Category Archives: Atherosclerosclerotic Cardiovascular Disease

Statins And Memory Loss: The Latest Findings

In 2017 I wrote a post  entitled “Do Statins Cause Memory Loss? The Science, The Media, The Statin-Denialist Cult, and The Nocebo Effect” which concluded that there was no scientific evidence for cognitive side effects of the widely-utilized statin cholesterol lowering drugs.

Despite this, a common concern of my patients when we discuss potentially utilizing statin drugs to reduce their long term risk of heart attack and stroke is that the drug will rob them of their memory.

More studies have been published in this area and they continue to show absolutely no evidence for adverse association between statins and cognition.

A recent summative review found no beneficial or detrimental associations between statins and cognition in elderly cohorts with normal baseline cognition, impaired cognition or with incident dementia.

Finally, and most recently we have reassuring evidence from Australian researchers who meticulously studied  over a thousand participants aged 70-90 years in the Sydney Memory and Ageing Study.

Over 6 years the study found

-no difference in the rate of decline in memory or global cognition between statin users and never users.

-Statin initiation during the observation period was associated with blunting the rate of memory decline.

-Exploratory analyses found statin use was associated with attenuated decline in specific memory test performance in participants with heart disease and apolipoprotein Eε4 carriage.

-There was no difference in brain volume changes between statin users and never users.

For those who see statins as part of a conspiracy please note that there was absolutely no connection between the researchers and the statin pharmaceutical industry.

  • This study was supported by the Australian Government’s National Health and Medical Research Council (Dementia Research Grant 510124). Dr. Brodaty has served on the Nutricia Australia Advisory Board. Dr. Sachdev has served on the Australian Advisory Board of Biogen. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

My 2017 post was triggered by a call from a reporter who wanted to discuss the “cognitive side effects” of statins. It goes into a fair amount of detail about media and internet fear-mongering and how this contributes to the nocebo effect which makes it more likely patients will experience adverse side effects from medicine.

At the end I discuss how we handle potential side effects in my practice.

I’ve copied it below as it remains highly relevant 2 years later.


Since I regularly prescribe statin drugs to my patients to reduce their risk of heart attack and stroke,  I am very concerned about any possible side effects from them, cognitive or otherwise. However, in treating hundreds of patients with statins, I have not observed a consistent significant effect on brain function.

When the U.S. Food and Drug Administration (FDA) issued a statement in 2012 regarding rare postmarketing reports of ill-defined cognitive impairment associated with statin use it came as quite a surprise to most cardiologists.

The FDA made a change in the patient information on all statin drugs which stated:

Memory loss and confusion have been reported with statin use. These reported events were generally not serious and went away once the drug was no longer being taken

This FDA statement was surprising because prior observational and randomized controlled trials had suggested that patients who took statins were less likely to have cognitive dysfunction than those who didn’t.

Early studies implied that statins might actually protect against Alzheimer’s disease.

In fact these signals triggered two studies testing if statins could slow cognitive decline in patients with established Alzheimer’s disease  One study used 80 mg atorvastatin versus placebo and a second 40 mg simvastatin versus placebo and both showed no effect on the decline of cognitive function over 18 months.

More recently, multiple reviews and meta-analyses have examined the data and concluded that there is no significant effect of statins on cognitive function. Importantly, these have been written by reputable physician-scientists with no financial ties to the pharmaceutical industry.

Data Show No Evidence of Causality Despite Case Reports

The FDA added the warning to statin patient information based on case reports  Occasional reports of patients developing memory loss on a statin do not prove that statins are a significant cause of cognitive dysfunction.

Case reports have to  be viewed in the context of all the other scientific studies indicating no consistent evidence of negative effects of the statins. Case reports are suspect for several reasons:

First, patients receiving statins are at increased risk for memory loss because of associated risk factors for atherosclerosis and advancing age. A certain percentage of such patients are going to notice memory loss independent of any medications.

Second. The nocebo effect: If a patient taking a statin is told that the drug will cause a particular side effect,that patient will be more likely to notice and report that particular side effect.

A recent study in The Lancet looked at reported side effects in patients taking atorvastatin versus placebo and found substantial evidence for the nocebo effect.

Analysis of the trial data revealed that when patients were unaware whether they were taking a statin or a placebo, the number of side effects reported was similar in those taking the statin and those taking placebo. However, if patients knew they were taking statins, reports of muscle-related side effects in particular increased dramatically, by up to 41 per cent.

Third, a review of the FDA post-marketing surveillance data showed the rate of memory loss with statins is not significantly higher than for other non-statin cardiovascular medications (1.9 per million prescriptions for statins , 1.6 per million prescriptions for losartan) and clopidogrel (1.9 per million prescriptions for clopidogrel.)

What Most Media Prefer: Controversy And Victims

I thought my experience and perspective on statins and cognitive function might be useful for a wider audience of patients to hear so I agreed to be interviewed. After I expressed interest the  reporter responded:

I would like to interview you and also a person who has experienced memory and/or thinking problems that they attribute to statin use.  
 I responded with “let me see what I can find,”  although I was concerned that  this reporter was searching for a cardiologist to support attention-grabbing claims of  severe side effects of statins rather than seeking a balanced, unbiased perspective from a knowledgeable and experienced cardiologist.
If I produced a “victim” of statin-related memory loss this would boost ratings.
I then began racking my brain to come up with a patient who had clearly had statin-related memory loss or thinking problems. I asked my wonderful MA Jenny (who remembers details about patients that I don’t) if she could recall any cases. Ultimately, we both came up without any patients for the interview. (Any patient of mine reading this with definite statin memory loss please let me know and I will amend my post. However, I won’t be posting anecdotes outside of my practice.)
I have had a few patients relate to me that they feel like their memory is not as good as it was and wonder if it could be from a medication they are on.  Invariably, the patient has been influenced by one of the  statin fear-mongering sites on the internet (or a friend/relative who has been influenced by such a site.)
I wrote about one such site in response to a patient question a while back:
The link appears to be a promotional piece for a book by Michael Cutler, MD. Cutler’s website appears to engage in fear-mongering with respect to statins for the purpose of selling his books and promoting his “integrative” practice. I would refer you to my post entitled “functional medicine is fake medicine”. Integrative medicine is another code word for pseudoscientific medicine and practitioners should be assiduously avoided.
The piece starts with describing the case of Duane Graveline, a vey troubled man who spent the latter part of his life attempting to scare patients from taking statins. Here is his NY Times obituary.
You can judge for yourself if you want to base decisions on his recommendations.
There is no scientific evidence to suggest statins cause dementia.
An Internet-Driven Cult With Deadly Consequences
Steve Nissen recently wrote an eloquent article which accuses statin deniers of  being  an “internet–driven cult with deadly consequences.”  Nissen has done extremely important research helping us better understand atherosclerosis  and is known for being a patient advocate: calling out drug companies when they are promoting unsafe drugs.
I have immense respect for his honesty, lack of bias, and his courage to be outspoken .  He writes:

“Statins have developed a bad reputation with the public, a phenomenon driven largely by proliferation on the Internet of bizarre and unscientific but seemingly persuasive criticism of these drugs. Typing the term statin benefits into a popular Internet search en- gine yields 655 000 results. A similar search using the term statin risks yields 3 530 000 results. One of the highest-ranking search results links to an article titled “The Grave Dangers of Statin Drugs—and the Surprising Benefits of Cholesterol”. We are losing the battle for the hearts and minds of our patients to Web sites de- veloped by people with little or no scientific expertise, who often pedal “natural” or “drug-free” remedies for elevated cholesterol levels. These sites rely heavily on 2 arguments: statin denial, the proposition that cholesterol is not related to heart disease, and statin fear, the notion that lowering serum cholesterol levels will cause serious adverse effects, such as muscle or hepatic toxicity— or even worse, dementia.”

He goes on to point out that this misinformation is contributing to a low rate of compliance with taking statins. Observational studies suggest that noncompliance with statins significantly raises the risk of death from heart attack.

The reasons for patient noncompliance, Nissen goes on to say, can be related to the promotion of totally unproven supplements and fad diets as somehow safer and more effective than statin therapy:

“The widespread advocacy of unproven alternative cholesterol-lowering therapies traces its origins to the passage of the Dietary Supplement Health and Education Act of 1994 (DSHEA). Incredibly, this law places the responsibility for ensuring the truthfulness of dietary supplement advertising with the Federal Trade Commission, not the U.S. Food and Drug Administra-tion. The bill’s principal sponsors were congressional representatives from states where many of the companies selling supplements are headquartered. Nearly 2 decades after the DSHEA was passed, the array of worthless or harmful dietary supplements on the market is staggering, amounting to more than $30 billion in yearly sales. Manufacturers of these products commonly imply benefits that have never been confirmed in formal clinical studies.”

Dealing With Statin Side Effects In My Practice

When a patient tells me they believe they are having a side effect from the statin they are taking (and this applies to any medication they believe is causing them side effects), I take their concerns very seriously. After 30 years of practice, I’ve concluded that in any individual patient, it is possible for any drug to cause  side effects.  And, chances are that if we don’t address the side effects the patient won’t take the medication.

If the side effect is significant I will generally tell the patient to stop the statin and report to me how they feel after two to four weeks.

If there is no improvement I have the patient resume the medication and we generally reach a consensus that the side effect was not due to the medication.

If there is a significant improvement, I accept the possibility that the side effect could be from the drug. This doesn’t prove it, because it is entirely possible that the side effect resolved for other reasons coincidentally with stopping the statin. Muscle and joint aches are extremely common and they often randomly come and go.

At this point, I will generally recommend a trial at low dose of another statin (typically rosuvastatin or livalo.)  If the patient was experiencing muscle aches and they return we are most likely dealing with a patient with statin related myalgias. However, most patients are able to tolerate low dose and less frequent administration of rosuvastatin or Livalo.

For all other symptoms, it is extremely unusual to see a return on rechallenge with statin and so we continue statin long term therapy.

Today a patient told me he thought the rosuvastatin we started 4 weeks ago was causing him to have more diarrhea. I informed him that there is no evidence that rosuvastatin causes diarrhea more often than a placebo and had no reason based on its chemistry to suspect it would. (Although I’m sure there is a forum somewhere on the internet where patients have reported this). Fortunately he accepted my expert opinion and will continue taking the drug.

If the symptoms persist and the patient continue to believe it is due to the statin, we will go through the process I described above. And, since every patient is unique, it is possible that my patient is having a unique or idiosyncratic reaction to the statin that only occurs in one out of a million patients and thus is impossible to determine causality.

Since statins are our most effective and best tolerated weapon in the war against our biggest killer, it behooves both patients and physicians to have a high threshold  for stopping them altogether. Having such a high threshold means filtering out the noise from attention-seeking media and the internet-driven denials cult thus minimizing the nocebo effect

Antinocebonically Yours

-ACP

ISCHEMIA Shows Medical Therapy Outcomes As Good As Coronary Stents or Bypass For Most CAD Patients

The ISCHEMIA (International Study of Comparative Health Effectiveness With Medical And Invasive Approaches) study presented at the AHA meeting this week provides further evidence that a conservative approach utilizing optimal medical therapy is an acceptable strategy for most patients with stable coronary disease (CAD).

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), coronary 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 stabilize atherosclerotic plaque, dilate the coronary artery or slow the heart’s pumping action 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.

What Did ISCHEMIA Prove?

ISCHEMIA (paper unpublished but slides available here) showed that an invasive strategy (employing cardiac catheterization with resulting stenting or coronary bypass surgery (CABG)) offered no benefit over optimal medical therapy in preventing cardiovascular events in patients with moderate to severe CAD.

Screen Shot 2019-11-17 at 10.39.42 AM

Rates of all-cause death were nearly superimposable over the years studied, reaching 6.5% and 6.4% at 4 years for the invasive and conservative groups,

Screen Shot 2019-11-17 at 10.40.47 AM

Inclusions and exclusion criteria are listed below. Patients with unnaceptable angina despite optimal medical therapy were not included. These patients clearly benefit symptomatically from revascularization (as long as their chest pain is actually angina and not from another cause.)

All patients had stress imaging studies demonstrating moderate to severe amounts of ischemia. Such patients with very abnormal stress tests in the past have typically been sent immediately to the cath lab.

Based on ISCHEMIA we now know in these patients there is no need to do anything urgently other than institute OMT.

Screen Shot 2019-11-17 at 10.37.21 AM

These patients were on good medical therapy which likely explains the very good outcomes in both conservative and invasive arms. The “high level of medical therapy optimization” is what cardiologists should be shooting for with LDL<70, on a statin with systolic blood pressure <140 mm Hg, on an antiplatelet drugg and not smoking.

Screen Shot 2019-11-17 at 10.38.50 AM

Interestingly coronary CT angiography (CCTA) was utilized prior to patients receiving catheterization. I’ve been  utilizing this noninvasive method for visualizing the coronary arteries increasingly prior to committing to an invasive approach.

Quality Of Life 

Finally, in a separate presentation the ISCHEMIA trial showed that the invasive strategy did improve symptoms and quality of life modestly. It did not improve quality of life in those without angina symptoms.

The ORBITA study (which I wrote about here) showed that a large amount of the symptomatic improvement in patients following stenting may be a placebo effect.

Importance Of ISCHEMIA

Hopefully the results of ISCHEMIA will cut down on the number of unnecessary catheterizations, stents and bypass operations performed. This, in turn, will save our health system millions of dollars and prevent unnecessary complications.

Outside the setting of an acute heart attack the best approach to patients with blocked coronary arteries is a calm, thoughtful, and measured one which allows ample time for shared decision-making between informed patients and knowledgeable physicians. Such decisions should carefully consider the ISCHEMIA, COURAGE and ORBITA results.

Nonischemically Yours,

-ACP

N.B. Ischemia is a fantastic acronym for this study. Doctors use it a lot to describe the absence of sufficient blood flow to tissues.

N.B.2 Although I deplore the number of unnecessary caths and stents performed in the US, especially in patients without symptoms and those with noncardiac chest pain, I still utilize them in my patients with flow-limiting coronary stenoses and unacceptable anginal chest pain with symptoms despite optimal medical therapy and have noticed outstanding results. This angiogram shows a tight, eccentric LAD blockage in such a patient who now, post stent, has had complete resolution of the chest pain that limited him from even short walks.

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Is Bernie Sanders Fit To Be President After His Heart Attack?

While campaigning in Las Vegas on Tuesday of last week, Vermont Senator Bernie Sanders began experiencing tightness in his chest. He was rushed to a hospital where he was diagnosed with a heart attack and had two stents implanted to open blocked arteries.

Little to nothing beyond these bare details of his health condition is known but, as Politico put it, this event has “cast a cloud over his candidacy.”

Is it appropriate for voters to lose confidence in Sanders at this point? He was already the oldest candidate in the race at age 78 years. Would he survive a 4 year term in the grueling position of head of the free world?

An American Federation of Aging white paper, Longevity and Health of U.S. Presidential Candidates for the 2020 Election, used data from national vital statistics to estimate lifespan, healthspan (years of healthy living), disabled lifespan, and four- and eight-year survival probabilities for U.S. citizens with attributes matching those of the 27 then candidates for Presidency.

Its conclusions:

Given the favorable health and longevity trajectories of almost all of the presidential candidates relative to the average member of the same age and gender group in the U.S., and the apparent current good health of all of the candidates, there is reason to question whether age should be used at all in making judgments about prospective presidential candidates

I would agree that individual health is more important than  chronological age in evaluating longevity and in Sanders’ case the heart attack may be an indicator of a poor prognosis and an inability to withstand the rigors of campaigning for and serving as president.

Unfortunately we need to know a lot more about Sanders’ heart attack and overall health to make this determination.

Big Heart Attack Or Little Heart Attack?

A heart attack or  myocardial infarction (MI) occurs when heart muscle does not get enough blood/oxygen to keep the myocardial cells alive. This typically is due to a tight blockage in one of the coronary arteries supplying blood to the heart, thus constricting the blood flow to a segment of heart muscle (myocardium).

The size of Sanders’ heart attack is an important determinant of his prognosis. The more myocardial cells that died the larger the damage. We can detect and quantify heart attacks with a blood test using a cardiac specific protein called troponin.

Some heart attacks are tiny and only detected by very slight increases in the troponin in the blood whereas larger ones result in large increases in the troponin. What kind did Sanders have?

The more damage to the main pumping chamber of the heart, the left ventricle, the weaker the pumping action as measured by the ejection fraction.  The lower the ejection fraction the more likely the development of heart failure. What is Sanders ejection fraction? Does he have any evidence of heart failure?

Stunned or Hibernating Myocardium?

With some heart attacks the heart muscle doesn’t die but becomes stunned-weakened but still living. Under other circumstances a tightly blocked coronary artery doesn’t cause a heart attack but the reduced oxygen supply causes the muscle to stop working-in effect hibernating.  Thus, 3 months from now Sanders’ heart muscle function may improve as these stunned or hibernating myocardial cells come back to full function. What will Sanders’ ejection fraction be 3 months from now.? Will he have evidence of heart failure at that time?

Troponin levels and EF are just two of many factors that will determine Sanders’ prognosis.

A recent review of such factors on the one year post MI prognosis concluded

Secular trends showed a consistent decrease in mortality and morbidity after acute MI from early to more recent study periods. The relative risk for all-cause death and cardiovascular outcomes (recurrent MI, cardiovascular death) was at least 30% higher than that in a general reference population at both 1–3 years and 3–5 years after MI. Risk factors leading to worse outcomes after MI included comorbid diabetes, hypertension and peripheral artery disease, older age, reduced renal function, and history of stroke.

Hopefully, prior to the Iowa caucases all the candidates will release their medical records for the public to review. Only by learning more details about Senator Sanders’ heart attack and his overall medical condition can we answer whether he is fit to serve as President. Similarly, heretofore unknown individual health conditions could markedly effect the prognosis of any of the other candidates and their medical records should be equally scrutinized.

Skeptically Yours,

-ACP

Graphic Cigarette Package Warnings May Soon Be Coming To Our Country

Two years ago I asked (and answered) the question Why Doesn’t The USA Have Graphic Warning Labels On Cigarette Packs Like The Netherlands?

Big tobacco had successfully blocked such labels but yesterday the FDA announced a proposed rule which would post new graphic health warnings on cigarette packages if approved:

The 13 proposed warnings, which feature text statements accompanied by photo-realistic color images depicting some of the lesser-known health risks of cigarette smoking, stand to represent the most significant change to cigarette labels in 35 years.

Here are some of the proposed graphics which aren’t quite as attention-grabbing as the ones I saw in Europe.

 

 

Cigarette smoking is by far the worse thing my patients do to compromise their health and I’m in favor of hammering home the horrible complications smokers face.

Do you want feet like this?

 

 

 

 

Or Lungs like these?

 

 

 

 

Or a scar on your chest from open heart surgery?

 

 

 

 

 

All this and more can be yours if you keep smoking!

I’ve reposted below my initial blog on the topic.


While strolling the delightful (and typically debris-free) streets of Haarlem in The Netherlands the skeptical cardiologist espied an unusual cigarette pack on the ground.

In comparison to the typical American cigarette pack I noted a very prominent and disgusting picture of a leg which had been ravaged by peripheral artery disease.

The large print translates “smoking clogs your arteries.”

This is one of many potential warnings on Dutch cigarette packs. My favorite is

Roken kan leiden tot een langzame, pijnlijke dood

(Smoking can lead to a slow, painful death)

Perhaps, if such warning had been on American cigarette packs in the 1990s my mother would have been able to walk without severe pain in her legs (claudication) from the severe blockages caused by her decades of cigarette smoking.

When cigarette smoking patients tell me that “you have to die from something” I tell them that although they are greatly increasing their chance of dying from lung and cardiac disease, the smoking may not kill them but  leave them miserable and unable to walk or breath.

Experts on tobacco control note that these large, graphic and direct warnings are much more effective than the first small boxed warnings:

After the implementation of the first warning labels in 1966, the FTC’s 1981 report concluded that the original warning labels were not novel, overexposed and too abstract to remember and be personally relevant.46 Warning labels, like advertisements, wear out over time.47 Written warning labels wear out faster than graphic ones.48,49 In response, Congress passed a law mandating four rotating warnings. Studies on them began appearing in the late 1980s, demonstrating that several years after the implementation, those written labels on cigarette packs were also not noticed and not remembered by smokers and adolescents.5053 Since then, the diffusion and evolution of tobacco warning labels have been propelled by observational and experimental studies showing the effectiveness of large graphic warning labels in informing consumers about the health harms of smoking and reducing their smoking behavior.45,54

Here’s how Australia’s warnings have evolved

autralia-cigarette.jpg

 

 

 

 

 

 

 

In 2011 the US Congress passed legislation moving America towards such effective graphic warnings:

However, the law was challenged by Big Tobacco and has never been enacted. From the FDA site:

The Family Smoking Prevention and Tobacco Control Act requires the FDA to include new warning labels on cigarette packages and in cigarette advertisements. On June 22, 2011, the FDA published a final rule requiring color graphics depicting the negative health consequences of smoking to accompany the nine new textual warning statements. However, the final rule was challenged in court by several tobacco companies, and on Aug. 24, 2012, the United States Court of Appeals for the District of Columbia Circuit vacated the rule on First Amendment grounds and remanded the matter to the agency.[1] On Dec. 5, 2012, the Court denied the government’s petition for panel rehearing and rehearing en banc. In 2013, the government decided not to seek further review of the court’s ruling.

The FDA has been undertaking research related to graphic health warnings since that time.

[1] R.J. Reynolds Tobacco Co., et al., v. Food & Drug Administration, et al., 696 F.3d 1205 (D.C. Cir. 2012)

What Other Countries Are Doing

According to a Canadian Cancer Society report from late 2016,

More than 100 countries/jurisdictions worldwide have now required pictorial warnings, with fully 105 countries/jurisdictions having done so. This represents a landmark global public health achievement.

Increasingly, the United States stands alone, because of a constitutional doctrine privileging commercial speech above public health.

Here are the countries requiring pictorial warnings courtesy of that Canadian Cancer Society report.

And some of their warning pictures:

And this a picture that FDA would have required:

 

Skeptically Yours,

-AcP

Are You Taking A Statin Drug Inappropriately Like Eric Topol Because of the MyGeneRank App?

The skeptical cardiologist was listening to a podcast discussion between Sam Harris and Eric Topol recently and became  flabbergasted.

Topol, the “world-renowned cardiologist” who is seemingly everywhere in media these days was discussing what he considers the overuse of imaging technology during the podcast which Harris’s website describes as follows:

In this episode of the Making Sense podcast, Sam Harris speaks with Eric Topol about the way artificial intelligence can improve medicine. They talk about soaring medical costs and declining health outcomes in the U.S., the problems of too little and too much medicine, the culture of medicine, the travesty of electronic health records, the current status of AI in medicine, the promise of further breakthroughs, possible downsides of relying on AI in medicine, and other topics.

Personally, I have been amazed at the hype and promotion that artificial intelligence (AI) has been getting given the near total absence in cardiology of any tangible benefits from it and I wanted to hear what the man who wrote ” Deep Medicine: How Artificial Intelligence Can Make Healthcare Human Again ” had to say about it.

About 28 minutes into the podcast, Harris, who has lately been preoccupied with promoting meditation as a cure for all ills, begins describing a procedure he underwent:

I’ve had a few adventures in cardiology. CT scan, calcium score scan.

Harris, who in neuroscience and philosophy might speak precisely, here is very vague. Did he get a coronary calcium scan (CAC) or a coronary CT angiogram? There is a huge difference and he is conflating the two imaging procedures.

Apparently he is unhappy with having undergone it but:

I might be telling a different story if my life was saved by it.

And his doctor’s rationale  for getting the scan was lacking:

The way this was dispensed to me. We now have this new tool, let’s use it.

Let me just say at this point that if your doctor’s rationale for performing a test is that he has a machine that performs the test just say no. Or demand an explanation of how the results will change your management or prognosis.

Apparently the scan that Harris had didn’t turn out either horrifically worse than expected or remarkably better and didn’t change management:

In my case at the end it didn’t make sense.

Now, I can forgive Sam Harris for being somewhat naive and misguided when it comes to coronary artery scans or coronary CT angiograms but Eric Topol , the world’s leading talking cardiology head should fully understand the value of coronary artery calcium scans.

This is where I first become flabbergasted.

Topol says in response at this point that coronary artery calcium scans are “terribly overused” and that “I’ve never ordered one.”

Eric, you cannot be serious!

Are you telling me that you wouldn’t order one on your 60 year old airline pilot friend whose father dropped dead of a massive MI at age 50 but whose lipids look fine?

Why doesn’t Eric order CACs?

Because “There are so many patients who have been disabled by the results of their calcium score even though they have no symptoms.”

This is where the degree of my flabbergastment increased by an order of magnitude.

Our job as preventive cardiologists is to identify those at high risk and lead them to lifestyle choices and medicine that dramatically lowers that risk.  We educate them that the large build up of subclinical atherosclerosis we identified does not have to result in sudden death, crippling heart attacks or strokes. We reassure them that with the right tools we can help them live a long, productive and happy life.

Eric, what do you tell these people? The calcium score is irrelevant? You’re fine. You shouldn’t have gotten it. Surely not! This would be the preventive cardiology equivalent of sticking one’s head in the sand.

This is not the first time Topol has opined on the dangers of CAC. An excerpt from his book, ‘The Patient Will See You Now: The Future of Medicine Is in Your Hands” posted on Scientific American describes the ills created in a 58 year old man who had a CAC score of 710.

My patient was told that he had a score of 710—a high calcium score—and his physician had told him that he would need to undergo a coronary angiogram, a roadmap movie of the coronary anatomy, as soon as possible. He did that and was found to have several blockages in two of the three arteries serving his heart. His cardiologists in Florida immediately put in five stents (even though no stress-test or other symptoms had suggested they were necessary), and put him on a regimen of Lipitor, a beta-blocker, aspirin and Plavix.

This case is not an example of inappropriate usage of CAC it is an example of really bad doctoring and failure to utilize the CAC information properly.

One should never order a cardiac catheterization/coronary angiogram solely on the basis of a high CAC score. Even ordering a stress test in this situation is debatable as I discuss here.

And Topol’s patients symptoms were most likely related to a beta-blocker that he didn’t need (see here).

My Gene Rank

Later in the podcast I reached maximum flabbergast  levels when Topol announced that as a result of a high score for CAD risk he received using an iPhone app called MyGeneRank he had started taking a statin drug.

He enthusiastically promoted the app which his Scripps Translational Science Institute developed and urged listeners to utilize this approach to better refine the estimate of their risk of heart attack and stroke.

Per the Scripps website:

The MyGeneRank mobile app is built using Apple’s ResearchKit, an open source framework that enables researchers and programmers to build customized mobile apps for research purposes. With user permission, the app connects with the 23andMe application program interface and automatically calculates and returns a genetic risk score for coronary artery disease.

In addition, the app calculates a 10-year absolute risk estimate for an adverse coronary event, such as heart attack, using a combination of genetic and clinical factors. Users are able to adjust behavioral risk factors to see the influence of lifestyle habits on their overall risk.

Elsewhere, Topol, has stated

“We are excited to launch a unique study that combines an iOS app and genomics to help guide important health decisions,” says Eric Topol, MD, Founder and Director of the Scripps Translational Science Institute and Professor of Molecular Medicine at The Scripps Research Institute. “Not only does participating in the study arm individuals with their own data, but it also gives them the opportunity to participate in new type of research – one that is driven by and for patients.”

Curious, I downloaded the MyGeneRank app, answered some questions and gave it permission to access my 23 and Me data. After requiring me to complete a survey on my health it then  yielded  my coronary artery disease risk score.

 

 

 

 

 

 

 

Oh, no! My genetic risk score was at the 81st percentile! In the red zone.  According to Eric Topol I should take a statin like him. Based on these results I probably should be incredibly anxious and crippled by fears of cardiac death.

Fortunately, I have superior information to allay my fears. I’ve had CAC scans in the past which are well below average for men my age. Despite my dad’s history of early CAD, a recent coronary CT angiogram showed minimal plaque. I know exactly where I stand risk-wise.

How many cardiac cripples has Topol’s MyGeneRank inappropriately created?

Is the data that MyGeneRank utilizes superior to that from CAC scans?

For coronary artery calcium scanning there is a wealth of data supporting improved risk prediction and we are looking directly at the atherosclerotic process that eventually causes the diseases we want to prevent.

It’s interesting that a recent study looking at a polygenetic risk score’s ability to predict cardiac events was comparing the risk score’s ability to predict subclinital atherosclerosis:

Each 1-SD increase in the polygenic risk score was associated with 1.32-fold (95% CI, 1.04-1.68) greater likelihood of having coronary artery calcification and 9.7% higher (95% CI, 2.2-17.8) burden of carotid plaque.

In the Scientific American article Topol quotes Mark Twain:, “To a man with a hammer, a lot of things looks like nails that need pounding.”

Topol’s hammer is artificial intelligence. We eagerly await the day he discovers a nail that he can bang on that  significantly advances medical care.

In the meantime I and the vast majority of progressive preventive cardiologists will be utilizing CAC scores intelligently to identify both those patients at high risk for cardiovascular events who need more aggressive treatment and those at low risk who can be reassured and have treatment de-escalated.

Polygenetic CAD risk scores do show promise to improve our predictive powers but more study is needed in this are before we make clinical treatment decisions based on the results.

Astoundingly Yours,

-ACP

Ilene Has High Cholesterol With A “Wonderful Ratio” And A Branch Retinal Vein Occlusion: Should She Take A Statin?

Recently the skeptical cardiologist was asked by Ilene, a reader with an HDL almost as high as her LDL and a history of branch retinal vein occlusion (BRVO) whether she should take the statin her cardiologist had prescribed.

I enjoy reading your articles and would appreciate your opinion on my situation.  I recently took a lipid panel blood test: total cholesterol: 244 HDL:112 LDL:121 VLDL:11  CRP: 1.77 Triglycerides: 57.  Also my Cardiac Agatston  score is 21.
I had a Branch Retinol Vein Occlusion a year ago in my left eye  (it’s healing beautifully) and as a precaution  am now taking Amlodipine 5mg daily (my blood pressure was never too high to begin with) along with a daily baby aspirin.
I am otherwise a healthy 72 year old woman, exercise and eat healthy.
My regular doctor (Integrative MD) says my cholesterol ratio is wonderful….my cardiologist wants me to take a statin (Atorvastatin) in a low dose.  The ONLY med I take is Amlodipine and I am not one to be taking a plethora of meds for the rest of my life (unless “absolutely” necessary.  What is your suggestion…take a statin or not.
While I can’t provide medical advice to Ilene specifically it is worthwhile  to ponder  the general aspects of her case and how I would approach it as it likely applies to thousands of other patients including many of my own.
In my mind there are two questions here: 1) Should Ilene and patients like her take a statin to prevent future heart attacks and strokes and 2) Do statins  effect the Branch Retinal Vein Occlusion (BRVO)?
Although I’m not a fan of integrative or functional medicine Ilene’s integrative MD is correct in saying that her ratio of total cholesterol to HDL cholesterol is wonderful. Perhaps that high  HDL is protecting her from a build-up of atherosclerotic plaque.
On the other hand, Ilene tells me that  “My father did have a heart attack in his 60’s”.  Perhaps she inherited something from him that puts her in a higher than average risk category.
With the information from the CAC we don’t have to guess about the influence of the high HDL and the family history of CAD. Her score is at the 48th percentile, slightly below average for white women her age, thus it would appear she is not destined for her father’s fate.
Frequent readers of skepcard (especially my posts on statin fence sitters) will know I  plug all these numbers (preferably with the calcium score available) into the MESA coronary calcium risk calculator
In this case, the CAC score does not significantly alter our risk estimate as it is so close to the average for her age
Even if we count her as having hypertension because she is on the amlodipine her 10 year risk of heart attack and stroke is low at 3.2%.
Guidelines don’t recommend statin treatment unless risk is >7.5%.
Also, note that I answered yes to “Family history heart disease” but most studies generally only consider this a risk factor if father had heart attack prior to age 55 years. If we make that a no the risk drops to <3%.
Now that we’ve answered Ilene’s real question let’s see if the BRVO warrants statin therapy.
Branch Retinal Vein Occlusion
BRVO is the blockage of a vein from the retina and the second most
common cause of vision loss from retinal vascular disease, following diabetic retinopathy. It typically  results in the painless loss of vision in one portion of one eye due to hemorrhage and edema in the retina.
A reasonable summary of BRVO provided by the American Academy of Ophthalmology can be found here.
BRVO is not clearly related to atherosclerosis or hyperlipidemia and there is no evidence that taking a statin would prevent recurrence or help the condition.

The leading theory for what causes BRVO is that the more delicate and distensible retinal veins are squished or compressed at points where the stiffer and thicker retinal arteries cross them.  Up to Date notes:

Whereas branch retinal vein occlusion (BRVO) appears to be related to compression of the branch vein by retinal arterioles at the arteriovenous crossing points, central retinal vein occlusion (CRVO) is usually associated with primary thrombus formation.

Although BRVO is more common in patients with hypertension and atherosclerosis it is not clear that one causes the other or that treatment of hypertension or atherosclerosis diminishes the risk of BRVO.  So statins are not recommended.
More Questions
Every patient case for me leads to more questions,  more investigations and more knowledge. Here are some questions that occurred to me from ilene’s case.
-Why would someone with no symptoms and no heart problems be seeing a cardiologist?
(“I started seeing a cardiologist just to make sure all systems were “go” and stayed that way!… we take care of our cars so why not my body. )
I kind of like this answer and I definitely see lots of patients with that philosophy but if we extrapolate the car analogy: going to a cardiologist would be like taking your car to a mechanic who only works on engines or perhaps one specific part of the engine (help me out here people who know about cars.)
-Why was Ilene unwilling to take a statin? (I pretty much know the answer to this (see here) for most patients.
‘m just afraid of the horrible muscle related side effects of statin drugs…and that’s why I’m taking Berberine 500mg twice a day.
Yep. I feel a post abut Berberine may be in the works!
-Finally, should a 72 year old with a CAC score of 21 and BRVO be taking a baby aspirin?
I’ve generally advocated aspirin in primary prevention for scores >100  so wouldn’t advise it for prevention of cardiovascular events in this situation.
In addition, I have seen nothing in the literature that recommends aspirin for BRVO. These two BRVO experts do not recommend either aspirin or anticoagulants.
Proretinally Yours,
-ACP
N.B. If you have a blockage of the the artery that supplies blood to the retina or a branch retinal artery occlusion ( BRAO)
you might benefit from a statin as this is often caused by a clot or plaque flying out of the heart or the carotid artery.

The Ultimate Guide To The Coronary Artery Calcium Scan (Score) Circa 2019

The skeptical cardiologist’s first post on coronary artery calcium (CAC) scan was posted in 2014 and had the wordy title “Searching for Subclinical Atherosclerosis: Coronary Calcium Score-How Old Is My Heart?”

This post still serves as a good introduction to the test (rationale, procedure, risks) but in the 5 years since it was published there has been a substantial body of data published on CAC and in 2018 it was embraced by major organizations.

Overall, I’ve written 20 posts in which CAC plays a predominant role since then and I feels it’s time to put the most important changes and concepts  in one spot.


Detection Of Subclinical Atherosclerosis: What’s Your Risk of Dropping Dead?

First, the rationale for using CAC (also known as a coronary calcium score or heart scan) is detection of “subclinical atherosclerosis”, a non-catchy but hugely important process which I describe in an early post on who should take aspirin to prevent heart attack or stroke:

We have the tools available to look for atherosclerotic plaques before they rupture and cause heart attacks or stroke. Ultrasound screening of the carotid artery, as I discussed here, is one such tool: vascular screening is an accurate, harmless and painless way to assess for subclinical atherosclerosis.

In my practice, the answer to the question of who should or should not take aspirin is based on whether my patient has or does not have significant atherosclerosis. If they have had a clinical event due to atherosclerotic cardiovascular disease (stroke, heart attack, coronary stent, coronary bypass surgery, documented blocked arteries to the legs) I recommend they take one 81 milligram (baby) uncoated aspirin daily. If they have not had a clinical event but I have documented by either

  • vascular screening (significant carotid plaque)
  • coronary calcium score (high score (cut-off is debatable, more on this in a subsequent post)
  • Incidentally discovered plaque in the aorta or peripheral arteries (found by CT or ultrasound done for other reasons)

then I recommend a daily baby aspirin (assuming no high risk of bleeding).


Help In Deciding Who Needs Aggressive Treatment

Second, CAC is an outstanding tool for further refining risk of heart attack and stroke and helping better determine who needs to take statins or undergo aggressive lifestyle reduction, something I described in detail in my post “Should All Men Over Sixty Take a Statin Drug”.

The updated AHA/ACC Cardiovascular Prevention Guidelines came out in 2013.

After working with them for 9 months and using the iPhone app to calculate my patients’ 10 year risk of atherosclerotic cardiovascular disease (ASCVD, primarily heart attacks and strokes) it has become clear to me that the new guidelines will recommend statin therapy to almost all males over the age of 60 and females over the age of 70.

As critics have pointed out, this immediately adds about 10 million individuals to the 40 million or so who are currently taking statins.

By identifying subclinical atherosclerosis, CAC scoring identifies those who do or don’t need statins.


This is particularly important for patients who have many reservations about statins or who are “on the fence” about taking them when standard risk factor calculations suggest they would benefit.


The Widowmaker

In 2015 I wrote about a documentary entitled “The Widowmaker” (see here and here) which is about the treatment and prevention  of coronary artery disease and what we can do about the large number of people who drop dead from heart attacks, some 4 million in the last 30 years:

The documentary, as all medical documentaries tend to do, simplifies, dumbs down and hyperbolizes a very important medical condition. Despite that it makes some really important points and I’m going to recommend it to all my patients.

At the very least it gets people thinking about their risk of dying from heart disease which remains the #1 killer of men and women in the United States.

Perhaps it will have more patients question the value of stents outside the setting of an acute heart attack. This is a good thing.

Perhaps it will stimulate individuals to be more proactive about their risk of heart attack. This is a good thing.

Although CAC has some similarities to mammography (both utilize low dose radiation, 0.5 mSV) I concluded that CAC was not “the mammography of the heart” as the documentary proclaims.

What We Can Learn From Donald Trump’s CAC?

In 2018 I noted that “Donald Trump Has Moderate Coronary Plaque: This Is Normal For His Age And We Already Knew It.”

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) .

Yesterday it was revealed by the White House doctor , Ronny Jackson, that Trump’s repeat score  was 133.

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.

What is most notable about the Trump CAC incident is that Trump, like all recent presidents and all astronauts underwent the screening. If the test is routine for presidents why is it not routine for Mr and Mrs Joe Q Public?

At a mininum we should consider what is recommended for aircrew to the general public:

A three-phased approach to coronary artery disease (CAD) risk assessment is recommended, beginning with initial risk-stratification using a population-appropriate risk calculator and resting ECG. For aircrew identified as being at increased risk, enhanced screening is recommended by means of Coronary Artery Calcium Score alone or combined with a CT coronary angiography investigation.

The 2018 guidelines Take A Giant Step Forward

In late 2018 I noted that CAC had been embraced by major guidelines:

I was very pleased to read that the newly updated AHA/ACC lipid guidelines (full PDF available here) emphasize the use of CAC for decision-making in intermediate risk patients.

 

 

 

For those patients aged 40-75 without known ASCVD whose 10 year risk of stroke and heart attack is between 7.5% and 20% (intermediate, see here on using risk estimator) the guidelines recommend “consider measuring CAC”.

If the score is zero, for most consider no statin. If score >100 and/or >75th percentile, statin therapy should be started.

A Few Final Points On CAC

First, it’s never too early to start thinking about your risk of cardiovascular disease. I have been using CAC more frequently in the last few years in  individuals <40 years with a strong family of early sudden death or heart attack and often we find very abnormal values (see here for my discussion on CAC in the youngish.)

coronary calcium scan with post-processing on a 45 year old white male with very strong history of premature heart attacks in mother and father. The pink indicates the bony structures of the spine (bottom) and the sternum (top). Extensive calcium in the LAD coronary artery is highlighted in yellow and in the circumflex coronary artery in ?teal. His score was 201, higher than 99% of white male his age.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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 were you stand and what you can do about it.

Included in my discussions with my patients with premature ASCVD is a strong recommendation to encourage their brothers, sisters and children to undergo a thoughtful assessment for ASCVD risk. With these new studies and the new ACC/AHA guideline recommendations if they are age 40-75 years there is ample support for making CAC a part of such assessment.

Hopefully very soon, CMS and the health insurance companies will begin reimbursement for CAC. As it currently stands, however, the 125$ you will spend for the test at my hospital is money well spent.

The Importance of Proactivity

In “The MESA App-Estimating Your Risk of Cardiovascular Disease With And Without Coronary Calcium Score” I recently wrote that:

If you want to be proactive about the cardiovascular health of yourself or a loved one, download the MESA app and evaluate your risk.  Ask your doctor if a CACS will help refine that risk further.

There are many other questions to answer with regard to CAC-should they be repeated?, how do statins influence the score?, is there information in the scan beyond just the score that is important? Is a scan helpful after a normal stress test?

I’ve touched on some of these in the past, including the really tough  question “Should All Patients With A High Coronary Calcium Score Undergo Stress Testing?

Like most things in cardiology we have a lot to learn about CAC. There are many more studies to perform. Many questions yet to be answered.

A study showing improved outcomes using CAC guided therapy versus non CAC guided therapy would be nice. However, due to the long time and thousands of patients necessary it is unlikely we will have results within a decade.

I don’t want to wait a decade to start aggressively identifying who of my patients is at high risk for sudden death. You only get one chance to stop a death.

Apothanasically Yours,

-ACP


 

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,

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).

 

 

 

 

Can The Apple Watch Or Kardia ECG Monitor Detect Heart Attacks?

The skeptical cardiologist recently received this email from a reader:

With the new Apple Watch that’s out now, people have suggested my husband (who had a heart attack at 36) should get it since it could detect a heart attack. But I keep remembering what you said – that these devices can’t detect heart attacks and that Afib isn’t related to a heart attack most of the time – is that still the case? I don’t really know how to explain to people that it can’t do this, since absolutely everyone believes it does.

The answer is a resounding and unequivocal NO!

If we are using the term heart attack to mean what doctors call a myocardial infarction (MI) there should be no expectation that any wearable or consumer ECG product can reliably diagnose a heart attack.

The Apple Watch even in its latest incarnation and with the ECG feature and with rhythm monitoring activated is incapable of detecting a myocardial infarction.

Similarly, although the AliveCor Kardia ECG monitor is superb at diagnosing rhythm abnormalities it is not capable of detecting an MI

To make this even clearer note that when you record an ECG on the Apple Watch it intermittently flashes the following warning:

 

Note: “Apple Watch never checks for heart attacks”

How did such this idea take root in the consciousness of so many Americans?

Perhaps this article in 9-5 Mac had something to do with it

The article begins
Scott Killian never imagined his Apple Watch might save his life, but that’s exactly what happened a few weeks ago when he had a heart attack in the middle of the night. Killian recently shared his personal experience with 9to5Mac, and the details of his story are absolutely amazing.
In reality,  the man received an alarm that his resting heart rate was high at night. Apparently he also was experiencing chest pain and went to an ER where a cardiac enzyme was elevated.  Subsequently he underwent testing that revealed advanced coronary artery disease and he had a bypass operation. 
Even if we assume all the details of this story are accurate it is absolutely not a case of Apple Watch diagnosing an MI.
 
A high resting heart rate is not neccessarily an indicator of an MI and most MIs are not characterized by high heart rates.  We have had the technology with wearables to monitor resting heart rate for some time and no one has ever suggested this can be used to detect MI.
 
The rate of false alarms is so high and the rate of failure to diagnose MI so low that this is a useless measure and should not provide any patient reassurance.
 
The writer of this story and the editors at 9-5 Mac should be ashamed of this misinformation.
 
Several other news sources have needlessly muddied the water on this question including Healthline and Fox News:
 
 
 
 
 
 
 
The Fox News article entitled “Could The Apple Watch Series 4 save you from a heart attack” quotes a non-physician who suggests that AW can detect early signs of a heart attack:
 

In clear cut cases the Apple Watch could make the difference between life and death,” says Roger Kay, president of Endpoint Technologies Associates. Because you wear the Apple Watch at all times, it can detect an early sign of a stroke or a heart attack, and that early indication is critical, he says.

And the Healthline article on the new Apple Watch also incorrectly implies it can diagnose MI:

The device, which was unveiled last week, has an electrocardiogram (ECG) app that can detect often overlooked heart abnormalities that could lead to a heart attack.

And if you are felled by a heart problem, the fall detector built into the Apple Watch Series 4 could alert medical professionals that you need help

Fox News and Healthline should modify their published articles to correct the misinformation they have previously provided.

And it is still true that  although both Apple Watch and Kardia can diagnose atrial fibrillation the vast majority of the time acute heart attacks are not associated with atrial fibrillation.

Readers, please spread the word far and wide to friends and family-Apple Watch cannot detect heart attacks!

Skeptically Yours,

-ACP