In October, 2016 the skeptical cardiologist predicted that Donald Trump’s coronary calcium score, if remeasured, would be >100 . At that time I pointed out that this score is consistent with moderate coronary plaque build up and implies a moderate risk of heart attack and stroke.
Trumps’ score gave him a seven-fold increase risk of a cardiovascular event in comparison to Hilary Clinton (who had a zero coronary calcium score) .
I was able to predict this score because we knew that Trump’s coronary calcium was 98 in 2013 and that on average calcium scores increase by about 10% per year.
I pointed out that his previous score was average for white men his age and his repeat score is also similar to the average white male of 71 years.
Entering Trump’s numbers into the MESA coronary calculator shows us he is at the 46th percentile, meaning that 46% of white men his age have less calcium.We can also calculate Trump’s 10 year risk of heart attack and stroke using the app from the ACC (the ASCVD calculator) and entering in the following information obtained from the White House press briefing:
Total Cholesterol 223
LDL Cholesterol 143
HDL Cholesterol 67
Systolic Blood Pressure 122
Never Smoked Cigarettes
Taking aspirin 81 mg and rosuvastatin (Crestor) 10 mg.
His 10 year risk of heart attack or stroke is 16.7%.
Given that his calcium score is average it doesn’t change his predicted risk and the conclusion is that his risk is identical to the average 71 year old white man-moderate.
We also know that Trump had an exercise stress echocardiogram which was totally normal and therefore can be reasonably certain that the moderate plaque build up in his arteries is not restricting the blood flow to his heart.
Here is what Dr. Jackson said about the stress echo:
He had an exercise stress echocardiogram done, which demonstrated above-average exercise capacity based on age and sex, and a normal heart rate, blood pressure, and cardiac output response to exercise. He had no evidence of ischemia, and his wall motion was normal in all images. the stress echo:
The New York Times article on this issue, entitled “Trump’s Physical Revealed Serious Heart Concerns, Outside Experts Say” however, presents a dramatically worrisome and misleading narrative.
It quotes several cardiologists who were very concerned about Trump’s high LDL level, weight and diet.
It’s interesting that some of the experts quoted in the NY Times piece feel that Trump’s Crestor dose should be increased in light of the recent NY Times piece questioning whether the elderly should take statins at all.
If we have serious concerns about Trump’s heart then we should have the same concerns about every 71 year old white man because he is totally average with regard to cardiac risk. In addition he is on a statin and on aspirin, the appropriate drugs to reduce risk.
In contrast to the average 71 year old male he has had a battery of cardiac tests which show exactly where he stands cardiac wise.
Most of these cardiac tests we would not recommend to an asymptomatic individual of any age. Jackson revealed that Trump had an EKG and an echocardiogram.
His ECG, or commonly EKG, was normal sinus rhythm with a rate of 71, had a normal axis, and no other significant findings.
He had a transthoracic echocardiogram done, which demonstrated normal left ventricular systolic function, an ejected fraction of 60 to 65 percent, normal left ventricular chamber size and wall thickness, no wall motion abnormalities, his right ventricle was normal, his atria were grossly normal, and all valves were normal.
So our President has a normal heart for a 71 year old white male. This automatically puts him at moderate risk for heart attack and stroke over the next 10 years but he is being closely monitored and appropriately treated and should do well.
N.B. I see that Trump’s LDL was reported previously as 93. The current LDL of 143 suggests to me that he has not been taking his Crestor.
N.B. Below is an excerpt from my prior post which explains coronary calcium
Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now. I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain patient’s risk of sudden death and heart attacks.
The CAC scan utilizes computed tomography (CT) X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.
Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.
The NY Times published an article earlier this month with the provocative title “You’re Over 75, and You’re Healthy. Why Are You Taking a Statin?”
It’s actually a balanced presentation of this difficult question (although it includes the seemingly obligatory anecdote of a patient getting severe muscle aches and weakness on Lipitor) and I agree with the concept that patients should demand a good thoughtful explanation from their PCP if they are on a statin. Shared physician and patient decision-making should occur irrespective of age when a statin is prescribed.
Unfortunately, the NY Times piece was triggered by and contains references to a weak observational study that was recently published in the Journal of the American Geriatric Society..
A much better article on this same topic was published earlier in January in what is arguably the most respected cardiology journal in the world (Journal of the American College of Cardiology).
It contains what I think is a very reasonable discussion of the problem: the elderly at are a substantially higher risk of adverse “statin-associated symptoms” but also at much higher risk of stroke, heart attack and cardiovascular-related death than the young.
Key Points To Consider For Use of Statins In Elderly
Some key points from that article to ponder for those over 75 years
Major European and North Americans national guidelines differ markedly in this area as this graphic illustrates
“At one end of the spectrum, the 2016 ESC/EAS guidelines miss great opportunities for safe, cheap, and evidence-based prevention in elderly individuals 66 to 75 years of age. At the other end of the spectrum, the 2014 NICE guideline provides near-universal treatment recommendations well into the very elderly >75 years of age where RCT evidence is sparse and more uncertain.”
2. Data on from 2 large primary prevention trial (JUPITER and HOPE-3) show that rosuvastatin (Ridker, et al)
reduced the risk of a composite endpoint (nonfatal MI, nonfatal stroke, or cardiovascular death) substantially by 49% (RR: 0.51; 95% CI: 0.38 to 0.69), and the risk was reduced by 26% (RR: 0.74; 95% CI: 0.61 to 0.91) in those ≥70 years of age. The efficacy was similar in individuals ≥70 and <65 years of age, indicating little heterogeneity in treatment effect by age. Today, nearly all apparently healthy elderly individuals have RCT evidence supporting statin efficacy.
3. The elderly compared to the younger are much more likely to have a nonfatal event which does not reduce their longevity but impacts their quality of life.
Thus, patient preferences are critical important for well-informed shared decision-making. If a patient only values longevity, there are little data to support primary prevention with statins in people >65 years of age. On the other hand, if preventing nonfatal and potentially disabling MI or stroke is of value to the patient, it might be reasonable to initiate statin therapy. From this perspective, it is noteworthy that the relative importance that people assign to avoiding death compared with avoiding nonfatal events appears to be highly age dependent. Although younger individuals <65 years of age weigh avoiding death highest, elderly individuals ≥65 years put a much higher weight on avoiding MI or stroke than death, These differences are compatible with elderly individuals having a greater focus on quality of life and avoiding disability than on extending life.
The Value of Derisking and Deprescribing
In my practice, I do a fair amount of deprescribing statins in the elderly. I have a very low threshold for initiating a trial of temporary statin cessation if there is any question that a patient’s symptoms could be statin-related (see here.)
The older the patient, the higher the bar for initiating statins and I think in all patients a search for subclinical atherosclerosis (coronary calcium scan or vascular ultrasound) helps inform the decision.
Previously, I had no term for this higher bar but I like the term the JACC paper introduces, derisking:
A promising approach to personalize treatment in elderly people is “derisking” by use of negative risk markers (i.e., absence of coronary artery calcification) to identify those at so low risk that statin therapy may safely be withheld . In the BioImage study of elderly individuals, for example, absence of coronary artery calcification was prevalent (≈1 of 3) and associated with exceptionally low ASCVD event rates
If you are >75 ponder all these factors and have an intense discussion with your doctor about taking a statin.
If you are still on the fence after this discussion consider a compromise approach that I have outlined here.
As we age our hearts and arteries become stiffer. This cardiovascular stiffening plays a key role in hypertension, atrial fibrillation, and heart failure in older individuals (1).
Age-related cardiac stiffening is worse in those who are sedentary compared to those who exercise regularly (2).
Recent studies strongly suggest that regular exercise can prevent or minimize these age-related changes, thereby hopefully reducing the high rate of heart failure, hypertension and atrial fibrillation in the elderly.
In my post on fitness as a vital sign I briefly mentioned a fascinating study from 2014 which looked at 102 healthy seniors (age>64 years) and stratified them into 1 of 4 groups based on their lifelong histories of endurance exercise training.
Consider which of these 4 categories you fall into:
Sedentary subject-exercised no more than once per week during the prior 25 years.
Casual exercisers-engaged in 2-3 sessions per week
Committed exercisers-performed 4-5 sessions per week
Competitive “Masters level” athletes-trained 6-7 times per week
Exercise sessions were defined as periods of “dynamic activity lasting at least 30 minutes.”
The participants had sophisticated measures of their exercise capacity (max VO2), the size and mass of their left ventricles (cardiac MRI) and the stiffness of their left ventricles (invasive pressure/volume curves to calculate LV compliance and distensibility.)
This graph shows the key finding of the study: a markedly different pressure/volume curve in the sedentary and casual exercisers (blue and red dots) versus the committed or master exercisers. The two curves on the left correspond to a very stiff heart, similar to curves found in patients with heart failure.
The far right curve of competitive exercisers resembles that of a young heart.
The black triangle curve of the committed exerciser is in between these extremes
The study concludes:
“low doses of casual, lifelong exercise do not prevent the decreased compliance and distensibility observed with healthy, sedentary aging. In contrast, 4 to 5 exercise sessions/week throughout adulthood prevent most of these age-related changes”
It would appear we need at least 4-5 30 minute exercise session per week to forestall the age-related stiffening of the heart and lower our chances of getting heart failure, hypertension and atrial fibrillation.
Since this was an observational study there is always a chance that lack of exercise is not the causes of poor cardiac stiffness. It is conceivable that those of us with stiffer hearts tend to be more sedentary because of the poor cardiac function.
Can You Reverse The Age-Related Changes In Cardiac Stiffness?
If you have already reached middle age there is still hope for you as these same investigators recently published a study showing that cardiac stiffness can be improved with exercise. These findings imply that lack of exercise is the cause of worsening cardiac stiffness with aging.
This study identified 61 sedentary men in their mid-fifties and randomly assigned them to either 2 years of exercise training or attention control (a combination of yoga, balance, and strength training 3 times per week for 2 years) and measured their LV stiffness and max VO2 before and after intervention.
Max VO2 increased by 18% and LV stiffness declined from .072 to .051 in the exercise group but did not change in the control group.
The exercise training arm of this study involved a mixture of continuous moderate-intensity aerobic exercise combined with high intensity training. The high intensity portion of the program involved exercising at 90-95% of HR maximum for 4 minutes followed by a 3 minute active recovery period, repeated 4 times.
Over a period of 6 months under the guidance of exercise physiologists the participants had their exercise levels gradually increased. After 6 months they were training 5-6 hours per week, including 2 of the “high intensity interval” session and 1 long (>/= 1 hour) and one 30-minute base pace session each week.
By the sixth month, participants were training 5 to 6 hours per week, including 2 interval sessions, and 1 long (at least an hour) and one 30-minute base pace session each week.
How Much Exercise Do We Need To Minimize Cardiac Aging?
This chart from recent European guidelines on lifestyle for prevention of disease describes different intensities of aerobic exercise:
These guidelines suggest that if you engage in vigorous exercise such as running or jogging, cycling fast or singles tennis, you only need to achieve 75 minutes per week. Moderate exercise such as walking or elliptical work-outs requires at least 150 minutes/week.
Based on these recent studies on exercise and cardiac stiffness and the bulk of scientific literature on the overall health benefits of exercise I would advise for all individuals with or without heart disease
-If you are sedentary, become a committed exerciser.
-Committed exercise means some form of dynamic exercise 4-5 times per week
-If you are already a committed exerciser at moderate intensity levels consider adding to your routine one or two sessions of high intensity interval exercise.
-High intensity exercise will require you to get your heart rate up to 90-95% of your maximum
-Predicted maximal HR=220 -age. For a 60 year old this equals 160 BPM. 90% of 160 equals 144 BPM.
When the skeptical cardiologist trained in medicine and cardiology in the 1980s the standard protocol for obtaining a lipid profile (LDL and HDL cholesterol plus triglycerides) involved having the patient fast for >8 hours before the blood was drawn.
Beginning in 2009, however, various national organizations began recommending the use of nonfasting lipid profiles. In 2011 the American Heart Association endorsed the fasting lipid profile and shortly thereafter I began telling my patients they did not need to fast for these tests.
Old habits and ideas are hard to kill and to this day most of my patients think that fasting is a requirement. Lab personnel seem to be stuck in the past as well and I typically instruct my patients to lie if they are asked if they have eaten.
In University City, like much of the country these past two weeks, we’ve been enveloped in extreme unremitting cold but just a month ago I was writing about leaves. My goal was to discuss leaf blowers. What follows is what I wrote before becoming distracted.
The street on which my humble abode abides is heavily populated by large, beautiful trees. With autumn, Thoreau noted, their beauty is enhanced and nature,
“like an athlete, begins to strip herself in earnest for her contest with her great antagonist Winter. In the bare trees and twigs what a display of muscle.”
Dendrophile that I am, my heart quickened when I witnessed the glorious display of colors that issued forth from their branches a month ago. I was so inspired I took the picture below from my front doorstep.
Alas, I had forgotten that the vivid reds and yellows were a precursor to a constant deluge of dead and decaying dendrophitic detritus upon my lawn.
Now the once beautiful leaves have become a nuisance-a funereal layer of death choking my lawn and once more I must grapple with how to handle them.
The first time I was presented with this problem I pondered just leaving the leaves. After watching my neighbors dutifully raking and blowing their leaves into the street I concluded this was not acceptable. I purchased a rake or two and raked.
Today I raked thousands of leaves into the street from which they will soon be sucked up by the leaf-sucking trucks of University City .
Once more I pondered the wisdom of this approach. I wondered if I was somehow interfering in the cycle of nature on one hand and on another I considered buying a leaf blower.
A prolonged surfing expedition led by Google led me to the following statement:
To treat leaves as trash is both environmentally foolish and financially ruinous. Currently, many municipalities encourage residents to rake leaves to the curb for collection, but before they are collected, heavy rains often wash the leaves into catch basins. There, they decompose and release phosphorus and nitrogen into streams and rivers that flow through the community. These excess nutrients contribute to algae blooms during the summer, which result in lower oxygen levels, making it difficult for fish and other aquatic species to survive.
Municipalities, both large and small, spend thousands, even millions, of dollars each year to collect, transport, and process autumn leaves, tying up resources that could be used elsewhere in our communities. If we all keep our leaves on our properties, we will improve our gardens, save money, and enhance the environment we all share.
University City Leaf Disposal and Mulching Operation
After encountering this sobering statement which implies that the leaf removal operation is wreaking all manner of havoc I posted it on a discussion regarding the leaf removal schedule on Next Door .
Fellow Ucitians informed me that UCity no longer disposes of the leaves themselves but has contracted with St. Louis Composting
St. Louis Compositing was” founded in 1992 by eco-enthusiast Patrick Geraty” and has “blossomed into the region’s largest compost producer. St. Louis Composting’s mission is to help make the world a little greener and reduce landfill waste by producing compost of the highest quality. Together, our six composting facilities process roughly 600,000 cubic yards of green material annually – more than one-third of all yard waste generated in St. Louis County.”
So, it seems it would be OK to blow or rakes leaves into the street. After much pondering, however, I decided to purchase a corded electric mower and perform the mulching myself.
Blowing is twice as fast as raking but the rake is superior in terms of personal fitness and earth friendliness:
“we burned more than twice as many calories raking as we did blowing, and no fossil fuels (barring those that went into the manufacturing of the rake). On the other hand, raking isn’t healthy if you spend the next day in bed with a pulled back.”
As your cardiologist I advise embracing the raking as a useful combination of aerobic exercise and upper body strength training!
Science continued to progress in the field of cardiology in 2017. Some cardiology interventions were proven to be more beneficial (TAVR) and some less (coronary stents). A class of cholesterol lowering drugs had a big winner and a big loser. A supplement that many thought, based on observational studies, was crucial to prevent heart disease, turned out to be unhelpful. More evidence emerged that saturated fat is not a dietary villain.
From the skeptical cardiologist’s viewpoint, the following were the major scientific studies relevant to cardiology:
1. “Thousands of heart patients get stents that may do more harm than good”
Cardiologists have known for a decade (since the landmark COURAGE study) that outside the setting of an acute heart attack (acute coronary syndrome or ACS), stents don’t save lives and that they don’t prevent heart attacks.
Current guidelines reflect this knowledge, and indicate that stents in stable patients with coronary artery disease should be placed only after a failure of “guideline-directed medical therapy.” Despite these recommendations, published in 2012, half of the thousands of stents implanted annually in the US continued to be employed in patients with either no symptoms or an inadequate trial of medical therapy.
Yes, lots of stents are placed in asymptomatic patients. And lots of patients who have stents placed outside the setting of ACS are convinced that their stents saved their lives, prevented future heart attacks and “fixed” their coronary artery disease. It is very easy to make the case to the uneducated patient that a dramatic intervention to “cure” a blocked artery is going to be more beneficial than merely giving medications that dilate the artery or slow the heart’s pumping to reduce myocardial oxygen demands.
Stent procedures are costly in the US (average charge around $30,000, range $11,000 to $40,000) and there are significant risks including death, stroke and heart attack. After placement, patients must take powerful antiplatelet drugs which increase their risk of bleeding. There should be compelling reasons to place stents if we are not saving lives.
I, along with the vast majority of cardiologists, still recommended stents for those patients with tightly blocked coronary arteries and stable symptoms, which were not sufficiently helped by medications. ORBITA calls into question even this indication for stenting.
The ORBITA study investigators recruited 230 patients to whom most American cardiologists would have recommended stenting. These patients appeared to have a single tightly blocked coronary artery and had chest pain (angina) that limited their physical activity.
They treated the patients for 6 weeks with aspirin/statins/ and medications that reduce anginal symptoms such as beta-blockers, calcium-channel blockers or long-acting nitrates. At this point patients were randomized to receive either a stent or to undergo a catheteriation procedure which did not result in a stent, a so-called sham procedure.
The performance of a sham procedure was a courageous move that made the study truly double-blinded; neither the patients nor the investigators knew which patients had actually received a stent. Thus, the powerful placebo effects of having a procedure were neutralized.
Surprisingly, the study found that those patients receiving stents had no more improvement in their treadmill exercise time, angina severity or frequency or in their peak oxygen uptake on exercise.
ORBITA hopefully will cause more cardiologists to avoid the “oculo-stenotic” reflex wherein coronary artery blockages are stented without either sufficient evidence that the blockage is causing symptoms or that a medical trial has failed.
Although this was a small study with a very narrowly defined subset of patients, it raises substantial questions about the efficacy of coronary stenting. If ORBITA causes more patients and doctors to question the need for catheterization or stenting, this will be a very good thing.
2. Vitamin D Supplementation Doesn’t Reduce Cardiovascular Disease (or fractures, or help anything really).
One of my recurring themes in this blog is the gullibility of Americans who keep buying and using useless vitamins, supplements and nutraceuticals, thereby feeding a $20 billion industry that provides no benefits to consumers (see here and here).
Vitamin D is a prime player in the useless supplement market based on observational studies suggesting low levels were associated with increased mortality and cardiovascular disease
Despite well done studies showing a lack of benefit of Vitamin D supplementation, the proportion of people taking more than 1,000 IU daily of Vitamin D surged from just 0.3 percent in 1999-2000 to 18 percent in 2013-2014.
Most recently a nicely done study showed that Vitamin D supplementation doesn’t reduce the risk of heart disease.
In a randomized clinical trial that included 5108 participants from the community, the cumulative incidence of cardiovascular disease for a median follow-up period of 3.3 years was 11.8% among participants given 100 000 IU of vitamin D3 monthly, and 11.5% among those given placebo.
Aaron Carroll does a good job of summarizing the data showing Vitamin D is useless in multiple other areas in a JAMA forum piece:
Last October, JAMA Internal Medicine published a randomized, controlled trial of vitamin D examining its effects on musculoskeletal health. Postmenopausal women were given either the supplement or placebo for one year. Measurements included total fractional calcium absorption, bone mineral density, muscle mass, fitness tests, functional status, and physical activity. On almost no measures did vitamin D make a difference.
The accompanying editor’s note observed that the data provided no support for the use of any dose of vitamin D for bone or muscle health.
Last year, also in JAMA Internal Medicine, a randomized controlled trial examined whether exercise and vitamin D supplementation might reduce falls and falls resulting in injury among elderly women. Its robust factorial design allowed for the examination of the independent and joined effectiveness of these 2 interventions. Exercise reduced the rate of injuries, but vitamin D did nothing to reduce either falls or injuries from falls.
In the same issue, a systematic review and meta-analysis looked at whether evidence supports the contention that vitamin D can improve hypertension. A total of 46 randomized, placebo controlled trials were included in the analysis. At the trial level, at the individual patient level, and even in subgroup analyses, vitamin D was ineffective in lowering blood pressure.
Finally, if the Vitamin D coffin needs any more nails, let us add the findings of this recent meta-analysis:
calcium, calcium plus vitamin D, and vitamin D supplementation alone were not significantly associated with a lower incidence of hip, nonvertebral, vertebral, or total fractures in community-dwelling older adults.
3. PCSK9 Inhibitors: Really low cholesterol levels are safe and reduce cardiac events
I reported the very positive results for evolocumab and disappointing results for bosocizumab on the physician social media site SERMO in March but never put this in my blog.
As a practicing cardiologist I’ve been struggling with how to utilize the two available PCSK9 inhibitors (Amgen’s Repatha (evolocumab) and Sanofi’s Praluent (alirocumab) in my clinical practice. I would love to use them for my high risk statin-intolerant patients but the high cost and limited insurance coverage has resulted in only a few of my patients utilizing it.
The lack of outcomes data has also restrained my and most insurance companies enthusiasm for using them.
The opening session at this year’s American College of Cardiology Scientific Sessions in DC I think has significantly changed the calculus in this area with two presentations: the first showing Amgen’s “fully humanized” evolocumab significantly lowers CV risk in high risk patients on optimal statin therapy and the second showing that Pfizer’s “mostly humanized” bococizumab loses efficacy over time and will likely never reach the market.
The FOURIER study of evolocumab randomized 27, 564 high risk but stable patients who had LDL>70 with prior MI, prior stroke or symptomatic PAD to receive evolocumab or placebo on top of optimized lipid therapy. 69% of patients were recieving high intensity statin therapy and the baseline LDL was 92. LDL was reduced by 59% to average level of 30 in the treated patients. The reduction in LDL was consistent through the duration of the study.
IN 1/4 of the patients LDL was <20! These are unprecedented low levels of LDL.
Active treatment significantly reduced the primary endpoint by 15% and reduced the secondary endpoinf of CV death, MI, stroke by 20%. absolute difference 2% by 3 years.
There was no difference in adverse effects between placebo and Evo.
The next presentation featured data using Pfizer’s candidate in the PCSK9 wars and the acronym SPIRE (Studies of PCSK9 Inhibition and the Reduction in vascular Events (SPIRE) Bococizumab Development Program).
Paul Ridker presented the outcomes data for bococizumab which was actually similar to evolocumab data but given the declining efficacy and development of antibodies to the Pfizer drug over time these were very disappointing for Pfizer and I would presume their drug will never reach the market.
How will these results impact clinical practice?
I am now more inclined to prescribe evolocumab to my very high risk patients who have not achieved LDL< 70. I’m willing to do what I can to jump through insurance company hoops and try to make these drugs affordable to my patients.
I am less worried about extremely low LDL levels and have more faith in the LDL hypothesis: the lower the LDL the lower the risk of CV disease.
Cost is still going to be an issue for most of my patients I fear and the need for shared decision-making becomes even more important.
4. “Pure Shakes Up Nutritional Field: Finds High Fat Intake Beneficial.”
As one headline put it.
I recorded my full observations on this observational international study here
Here is a brief excerpt:
The Prospective Urban Rural Epidemiology (PURE) study, involved more than 200 investigators who collected data on more than 135000 individuals from 18 countries across five continents for over 7 years.
There were three high-income (Canada, Sweden, and United Arab Emirates), 11 middle-income (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, and Turkey) and four low-income countries (Bangladesh, India, Pakistan, and Zimbabwe)
This was the largest prospective observational study to assess the association of nutrients (estimated by food frequency questionnaires) with cardiovascular disease and mortality in low-income and middle-income populations,
The PURE team reported that:
-Higher carbohydrate intake was associated with an increased risk of total mortality but not with CV disease or CV disease mortality.
This finding meshes well with one of my oft-repeated themes here, that added sugar is the major toxin in our diet (see here and here.)
I particular liked what the editorial for this paper wrote:
Initial PURE findings challenge conventional diet–disease tenets that are largely based on observational associations in European and North American populations, adding to the uncertainty about what constitutes a healthy diet. This uncertainty is likely to prevail until well designed randomised controlled trials are done. Until then, the best medicine for the nutrition field is a healthy dose of humility
I wish for all those following science-based medicine a healthy dose of humility. As science marches on, it’s always possible that a procedure we’ve been using might turn out to be useless (or at least much less beneficial than we thought), and it is highly likely that weak associations turn out to be causally nonsignificant. Such is the scientific process. We must continually pay attention, learn and evolve in the medical field.
Happy New Year to Be from the Skeptical Cardiologist the EFOSC!
The KardiaBand for Apple Watch from AliveCor has delivered on its unique promise of a medical grade single lead ECG recording made by placing your thumb on your wristwatch band.
The ECG recordings are equivalent in quality to those made by their previously available KardiaMobile (see my prior post here.) After more experience with the Band I think the ease of recording is superior to KardiaMobile and the ability to discriminate atrial fibrillation from normal sinus rhythm is similar to KardiaMobile.
By combining either a KardiaBand or a KardiaMobile device with Kardia’s SmartRhythm monitoring system for Apple Watch we now have the promise of personal monitoring to detect atrial fibrillation.
What is SmartRhythm?
SmartRhythm is AliveCor’s term for its system for monitoring your heart rate and activity levels in order to identify when your rhythm is abnormal.
The system “takes your heart rate and activity data gathered from the Apple Watch and evaluates it using a deep neural network to predict your heart rate pattern.”
The heart rate is obtained from the Apple Watch PPG sensor every 5 seconds. If it differs from what is predicted SmartRhythm notifies you to record an ECG.
If you’d like to learn more detail about the development of SmartRhythm and how it functions, AliveCor has an excellent informational piece here.
You can choose to have the Kardia SmartRhythm display come up whenever your Apple Watch awakens. It’s got information on your heart rate and activity over the preceding several hours
The AliveCor FAQ on SmartRhythm stresses that a notification does not always mean an abnormal rhythm. Clearly false positives can and will occur. The first day I wore my KardiaBand I had several of these.
Causes for false positives include exercise that Apple Watch couldn’t detect, stress or anxiety-in other words, situations where your heart rate is higher than predicted by how much activity you are doing.
The long term record of your SmartRhythm recordings resides on your iPhone . Here’s my record for the last week
Note that Kardia , in addition to tracking your heart rate, also shows you by the green, yellow and orange dots, the times that ECG recordings were made.
Green dots indicate recordings classified as normal and yellow as “unclassified.” In my case most of the unclassified recordings were due to heart rate >100 BPM associated with exercise.
There is one orange dot indicating that Kardia felt the ECG showed “possible atrial fibrillation.”
This happened when I took my Apple Watch off my wrist and put it on one of my patients who has permanent atrial fibrillation. I had him push on the KardiaBand sensor to make an ECG recording and it was correctly identified as atrial fibrillation.
Thus far I have had no notifications of “possible atrial fibrillation” while I have been wearing my watch thus the false positive rate appears acceptably low.
How Does SmartRhythm Perform During Exercise?
I checked out SmartRhythm’s ability to predict normal and abnormal heart patterns by wearing it during a session on my indoor bike trainer. The device did a good job of tracking both my heart rate and activity during the workout. You can view the most recent data by viewing your Apple Watch screen during the workout as below
Or for more detailed information you can view the complete history on your iPhone as below
The system accurately tracked my heart rate and activity (although AliveCor lists stationary bike as an activity that may result in false positives). During a session of weights after the aerobic workout despite erratic heart rates and arm movements it did not notify me of an abnormality. I also did 100 jumping jacks (which involves wildly flailing my arms) and the heart rate remained within the predicted boundaries.
What is more remarkable is that I was able while cycling at peak activity to make a very good quality ECG recording by taking my right hand off the handle bar and pushing my thumb down on the KardiaBand sensor on my left wrist.
This recording clearly displays p waves and is sinus tachycardia. It’s unclassified by Kardia because the rate is >100 BPM.
Afib Patient Experience
One of my patients last week, a 70 year old woman with paroxysmal atrial fibrillation, had already set up SmartRhythm monitoring on her Apple Watch.
I have this patient like many of my afibbers utilizing KardiaMobile to check an ECG when they think they are in afib.
However, she, like many of my afib patients, is totally unaware when her heart is out of rhythm. Such asymptomatic patients are alerted to the fact that they are in afib by detection of a rapid heart rate (from a heart rate tracking wearable or BP monitor) or an irregular heart beat (from BP monitor or by someone checking the pulse) or by a random recording of an ECG.
She’s started using SmartRhythm in the hopes that it will provide a reliable and early warning of when she goes into atrial fibrillation.
We discussed the possibility of stopping the flecainide she takes to maintain normal rhythm to test the accuracy of the SmartRhythm system for detecting atrial fibrillation in her but decided not to. She’s on an oral anticoagulant and therefore protected from stroke so development of atrial fibrillation will not be dangerous for her.
I eagerly await the first real world, real patient reports of SmartRhythm’s performance in atrial fibrillation detection.
If there are any afibbers out there who have had an episode of atrial fibrillation detected by SmartRhythm please let me know the details.
We need such anecdotes along with controlled trials to determine how useful SmartRhythm will be as a personal wearable system for detection of afib.
N.B. I’ve copied a nice section from AliveCor’s website which describes in detail the difference between measuring heart rate from the PPG sensor that all wearable devices use versus measuring the electrical activity of the heart with an ECG.
To understand how Kardia for Apple Watch works, let’s start by talking about your heart, how the Apple Watch and other wearable devices can measure your heart rate, and how an ECG is different from the information you get from a heart rate sensor alone.
Your heart is a pump. With each beat of your heart, blood is pumped through your arteries and causes them to expand. In the time between beats, your arteries relax again. On the underside of the Apple Watch is a sensor, called a photoplethysmogram (PPG), that uses green and infrared LEDs to shine light onto your skin, and detects the small changes in the amount of light reflected back as your arteries expand and relax with each beat of your heart. Using this sensor, the Apple Watch can tell how fast your heart is beating, and how your heart rate changes over time.
But, your heart rate does not tell everything there is to know about your heart. The PPG sensor on the Apple Watch can only see what happens after each heartbeat, as blood is pumped around your body. It can’t tell you anything about what is making your heart beat, or about what happens inside your heart during each beat. An ECG is very different, and tells you a lot more!
An ECG measures the electrical activity in your heart muscles. It detects the small pulse of electricity from the sinoatrial node (the body’s natural pacemaker, which normally initiates each heartbeat) and the large electrical impulses produced as the lower chambers of the heart (the ventricles) contract and relax. By looking at an ECG, a doctor can discern a wealth of information about the health and activity of your heart muscle, much more than you can tell from your heart rate alone. ECGs are the required gold standard for diagnosis of arrhythmias and many cardiac abnormalities, and can even be used to see evidence of acute heart attacks and even events that have occurred in the past.
Research has shown that taking frequent ECGs increases the likelihood of detecting certain arrhythmias, and decreases the mean time to diagnosis.
The skeptical cardiologist has been evaluating the Kardia Band from AliveCor which allows one to record single lead medical grade ECGS on your Apple Watch. What follows is my initial experience with setting up the device and using it to make recordings.
After ordering my Kardia Band for Apple Watch on 11/30 from AliveCor the device appeared on my door step 2 days later on a Saturday giving me most of a Sunday to evaluate it.
What’s In The Box
Inside the box I found one small and one large black rubber wrist watch band
The larger one had had a small squarish silver metallic sensor and the smaller one had a space to insert a sensor. It turns out my wrist required the smaller band and it was very easy to pop out the sensor and pop it into the smaller band.
After replacing my current band with the Kardia band (requires pushing the button just below the band and sliding the old band out then sliding the new one in) I was ready to go.
The Eternal fiancée did not complain about the appearance of the band so I’m taking that to mean it passes the sufficiently stylish test. She did inquire as to different colors but it appears AliveCor only has one style and one color to choose from right now.
I have had problems with rashes developing with Apple’s rubbery band and switched to a different one but thus far the Kardia band is not causing wrist irritation.
I didn’t encounter any directions in the box or online so I clicked on the Kardia app on the watch and the following distressing message appeared.
Prior to 11/30 Kardia Band only worked in certain countries in Europe so I suspected my AliveCor app needed to be updated.
I redownloaded the Kardia app from the Apple App Store , deleted it off my Watch and reinstalled it.
I was thrilled when the app opened up and gave me the following message
However, I was a little puzzled as I was not aware that setting up Smart Rhythm was a requirement to utilize the ECG recording aspect of Kardia Band. Since I have been granted a grandfathered Premium membership by AliveCor I knew that I would have access to Smart Rhythm and went through the process of entering my name and email into the Kardia app to get this started.
Alas, when the Watch Kardia app was accessed after this I continued to get the same screen. Clicking on “need help” revealed the following message:
Bluetooth was clearly on and several attempts to restart both the watch and the iPhone app did not advance the situation.
I sent out pleas for assistance to AliveCor.
At this point the Eternal Fiancee had awoken and we went to Sardella for a delightful brunch . I had this marvelous item:
Later on that day I returned to my Kardia Band iPhone and deinstalled, reinstalled , reloaded and restarted everything.
The First Recording
At this point it worked and I was able to obtain my first recording by pushing the record ECG button and holding my thumb on the sensor for 30 seconds.
I’ve made lots of recordings since then and they are good quality and have accurately recognized that I am in normal sinus rhythm.
The Smart Rhythm component has also been working. Here is a screen shot of today’s graph.
You’l notice that the Smart Rhythm AI gave me a warning sometime in the morning (which I missed) as it felt my rhythm was abnormal. I missed making the recording but am certain that I was not in afib.
Comparison of the Kardia Band recording (on the right) versus the separate Kardia device recording (on left) shows that they are very similar in terms of the voltage or height of the p waves, QRS complexes and T waves.
I felt a palpitation earlier and was able to quickly activate the Kardia Watch app and make a recording which revealed a PVC.
In summary, after some difficulty getting the app to work I am very pleased with the ease of recording, the quality of the recording and the overall performance of Kardia Band. The difficulties I encountered might reflect an early adoption issue which may already be resolved. Please give me feedback on how the device set up worked for you.
I’ll be testing this out on patients with atrial fibrillation and report on how it works in various situations in future posts.
After more experience with the Smart Rhythm monitoring system which I think could be a fantastic breakthrough in personal health monitoring I’ll give a detailed analysis of that feature.
I note patient awareness of the possibility of OSA is rising exponentially and many of my patient’s are being subjected to sleep studies because their wives are bothered by their excessive snoring.
The AASM guidelines state that
Increased risk of moderate to severe OSA is indicated by the presence of excessive daytime sleepiness and at least two of the following three criteria: habitual loud snoring; witnessed apnea or gasping or choking; or diagnosed hypertension
Although I have no reason to suspect that I have sleep disordered breathing (SDB-I feel like this term is becoming popular as it avoids the stigma of apnea), I decided to determine my Epworth Sleepiness Scale which is often utilized to measure excessive daytime sleepiness.
Developed by Dr. Murray Johns, this scale has its own website where you will learn that:
Johns (2002) introduced the term somnificity to describe the effects of different postures and activities on sleep propensity.
The somnificity of any particular posture, activity and situation is a measure of its ability to facilitate or impede sleep onset in the majority of people. It is not a characteristic of individual people or their sleep disorders.
and (no doubt after years of intense sleepiness research) Dr. Johns has discovered that:
Simply to lie down rather than stand up increases one’s likelihood of falling asleep – the change of posture increases one’s sleep propensity at the time.
After stumbling up on this revelation I have decided to test my hypothesis that playing electric guitar while standing has extremely low somnificity. (I also hope to use the word somnificity in a normal daily conversation without biting my tongue.)
This self-administered questionnaire asks you to rate how likely you are (on a scale of 0=never to 3=high chance of dozing) to doze off or fall asleep in certain situations. What follows are the situations with my observations and my self-rated score.
Sitting and reading (Principles of Nuclear Medicine=3, Brave New World=0) 1
Watching TV 1
Sitting, inactive in a public place (theatre or a meeting) 1
As a passenger in a car for an hour without a break 2
Lying down to rest in the afternoon when circumstances permit 3
sitting and talking to someone 1
sitting quietly after a lunch without alcohol 1
In a car while stopped for a few minutes in the traffic 2
They don’t ask about falling asleep while driving which seems much more important than the other situations. I’ve done that a lot.
The biggest soporific situation for me is sitting in a barber’s chair. No matter what small talk the hairdresser throws at me, I am asleep within 5 minutes. My bobbing head requires the rare skill of trimming a moving target.
My total score was 12 which puts me solidly in the land of sleep disordered breathing. In the original study by Johns the patient’s with sleep apnea (OSA-line 3 in below chart) had an average score of 11.7.
The AASM guidelines indicate that I could have gotten into some OSA studies with my score, especially if I add in that I have been caught snoring, gasping and choking (sometimes all three simultaneously!) and I have hypertension.
The Eternal fiancée got a respectable score of 7. Apparently she never falls asleep at traffic lights, watching TV/movie or sitting after lunch and believes these are masculine traits. However, I think she should get double points for taking long, intentional naps throughout the day.
AliveCor has finally gotten approval from the FDA to release its Kardia Band in the United States.
The skeptical cardiologist is quite excited to get his hands (or wrist) on one and just gave AliveCor $199 to get it.
The device incorporates a mobile ECG sensor into a wrist band that works with either 42 or 38 mm Apple watches. I’ve written extensively about AliveCor’s previous mobile ECG product (here and here) which does a good job of recording a single lead ECG rhythm strip and identifying atrial fibrillation versus normal rhythm,
Hopefully, the Kardia Band will work as well as the earlier device in accurately detecting atrial fibrillation.
According to this brief video to make a recording you tap the watch screen then put your thumb on the sensor on the band.
The app can monitor your heart rate constantly and alerts you to make a recording if it thinks you have an abnormal rhythm.
I was alerted to the release of Kardia by Larry Husten’s excellent Cardio Brief blog and in his post he indicates that the alert service , termed Smart Rhythm, requires a subscription of $99 per year.:
AliveCor simultaneously announced the introduction of SmartRhythm, a program for the Apple Watch that monitors the watch’s heart rate and activity sensors and provides real-time alerts to users to capture an ECG with the Kardia Band. The program, according to an AliveCor spokesperson, “leverages sophisticated artificial intelligence to detect when a user’s heart rate and physical activity are out of sync, and prompts users to take an EKG in case it’s signaling possible abnormalities like AFib.”
The Kardia Band will sell for $199. This includes the ability to record unlimited ECGs and to email the readings to anyone. The SmartRhythm program will be part of the company’s KardiaGuard membership, which costs $99 a year. KardiaGuard stores ECG recordings in the cloud and provides monthly summary reports on ECGs and other readings taken.
AliveCor tells me my Kardia Band will be shipped in 1-2 days and I hope to be able to give my evaluation of it before Christmas.
Please note that I paid for the device myself in order to avoid any bias that could be introduced by receiving largesse from AliveCor.
N.B. Larry Husten’s article includes some perspective and warnings from two cardiologist and can be read here.
Another article on the Kardia Band release suggests that the Smart Rhythm program at $99/ year is a requirement.
Perhaps, AliveCor’s David Albert can weigh in on whether the annual subscription is a requirement for making recordings or just allows the continuous monitoring aspect.