Is Dean Ornish’s Lifestyle Program “Scientifically Proven To Undo (Reverse) Heart Disease?”

Supporters of vegetarian/ultra low fat diets like to claim that there is solid scientific evidence of the cardiovascular benefits of their chosen diets.

To buttress these claims they will cite the studies of Esseslystn, Pritikin and Ornish.

I’ve previously discussed the bad science underlying the programs of Esselsystn and Pritikin but have only briefly touched on the inadequacy of Dean Ornish’s studies.

The Ornish website proclaims that their program is the first program “scientifically proven to undo (reverse) heart disease.” That’s a huge claim. If it were true, wouldn’t the Dietary Guidelines for Americans, the American Heart Association, and most cardiologists and nutrition experts be recommending it?

Who Is Dean Ornish?

Dean Ornish has an MD degree from Baylor University and trained in internal medicine but has no formal cardiology or nutrition training (although many internet sites including Wikipedia describe him as a cardiologist.)

Ornish, according to the Encyclopedia of World Biographies became depressed and suicidal in college and underwent psychotherapy “but it was only when he met the man who had helped his older sister overcome her debilitating migraine headaches that his own outlook vastly improved. Under the watch of his new mentor, Swami Satchidananda, Ornish began yoga, meditation, and a vegetarian diet, and even spent time at the Swami’s Virginia center.”

Can Ornish’s Program Reverse Heart Disease?

After his medical training Ornish founded the Preventive Medicine Research Institute and has has widely promoted his Ornish Lifestyle Program.  the website of which claims:

Dr. Ornish’s Program for Reversing Heart Disease® is the first program scientifically proven to “undo” (reverse) heart disease by making comprehensive lifestyle changes.

The Ornish claims are based on a study he performed between 1986 and 1992 which originally had 28 patients with coronary artery disease in an experimental arm and 20 in a control group. You can read the details of the one year results here.and the five year results here.

There are  so many limitations to this study that the mind boggles that it was published in a reputable journal.

-Recruitment of patients. 

193 patients with significant coronary lesions from coronary angiography were “identified” but only 93 “remained eligible.” These were “randomly” assigned to the experimental or control groups. Somehow , this randomization process assigned 53 to the experimental group and 40 to the usual-care control group.

If this were truly a 1:1 randomization the numbers would be equal and the baseline characteristics equal.

Only 23 of the 53 assigned to the experimental group agreed to participate and only 20 of the control group.

The control group was older, less likely to be employed and less educated.

“The primary reason for refusal in the experimental group was not wanting to undergo intensive lifestyle changes and/or not wanting a second coronary angiogram; control patients refused primarily because they did not want to undergo a second angiogram.”

In other words, all of the slackers were weeded out of the experimental group and all of the patients who were intensely motivated to change their lifestyle were weeded out of the control group. Gee, I wonder which group will do better?

-The Intervention.

The experimental patients received “intensive lifestyle changes (<10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support).
The control group had none of the above.

Needless to say this was not blinded and the researchers definitely knew which patients were in which group.

Control-group patients were “not asked to make lifestyle changes, although they were free to do so.”

There is very little known about the 20 slackers in the control group. I can’t find basic information about them-crucial things like how many smoked or quit smoking or how many were on statin drugs.

-The Measurement

Progression or regression of coronary artery lesions was assessed in both groups by quantitative coronary angiography (QCA) at baseline and after about a year.

QCA as a test for assessing coronary artery disease has a number of limitations and as a result is no longer utilized for this purpose in clinical trials. When investigators  want to know if an intervention is improving CAD they use techniques such as intravascular ultraound or coronary CT angiography (see here) which allow measurement of total atherosclerotic plaque burden.

Rather than burden the reader  with the details at this point I’ve included a discussion of this as an addendum.

-The Outcome

Ornish has widely promoted  this heavily flawed study as showing “reversal of heart disease” because at one year the average percent coronary artery stenosis by angiogram had dropped from 40% to 37.8% in the intensive lifestyle group and increased from 42.7% to 46.1% in the control patients.

The minimal diameter (meaning the tightest stenosis) changed from 1.64 mm at baseline in the experimental to 1.65 at one year. At 5 years the minimal diameter had increased another whopping .001 mm to 1.651. 

 

 

In other words even if we overlook the huge methodologic flaws in the study the  so-called  “reversal” was minuscule.


Utlimately, dropping coronary artery blockages by <5 % doesn’t really matter unless that is also helping to prevent heart attacks or death or strokes or some outcome that really matters.

There were no significant differences between the groups at 5 years in hard events such as heart attack or death.
In fact 2 of the experimental group died versus 1 of the control group by 5 years.

There were less stents and bypasses performed in the Ornish group but the decision to proceed to stent or bypass is notoriously capricious when performed outside the setting of acute MI. The patients in the experimental group under the guidance of Ornish and their Ornish counselors would be strongly motivated to do everything possible to avoid intervention.

I’ve gotten a lot of flack for humorously suggesting that Nathan Pritikin killed himself as a result of the austere no fat diet he consumed but the bottom line on any lifestyle change is both quality and quantity of life.

If you are miserable most days due to your rigid diet you might consider that life is no longer worth living

Ornish’s Lifestyle Intervention Is Not A Trial Of Diet …And Other Points

 

Although often cited as justification of ultralow fat diet, the Ornish Lifestyle trial doesn’t test diet alone.

It is a trial of multiple different interventions with frequent counseling and meetings to reinforce and guide patients.

The interventions included things that we know are really important for long term health-regular exercise, smoking cessation, and weight management. These factors alone could account for any differences in the outcome but they are easily adopted without becoming a vegetarian.

The patients who agreed to the experimental arm were a clearly highly motivated bunch who agreed to this really strict regimen. Even in this population there was a 25% drop out rate.

Since investigators clearly knew who the “experimental patients” were and they were clearly interested in good outcomes in these patients there is a high possibility of bias in reporting outcomes and referring for interventions.

Despite all the limitations the study does raise an interesting hypothesis. Should we all be eating vegan diets?

 if Ornish really wanted to scientifically prove his approach he should have repeated it with much better methodology and much larger numbers.

Finally, this tiny study has never been reproduced at any other center.

Because of the small numbers, lack of true blinding, lack of hard outcomes and use of multiple modalities for lifestyle intervention, this study cannot be used to support the Ornish/Esselstyn/Pritikin dietary approach.

It most certainly doesn’t show that the Ornish Lifestyle Program “reverses heart disease.” Consequently, you will not find any evidence-based source of nutritional information or guideline (unless it has a vegan/vegetarian philosophy or is being funded by the Ornish/Pritikin lifestyle money-making machines) recommending these diets.

Skeptically Yours,

-ACP

N.B.1 A recent paper on noninvasive assessment of atherosclerotic plaque has a great infographic which shows how coronary artery disease progresses and how and when in the progression various imaging modalities are able to detect plaque:

I’ve inserted a vertical red arrow which shows how IVUS detects very early atheroma whereas angiography (ICA, green line) only detects later plaque when it has started protruding into the lumen of the artery.

The paper notes that “Intravascular ultrasound (IVUS)  constitutes the current gold standard for plaque quantification. Multiple studies using IVUS and other techniques have revealed a robust relation between statin therapy and plaque regression. In the ASTEROID trial coronary atheroma volume regressed by 6.8% during 24 months of high-intensity lipid therapy. A meta-analysis of IVUS trials including 7864 patients showed an association between plaque regression and decreased cardiovascular events.”

While I believe Ornish started off as a legitimate scientist several authors have pointed out that he has joined the ranks of pseudoscientific practiioners.

Here’s one analysis from Science Blogs :

In the end, the problem is that Dr. Ornish has yoked his science to advocates of pseudoscience, such as Deepak Chopra and Rustum Roy. Why he’s done this, I don’t know. The reason could be common philosophy. It could be expedience. It could be any number of things. By doing so, however, Dr. Ornish has made a Faustian deal with the devil that may give him short-term notoriety now but virtually guarantees serious problems with his ultimately being taken seriously scientifically, as he is tainted by this association. Let me yet again reemphasize that this relabeling of diet, exercise, and lifestyle as somehow being “alternative” is nothing more than a Trojan Horse. Inside the horse is a whole lot of woo, pseudoscience and quackery such as homepathy, reiki, Hoxsey therapy, acid-base pseudoscience, Hulda Clark’s “zapper,” and many others,

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

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

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

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

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

 

 

 

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

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

Kardia 6L Setup And Hardware

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

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

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

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

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

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

The  Diagnostic Power Of Six Leads

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

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

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

 

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

The History of ECG Leads

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

 

 

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

Old string galvanometer electrocardiograph showing the big machine with the patient rinsing his extremities in the cylindrical electrodes filled with electrolyte solution.

 It is mind-boggling to consider that we can now record  6 ECG leads with a smartphone and a device the size of a stick of gum

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

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


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

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

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

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

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

Stockingfreely Yours,

-ACP

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

 

Can Catheter Ablation Improve Quality of Life?

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

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

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

Skeptically Yours,

-ACP


Update 6/12/2019 357 PM.

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

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

This review article gives an overview:

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

 


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

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

Feel Free To Skip Breakfast Again And Again And Again

It seems like every 2 years the skeptical cardiologist has to defend skipping breakfast.

I first described how irritating and puzzling I find the concept that skipping breakfast causes obesity and heart disease in a 2013 post entitled “Breakfast is not the most important meal of the day: feel free to skip it.” When I’m irritated with a ridiculous concept I ask lots of questions:

Why would I eat breakfast if I am not hungry in order to lose weight? What constitutes breakfast? Is it the first meal you eat after sleeping? If so, wouldn’t any meal eaten after sleeping qualify even it is eaten in the afternoon? Is eating a donut first thing in the morning really healthier than eating nothing? Why would your first meal be more important than the last? isn’t it the content of what we eat that is important more than the timing?

Most of the studies on the proposed effect of breakfast on obesity (PEBO), I pointed out, are observational studies which cannot prove causality and the few, small prospective randomized studies don’t clearly support the hypothesis.

I suggested that PEBO comes from the breakfast food and cereal industry and should be ignored.



Writing an update on my post in 2015 I referenced Melanie Warner’s excellent book on the methods of the food industry entitled “Pandora’s Lunchbox”

“Walk down a cereal aisle today or go onto a brand’s Web site, and you will quickly learn that breakfast cereal is one of the healthiest ways to start the day, chock full of nutrients and containing minimal fat. “Made with wholesome grains,” says Kellogg’s on its Web site. “Kellogg’s cereals help your family start the morning with energy by delivering a number of vital, take-on-the-day nutrients—nutrients that many of us, especially children, otherwise might miss.” It sounds fantastic. But what you don’t often hear is that most of these “take-on-the-day” nutrients are synthetic versions added to the product, often sprayed on after processing. It’s nearly impossible to find a box of cereal in the supermarket that doesn’t have an alphabet soup of manufactured vitamins and minerals, unless you’re in the natural section, where about half the boxes are fortified.”

The Kellogg’s and General Mills of the world strongly promoted the concept that you shouldn’t skip breakfast because they had developed products that stayed fresh on shelves for incredibly long periods of time. They could be mixed with easily accessible (low-fat, no doubt) milk to create inexpensive,  very quickly and easily made, ostensibly healthy breakfasts.

Unfortunately, the processing required to make these cereals last forever involved removing the healthy components.

As Warner writes about W.K. Kellogg:

“In 1905, he changed the Corn Flakes recipe in a critical way, eliminating the problematic corn germ, as well as the bran. He used only the starchy center, what he referred to as “the sweetheart of the corn,” personified on boxes by a farm girl clutching a freshly picked sheaf. This served to lengthen significantly the amount of time Corn Flakes could sit in warehouses or on grocers’ shelves but compromised the vitamins housed in the germ and the fiber residing in the bran”



In 2017 I felt compelled to revisit the topic when a New York Times piece made the case for making breakfast a feast:

The writer, Roni Rabin (who has a degree in journalism from Columbia University)  struggles to support her sense that there is a “growing body of research” suggesting we should all modify our current dietary habits in order to eat a  breakfast and make breakfast the largest meal of the day

My post entitled  “Ignore The New York Times and The American Heart Association and Feel Free to Skip Breakfast” examined the weak evidence for benefits of “mindful” eating and harms of skipping breakfast.


A new study has popped up and, of course, been widely publicized as supporting eating breakfast. Fortunately, it caught the eye of Peter Attia thus saving me from having to read the article.

Below are some of his scathing comments, taken from one of his non-lame weekly emails:

You’ve probably heard that breakfast is the most important meal of the day. “What is less commonly mentioned,” writes Alex Mayyasi in The Atlantic, “is the origin of this ode to breakfast: a 1944 marketing campaign launched by General Foods, the manufacturer of Grape Nuts, to sell more cereal.”

Seventy-five years later, here’s the latest report from the April issue of the Journal of the American College of Cardiology: “Taken together, these studies [showing a positive association between skipping breakfast and CVD and CVD risk factors] as well as our findings underscore the importance of eating breakfast as a simple way to promote cardiovascular health and prevent cardiovascular morbidity and mortality.”
What were the findings? Let’s look at a few newspapers:

  • “Want to Lower Your Risk for Heart Disease? Eat Breakfast Every Morning” (Healthline)
  • “Eating breakfast? Skipping a morning meal has higher risk of heart-related death, study says” (USA TODAY)
  • “Study: Skipping breakfast increases risk of heart disease mortality by 87 percent (FOX)”

(You may notice that all three headlines imply causality.)

Looks like General Foods was right. Time to reach for the Lucky Charms? Perhaps it’s time to put on our critical thinking cap instead. The actual study, and the media coverage of it, is a part of the Groundhog Day that is observational epidemiology (for more on the limitations of this type of research, check out Studying Studies: Part II). This was a prospective cohort study pulling data from NHANES III, looking at people who reportedly eat breakfast every day to people who never eat breakfast, and then following up with them (about 19 years later on average), tallying up the deaths from CVD and deaths from all causes.

One question to ask about the population studied is: was eating breakfast or not eating breakfast the only difference between these two groups? In other words, were there any confounding factors (for more on confounding, see Studying Studies: Part IV)? The authors reported that, “participants who never consumed breakfast were more likely to be non-Hispanic black, former smokers, heavy drinkers, unmarried, physically inactive, and with less family income, lower total energy intake, and poorer dietary quality, when compared with those who regularly ate breakfast.” Not only that, “participants who never consumed breakfast were more likely to have obesity, and higher total blood cholesterol level than those who consumed breakfast regularly.” They also had a higher reported incidence of diabetes and dyslipidemia. Read that again, please.

While the study used statistical models to “adjust for” many of these potential confounders, it’s extremely difficult (actually, it’s impossible) to accurately and appropriately adjust for what amounts to fundamentally different people. The healthy user bias (or the inverse, an unhealthy user bias) is virtually impossible to tease out of these studies (the healthy user bias is covered in more depth in Studying Studies: Part I). Not only that, you never really know what you’re not looking for. This is typically referred to as residual confounding in the literature, where other factors may be playing a role that go unmeasured by the investigators.

I haven’t even yet mentioned the misleading nature of reporting relative risk — in this case, an associated 87% (reported in the study as a hazard ratio of 1.87) — without reporting absolute risk. The question you should always ask is, 87% greater than what? To get an idea of the associated absolute risk, the number of CVD deaths in the “every day” breakfast group were 415 out of a total of 3,862 people over 16.7 years (that’s an unadjusted rate of 10.7%) while the numbers for the “never” breakfast folks were 41 CVD deaths out of a total of 336 people over 16.7 years (unadjusted rate of 12.2%). That’s an absolute difference of 1.5% over almost 17 years (annually, this is an absolute difference of 0.09%). Granted, this is before adjustment of the myriad confounders (including the biggest “risk factor” for CVD death, age, in which the “never” breakfast group was younger on average at baseline), but it gives you an idea that we’re looking at small differences even over the course of a couple of decades. This looks a lot difference on paper than an associated 87% increased risk of CVD death. (For more on absolute risk and relative risk, see Studying Studies: Part I.)

There’s more:

  • What were the participants actually eating for breakfast? We don’t know. The investigators didn’t have information about what foods and beverages they consumed.
  • Did participants change their breakfast eating (or abstaining) habits over the course of almost 20 years? We don’t know. Information on breakfast eating was only collected at baseline.
  • Could there be errors in the classification of the causes of death in the participants? It’s possible.
  • What constitutes skipping breakfast? Was it the timing of the first meal of the day? We don’t know. Participants were asked, “How often do you eat breakfast?” but there was no definition of what that means, exactly.

What’s more likely: reported skipping breakfast was a marker for a lifestyle and environment that may have predisposed these people to a higher risk of CVD death or that skipping breakfast itself causes CVD death?

Go ahead and skip all the breakfasts you want. And please forward this to the next 10 people who tell you it’s unhealthy to do so.

And ditto for this post.

Breakfastingly Yours,

-ACP

A Voodoo Coronary Calcium Scan Could Save Your Life

The skeptical cardiologist received this reader comment recently:

So I went and got a Cardiac Calcium Score on my own since my cardiologist wouldn’t order one because he says they are basically voodoo.. Family History is awful for me.. I got my score of 320 and I’m 48 years old.. Doc looked at it and basically did the oh well.. so I switched docs and the other doc basically did the same thing.. I try so very hard to live a good lifestyle..I just don’t understand why docs wait so long to actually take a look at your heart.. I would have thought a score of 320 would have brought on more testing.. It did not..

I was shocked that a cardiologist practicing in 2019 would term a coronary artery calcium (CAC) scan (aka, heart scan or calcium score) “voodoo.”

I’m a strong advocate of what I wrote in a recent post with the ridiculously long title, “Prevention of Heart Attack and Stroke-Early Detection Of Risk Using Coronary Artery Calcium Scans In The Youngish“:

It’s never too early to start thinking about your risk of cardiovascular disease. If heart disease runs in your family or you have any of the “risk-enhancing” factors listed above, consider a CAC, nontraditional lipid/biomarkers, or vascular screening to better determine where you stand and what you can do about it.

Here’s what I told this young man:

If your cardiologist tells you coronary calcium scores are voodoo I would strongly consider changing cardiologists.

A score of 320 at age 48 puts you in a very high risk category for stroke and heart attack over the next 10 years.

You need to find a physician who understands how to incorporate coronary calcium into his practice and will help you with lifestyle changes and medications to reduce that risk


Let’s analyze my points in detail and see if these off the cuff remarks are really justified

1,  Changing cardiologists.

Recent studies and recent guideline recommendations (see here) all support utilization of CAC in this kind of patient. If you have a strong family history of premature heart disease or sudden death you want a cardiologist who is actively keeping up on the published literature in preventive cardiology,  Such cardiologists are not dismissing CAC as “voodoo” they are incorporating it into their assessment of patient’s risk on a daily basis.

2. High risk of CAC score 320  at age 48

I plugged normal numbers for cholesterol and BP into the MESA risk calculator (see my discussion on how to use this here) for a 48 year old white male.

As you can see the high CAC score puts this patient at almost triple the 10 year risk of heart attack and stroke.

Immediate action is warranted to adjust lifestyle to reduce this risk! This high score will provide great motivation to the patient to stop smoking, exercise, lose excess weight, and modify diet.

Hidden risk factors such as lipoprotein(a),  hs-CRP and LDL-P need to be assessed.

Drug treatment should be considered.

3. Find physician who will be more proactive in preventing heart disease

This may be the hardest part of all my recommendations. On your own you can get a CAC performed and advanced lipoprotein analysis.

However, finding progressive, enlightened, up-to-date preventive cardiologists can be a challenge.

We need a network of such cardiologists.

I frequently receive requests from readers or patients leaving St. Louis for recommendations on cardiologists.

If you are aware of such preventive cardiologists in your area email me or post in comments and I will keep a log and post on the website for reference.

Voodoophobically Yours,

-ACP

Jellyfish Memory Supplement Prevagen Is A “Clear-Cut Fraud” According To The FTC: Stop Buying This And Other Useless Brain Supplements

A JAMA viewpoint article entitled “The Rise of Pseudomedicine for Dementia and Brain Health ” caught my eye recently and I immediately thought of the widely advertised,  jellyfish-derived and totally useless supplement,  Prevagen.

The  article, written by three prominent neurologists and dementia researchers at UC San Francisco, discusses the lack of science behind the $3.2 billion  industry promoting unproven supplements for improved cognition and  brain health.

Unproven supplements like Prevagen (made from jellyfish! and with a hard to pronounce crucial ingredient!) utilize a facade of “proven benefits” and succeed by promoting themselves as science-backed on radio, television and the internet.

The JAMA articles notes that this industry thrives due to the increasing prevalence of Alzheimer’s disease, and it’s lack of effective treatments.

Consumers, it goes on to say,  who are intent on finding methods to prevent dementia need to know three things:

  1. There is no known dietary supplement that prevents cognitive decline for dementia,.
  2. Supplements do not undergo FDA testing for safety or review for effiacy.
  3. Some supplements may cause harm. For example, Vitamine E-increases risk of hemorrhagic stroke and in high doses, increase risk of death.

The Facade of Science-Backed Research.

Companies like Quincy Bioscience, the maker of Prevagen,  utilize sophisticated techniques that supply false scientific backing for brain health interventions.

The website for Prevagen states “prevagen improves memory” and “has been clinically shown to help with mild memory loss associated with aging.”

A tab promises to show the research behind this claim:

As the JAMA articled pointed out, these bogus brain supplement companies quote scientific articles which appear valid yet lack essential  features such as “sufficient participant characterization, treatment randomization and fail to include limitations.”  These bad papers are often published in predatory open access journals.

In the case of Prevagen, despite marketing which includes “The Science Behind Prevagen” there isn’t even a single study published  in the peer-reviewed scientific literature, predatory or otherwise.

If you click on the “view the study” link  you will be taken to a PDF of the “Madison Memory Study” which is a study sponsored by Quincy Bioscience, performed by an employee of Quincy Bioscience and published in house by Quincy Bioscience.

In the world of real science, this type of study is ignored and considered extremely preliminary until it is reproduced by a reputable unbiased  scientific lab and published in a peer-reviewed journal. The chances for biased results are way too high to trust.

FTC Files Suit Against Quincy Bioscience

According to the Federal Trade Commission (FTC), which charged Quincy Bioscience with false and deceptive advertising in 2017, the initial version of this company study found that Prevagen was no more effective than a placebo at improving any of the nine cognitive skills, including memory, that the company measured.

“The marketing for Prevagen is a clear-cut fraud, from the label on the bottle to the ads airing across the country,” said New York Attorney General Eric Schneiderman. “It’s particularly unacceptable that this company has targeted vulnerable citizens like seniors in its advertising for a product that costs more than a week’s groceries, but provides none of the health benefits that it claims.”

“The marketers of Prevagen preyed on the fears of older consumers experiencing age-related memory loss,” said Jessica Rich, director of the FTC’s Bureau of Consumer Protection. “But one critical thing these marketers forgot is that their claims need to be backed up by real scientific evidence.”

The suit seeks to fine Quincy and force it to pay back consumers who bought the pills

Since then Quincy went back and “re-analyzed” their in-house data coming up with 3  parameters that improved and challenging the FTC in court. This process is called p-hacking and any significant findings gathered through this process are highly suspect.

A great article on the Prevagen case from the McGill University Office  of Science and Society summarizes the problems with this re-analysis.

This is an after-the-fact, unplanned exploration of the data to see if anything else of interest happened in the trial. Some might call it a fishing expedition. Scientists do this all the time, but with a big caveat: post hoc results are considered tentative, not conclusive. Before they’re accepted as valid outcomes, they need to be confirmed by additional studies.

That’s because random events happen all the time in scientific studies. Some of them may seem statistically significant, but they’re flukes and not the result of cause-and-effect.  And the more post hoc analyses you do (like the more than 30 Quincy Bioscience did), the more likely you’ll encounter these chance results.

Scientists guard against accepting them as real by setting a high bar for statistical significance and by not accepting post hoc findings until they’ve been tested again.

Despite the total lack of proven efficacy and the  lawsuit  by the FTC the company continues to heavily market Prevagen and reap millions of dollars in profits from the gullible. Prevagen is sold at the pharmacies of the companies below which should immediately remove this snake oil if their aim is to help consumers.

 

 

Anamnestically Yours,

-ACP

For more in-depth analysis see below.

Jann Bellamy at Science-Based Medicine delves deeply into the case and cases against Prevagen in “Prevagen goes P-hacking.

Prevagen goes P-hacking

And see here for the McGill University office of Science and Society: Separating Sense From Nonsense

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

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

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

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

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

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

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

A Tale Of Six Cardioversions

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

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

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

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

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

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

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

 

 

 

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

Amiodarone-The Big Medical Gun For Stopping Atrial Fibrillation

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

Amiodarone is a unique drug in the AF toolkit.

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

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

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

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

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

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

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

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

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

Medical Management With Antiarrhythmics Versus Ablation

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

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

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

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

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

Who posseses the right hands?

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

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

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

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

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

Unbenightedly Yours,

-ACP

I Want To Tell You About A Chord That George Harrison Did Not Invent

The skeptical cardiologist has of late been obsessed with a Beatles song. It is the fifth song on the second side of the four mop tops seventh studio album and the third George Harrison contribution to Revolver, arguably the best record album of all time.

With a subscription to Apple Music I can listen to the entire Beatles catalogue now and one day I Want To Tell You (IWTTY) began playing. I hadn’t closely listened to this song before but at 25 seconds in someone begins playing very loudly two notes on a piano and keeps playing them for 8 seconds. The effect is strikingly dissonant but mesmerizing.

It turns out much has been written about this section of I Want To Tell you (along with anything else remotely related  to The Fab Four.)

The two notes are F and E and they are being played by Paul McCartney emphasizing the flattened ninth (and highly dissonant) portion of the chord E 7 b9.

Tim Riley in his Beatles song by song analysis, “Tell Me Why” writes of IWTTY:

The guitar line is central, the backbone for the esoteric lyrics, and the piano’s annoying dissonant figure at the end of each verse disrupts its stability.

The piano conveys the frustration of the singer, and its single-note solo is the peace he wants to attain

I’ve also seen this section described as “creating a frustrated bitonal disonance ( G sharp 7 diminished against E7 or E7 flat 9)

Apparently Harrison:

Lacking formal music training, apart from in his sitar studies…later described the harsh-sounding E79 as, variously, “an E and an F at the same time”  and “an E7th with an F on top, played on the piano”.

The Wikipedia entry on IWTTY spends considerable time on the significance of the E7flat9.

Writing in Rolling Stone’s Harrison commemorative issue, in January 2002, Mikal Gilmore recognised his incorporation of dissonance on “I Want to Tell You” as having been “revolutionary in popular music” in 1966. Gilmore considered this innovation to be “perhaps more originally creative” than the avant-garde styling that Lennon and McCartney took from Karlheinz Stockhausen, Luciano Berio, Edgar Varese and Igor Stravinsky and incorporated into the Beatles’ work over the same period.

The Wikipedia entry goes on to say that the chord “became one of the most legendary in the entire Beatles catalogue.”

Harrison was deliberately using the chord’s dissonance to create an emotion.”The musical and emotional dissonance is then heightened by the use of E79, a chord that Harrison said he happened upon while striving for a sound that adequately conveyed a sense of frustration.”

“speaking in 2001, Harrison said: “I’m really proud of that as I literally invented that chord.”

 I thought it highly unlikely that George Harrison “invented” (literally or figuratively) the seventh flattened ninth chord but had no way of checking the accuracy of the Wikipedia quote (from Guitar World magazine.) or the context. Was Harrison that musically naive, was he joking or did he mean something else?

Later that day I sat at my Kawai baby grand piano and began playing songs from The Encylopedia of Jazz.

One of my favorites from this book  is Satin Doll (written in 1953 by Duke Ellington and Billy Strayhorn) and as I was playing it I realized that it was loaded with  flattened ninths. There’s a D7flat9 when the word Satin is sung. These chords make the song more complex and memorable.

Next I played my favorite song in this Jazz book i “Lullaby of Birdland” (music written by George Shearing in 1952) which features two 7flat9 chords (F# and B7) in the second measure (played with the words “that’s what I.”)  Later on in the song we are treated to 7flat 9 in D and the chord that George Harrison claimed to have literally invented E7b9.

Here’s Ella Fitzgerald singing it with Duke Ellington

So a cursory review reveals that the chord was being utilized a lot in 1953 (and that I have a special attraction to its complexity.)

Perhaps Harrison can claim he was the first to appropriate the chord in rock and roll music? Alas, we know that an F#7b9 is prominent in the Beach Boys’ Caroline, No which was released in March, 1966, 3 months before the Beatles released IWTTY.

He may not have invented the chord or even been the first to use it in rock and roll but his use in IWTTY coupled with McCartney’s hammering on the F and E have made me forever cognizant of that song’s beauty. 

For that plus his brilliant guitar work and songwriting during and after The Beatles I will be eternally grateful.

Nondissonantly Yours,

-ACP

N.B. Dear Readers. If any of you have access to the Guitar World interview of 2001 (from Wikipedia-Garbarini, Vic (January 2001). “When We Was Fab”. Guitar World. p. 200) wherein Harrison is alleged to claim he invented the magical 7b9 please share it with me. 

Also, please note there is a new button on my website which allows you to sign up for my weekly emal newsletter (which i promise will be mostly related to cardiology and not esoteric musical chords.)

Is An Unneeded Beta-Blocker Making You Feel Logy?

The skeptical cardiologist saw a patient recently who  had undergone stenting of a 95% blocked right coronary artery. Mr Jones had presented  a year ago to our ER 2 days after he first began experiencing a light pressure-type discomfort in his left shoulder and scapular region. This pain persisted, waxing and waning, without a clear relationship to exertion or position or movement of his shoulder.

Upon arrival in the ER, his ECG was normal but his cardiac enzymes were slightly elevated (troponin peaking 0.92), thus he was diagnosed with a non-ST elevation myocardial infarction (MI).

He’s done great since the stent procedure fixed the coronary blockage that caused his infarct and chest pain, but during our office visit he related that since his hospitalization he had been feeling “logy.” 

Being a lover of words, my ears perked up at this new-to-me adjective, and I asked him to describe what he meant by logy. For him, loginess was a feeling of fatigue or lacking energy.

Indeed, the online Merriam-Webster dictionary defines logy as sluggish or groggy. It is pronounced usually with a long o and a hard g.

The origin is unclear but has nothing to do with rum:

Based on surface resemblance, you might guess that “logy” (also sometimes spelled “loggy”) is related to “groggy,” but that’s not the case. “Groggy” ultimately comes from “Old Grog,” the nickname of an English admiral who was notorious for his cloak made of a fabric called grogram – and for adding water to his crew’s rum. The sailors called the rum mixture “grog” after the admiral. Because of the effect of grog, “groggy” came to mean “weak and unsteady on the feet or in action.” No one is really sure about the origin of “logy,” but experts speculate that it comes from the Dutch word log, meaning “heavy.” Its first recorded use in English, from an 1847 London newspaper, refers to a “loggy stroke” in rowing.

Fatigue is a common, nonspecific symptom that we all feel at times. It is more common as we age and it can be challenging for both patients and physicians to sort out when it needs to be further evaluated.

Occasionally, fatigue is the only symptom of a significant cardiac condition, but more frequently in the patient population I see it is either noncardiac (low thyroid, anemia, etc.) or iatrogenic

When a patient tells me they are feeling fatigued I immediately scan their med list for potential logigenic drugs.

In this case, my patient had been started on a low dosage of the beta-blocker carvedilol (brand name Coreg) after his stent, and I suspected this was why he had felt logy for the past year.

In cardiology, we utilize beta-blockers in many situations-arrhythmias, heart failure, and heart attacks to name a few, and they are well-known to have fatigue as a common side effect. There was a really good chance that Mr. Jones’s loginess was due to the carvedilol.

It’s important to review all medications at each patient visit to check for side effects, interactions and benefits, and in the case of Mr. Jones’ carvedilol, loginess.

Do All Patients Post-Revascularization or Post-MI Need To Take Beta-Blockers

Beta-blockers (BBs) are frequently started in patients after a stenting procedure or coronary bypass surgery, and continued indefinitely. However, the evidence for their benefit in such  patients with normal LV function long term is lacking.

If any post-revascularization population benefits from BBs, it is those, like Mr. Jones who have had a myocardial infarction (MI, heart attack) prior to the procedure, however the smaller the infarct, the less the benefits.

And with the widespread use of early stenting to treat MI, infarcts are much smaller and dysfunction of the left ventricle (LV) less likely.

In those patients with minimal damage and normal LV function, the benefits appear minimal. For this reason in the last 5 to 10 years I’ve been stopping BBs in this population if there are any significant side effects.

An “Expert Analysis” published in JACC in 2017 noted that:

A 2015 meta-analysis of 10 observational acute MI studies including more than 40,000 patients showed that beta-blockers reduced the risk of all-cause death  However, the benefit of these agents was not found in all subgroups and seemed confined to the patients with reduced LVEF, with low use of other secondary prevention drugs, or NSTEMI.

In a study of almost 180,000 patients post MI with normal LV systolic function in the UK between 2007 and 2013 there was no difference in mortality at one year in patients discharged with or without beta-blockers.

The only way to answer this question definitely would be with a randomized controlled trial and, to my surprise and delight, such a study (CAPITAL-RCT (Carvedilol Post-Intervention Long-Term Administration in Large-scale Randomized Controlled Trial) was published in PLOS One in August of 2018.

I’ll save readers the details, but the bottom line is that patients treated with optimal contemporary therapy for acute MI, whose LV function was not significantly impaired, did not benefit in any way from treatment with carvedilol, the beta-blocker my patient was taking.

It’s rare that we get such definitive evidence for a change in treatment that reverses what is in current guidelines. This has the potential to affect tens of thousands of patients and improve their quality of life. It should be trumpeted far and wide. The cynic in me suspects that if it were a study demonstrating the benefits of a new drug, physicians would be bombarded with the new information.

Helping Patients Feel Less Logy

We will be ordering an echocardiogram on Mr. Jones, and if his LV function is normal we will stop his carvedilol and see if he feels significantly better.  

I feel like stopping a drug that is not beneficial and that is causing a lifetime of loginess is an incredibly important intervention a cardiologist can make. It’s not as life-saving as stenting for acute MI, but saving quality of life is something this non-invasive cardiologist can do every day for every patient.

Skeptically Yours,

-ACP

N.B. The summary of the recent CAPITAL-RCT:

STEMI patients with successful primary PCI within 24 hours from the onset and with left ventricular ejection fraction (LVEF) ≥40% were randomly assigned in a 1-to-1 fashion either to the carvedilol group or to the no beta-blocker group within 7 days after primary PCI. The primary endpoint is a composite of all-cause death, myocardial infarction, hospitalization for heart failure, and hospitalization for acute coronary syndrome. Between August 2010 and May 2014, 801 patients were randomly assigned to the carvedilol group (N = 399) or the no beta-blocker group (N = 402) at 67 centers in Japan. The carvedilol dose was up-titrated from 3.4±2.1 mg at baseline to 6.3±4.3 mg at 1-year. During median follow-up of 3.9 years with 96.4% follow-up, the cumulative 3-year incidences of both the primary endpoint and any coronary revascularization were not significantly different between the carvedilol and no beta-blocker groups (6.8% and 7.9%, P = 0.20, and 20.3% and 17.7%, P = 0.65, respectively). There also was no significant difference in LVEF at 1-year between the 2 groups (60.9±8.4% and 59.6±8.8%, P = 0.06).

 

 

 

 

Foxglove Is Growing In My Garden: Bunnies Beware!

While surveying his garden this morning the skeptical cardiologist felt the cockles of his heart warm when he viewed the budding plant below:

The plant I beheld was the glorious, mystical and medicinal foxglove or digitalis purpurea upon which I have waxed poetic innumerable times (see here and here and here.)

It is from the foxglove that William Withering made his potions to treat dropsy (the ancient term for heart failure)  and since writing about my encounter with the foxglove  in Wales I’ve been on a quest to get some in my garden.

This mission was accomplished when Quiet Village Landscaping installed the plants a month ago.

Now if I can keep them growing I’ll be able to enjoy the tall, showy spikes of tubular pink or purple flowers with speckled throats that should emerge in summer.

Foxglove and its medicinal derivative digitalis can be toxic to both humans and animals. Let’s hope  that the five bunnies that were frolicking in my yard and eating my hosta earlier in the spring have the good sense to eschew chewing it.

My first encounter with foxglove is entitled “Withering Away in Wales” and I’ve copied it below.



The skeptical cardiologist was born in Wrexham, North Wales, not too far from the northern area in Wales known as Snowdonia, the ancestral lands of the great Princes of Wales.

I’ve been back to this wonderful area several times in the last dozen years, entranced by its beauty and connection with my ancestor, Prince Llewelyn the Great.

Most recently I stayed in Beddgelert, a small village nestled at the base of Mount Snowdon, which , according to (possibly tourism-inspired) legend, is named after the grave of Gelert, the faithful hound of Prince Llewelyn.

A brief hike along the gurgling Glaslyn river takes you to a stone monument with these words inscribed:

IMG_4547
Two Pearson children show their appreciation of Gelert’s heroic behavior. Note the purplish flower on the long green stalk in the background, next to the stone wall-FOXGLOVE!

“In the 13th century Llewelyn, prince of North Wales, had a palace at Beddgelert. One day he went hunting without Gelert, ‘The Faithful Hound’, who was unaccountably absent.                                                  On Llewelyn’s return the truant, stained and smeared with blood, joyfully sprang to meet his master. The prince alarmed hastened to find his son, and saw the infant’s cot empty, the bedclothes and floor covered with blood.                      The frantic father plunged his sword into the hound’s side, thinking it had killed his heir. The dog’s dying yell was answered by a child’s cry. Llewelyn searched and discovered his boy unharmed, but nearby lay the body of a mighty wolf which Gelert had slain.

The prince filled with remorse is said never to have smiled again. He buried Gelert here”.

IMG_0007While lingering in the little stone wall enclosure within which a statue of the faithful Gelert stood I espied a plant that looked like digitalis purpurea, more commonly known as foxglove.

Moving closer, I realized that I had indeed come face to face with a wildly growing foxglove,  the plant that William Withering had utilized to treat patients with dropsy in the late -1700s.

I was understandably ecstatic as I was  on a sort of mission to observe foxglove in its native environs. I had expected to view the medicinal plant in Shropshire where William Withering was born and where he had encountered “the old woman of Shropshire” who first inspired him to use foxglove for dropsy.

This unexpected foxglove experience seemed like a serendipitous harbinger of wonderful Witheringesque experiences to come.

Sure enough as we left the fog-enshrouded mountains of Snowdonia and drove on the left side of narrow, winding Welsh roads toward Shropshire we spotted  multiple large patches of wildly growing foxglove in a nearby meadow.

dpeating foxgloveAlthough my children were eager to taste the foxglove and see if the inotropic properties of the digitalis within would make their hearts beat stronger and make them more powerful, I restrained them, for Withering’s writings and subsequent years of clinical experience with digitalis tell us that the therapeutic window is narrow and toxicity manifested by nausea and vomiting common.

Witheringly Yours,

-ACP

Unbiased, evidence-based discussion of the effects of diet, drugs, and procedures on heart disease

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