone weighing 60 kg or 132 pounds.
My Search For Healthy Almonds Continues
The small amount of cyanide one gets from consuming a single bitter almond seems to have little effect. (Although the Mediterranean diet nutritionist Conner Middelman-Whitney , who spent time in Europe and encountered bitter almonds occasionally says that she does remember a weird, numb sensation in the mouth when they were consumed.) It’s extremely unlikely that one of my patients would consume 10 of the bitter almonds (without reflexively spitting them out as I did) in a short period of time.
When I have consumed them I noticed no adverse effects but after such an encounter I stopped eating the almonds for the day.
However, I’m not interested in testing that theory. (Ability to taste amygdalin or smell cyanide varies between individuals, thus I can’t be certain that the bitter taste would serve as a reliable warning.)
Therefore, I’ve concluded that I’m not going to distribute these potentially lethal almonds to my patients and will be removing them from the Dr. Pearson Health Nuts Packages.
My search for non-fumigated, non-cyanide-laced , non-carcinogenic almonds continues!
N.B. Famous deaths from cyanide poisoning include Hitler and Alan Turing.
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).
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 multiple 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 states 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.)