Tag Archives: heart attack

Bernie Sanders Is Back: Is His Heart Healthy? Why Is His Ejection Fraction Not Reported?

While campaigning in Las Vegas last October, 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.

Despite little details about his cardiac condition, the event cast a cloud over his candidacy.

At the time I asked (and answered) a few questions): 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?

We now have more details to better answer these questions.

On December 30 of 2019, a letter from Brian P. Monahan, MD MACP on a letter head which reads in all caps “THE ATTENDING PHYSICIAN:Congress of the United States” to The Honorable Bernard Sanders was released.

This letter summarized Sanders’ “general health history and current medications” as Sanders had requested

Monahan, an oncologist by training, examined Sanders on 12/19/2019 at which time he found the senator was:

” 6 feet tall and 174 pounds. His blood pressure was 102/56, with a pulse of 62 beats per minute. His total cholesterol was 117 milligrams per deciliter of blood, HDL cholesterol (or “good” cholesterol) was 32 milligrams, and LDL cholesterol (or “bad” cholesterol) was 58 milligrams.”

With the exception of the low HDL these are good numbers and they indicate that Sanders LDL/bad cholesterol was at the appropriate goal post MI of <70 mg/dl. I would be a little concerned about the lowish BP of 102/56 in a 78 year old man but this likely reflects to some extent medications he is receiving to strengthen and protect his heart muscle.

Past Medical History

Next, Monahan summarizes Sanders’ past medical history

Over the years you have been treated for medical conditions including gout, hypercholesterolemia, diverticulitis, hypothyroidism, laryngitis secondary to esophageal reflux, lumbar strain, and complete removal of superficial skin lesions. Your colorectal cancer screening is up to date. Your past surgical history consists of repair of left and right-side inguinal hernias by laparoscopic technique and a right true vocal cord cyst excision. In November 2019, a follow-up ENT evaluation of your vocal cords for hoarseness was stable. You have no history of tobacco use, exercise regularly, and seldom drink alcohol.

Now we know some Bernie’s characteristic voice is due to a vocal cord cyst and that he is following a healthy lifestyle with regular exercise and no cigarette smoking.

What Happened In Vegas: The Myocardial Infarction

Monahan’s description of the heart attack (myocardial infarction or MI) Sanders suffered in Las Vegas gives more information than I had seen previously but is still lacking in details which I felt were important to know: troponin level and ejection fraction

The most significant event in your recent health was your admission to the Desert Springs Hospital in Las Vegas Nevada on October 19 2019. You experienced myocardial infarction due to an acute blockage of a coronary artery. In the initial hours of your evaluation, you were found to have an elevation of cardiac muscle proteins in your blood accompanied by diminished heart muscle strength and chamber wall motion reduction as determined by echocardiogram. You underwent prompt cardiac catheterization with identification of the narrowed segment of the midportion of the left anterior descending coronary artery. The narrowed segment was re-opened followed by the placement of two drug-eluting stents, a procedure that is referred to as primary percutaneous coronary intervention (Per). You received standard treatment with medications to improve your heart function and provide antiplatelet therapy required by your stents. You were released from the hospital three days later and returned home.

The exact elevation of the cardiac muscle protein, aka troponin, level is not reported.

He indicates “diminished heart muscle strength” determined by an echocardiogram and this is the ejection fraction (EF) but the exact percent EF is not given.

In my previous post on Senator Sanders I wrote

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?

Heart Failure?: Signs Or Symptoms?

Later in his letter Monahan indicates

You have never had symptoms of congestive heart failure

This is an interesting turn of phrase. The doctor is not stating clearly that Sanders did not have congestive heart failure (CHF)

We diagnose CHF by eliciting certain symptoms such as shortness of breath or fatigue and observing certain signs such as crackles in the lungs, distention of the jugular veins, or swelling in the legs. These findings are combined with lab tests (BNP or pro BNP) and imaging studies (chest x-ray, echocardiography).

Given Monahan’s phrasing I suspect there were signs and/or abnormal labs that suggested CHF  on his presentation with chest pain. The good news is that subsequent testing indicates no CHF.

Bernie’s Medications:

Monahan goes on to describe current medications:

Your current daily medications include atorvastatin, aspirin, clopidogrel, levothyroxine, and lisinopril

The aspirin and clopidogrel are anti-platelet agents which are standard after implantation of drug-eluting stents like the two Sanders received at the time of his MI.  They help keep the stents from stenosing or clogging up.

The atorvastatin is a statin/cholesterol lowering drug which should be given post MI in high dosages (40 to 80 mg daily) to reduce the risk of progression of the atherosclerotic plaque in Bernie’s coronaries which caused his MI. The atorvastatin has lowered his LDL to <70.

Lisinopril is an ACE inhibitor which is likely being utilized in this case to help strengthen and protect his heart muscle after the MI. Typically this would be used in conjunction with a beta-blocker however later in the letter, Dr. Monahan indicates Sanders was taken off a beta-blocker:

Several of the medications you initially required (blood-thinner, beta blocker) were stopped based on your progress. Your heart muscle strength has improved

Why Was The Beta-Blocker Stopped?

I see two possibilities, one portending a good prognosis and the other a bad prognosis.

Beta-blockers have been shown to significantly improve outcomes post MI in patients with depressed EF. The normal EF is >55%. Did Sanders’ EF improve to the point where the doctors felt beta-blockers would no longer be beneficial? This would be a good prognostic sign.

The other possibility is that Sanders’ blood pressure was so low on the beta-blockers that he was weak or dizzy. This would be a bad prognostic sign.

A third possibility seems less likely to me: excessive heart rate slowing on a beta-blocker. Given his resting heart of 62 bpm on no beta-blocker he should have been able to tolerate at least a low dose of beta blocker.

Cardiac Testing Post MI

After Sanders returned to his home in Vermont he saw his personal cardiologist Martin LeWinter and underwent further testing which according to Monahan showed the following

The heart chamber sizes, wall thickness, estimated pressures, and heart valves are normal.

I’m presuming this information comes from an echocardiogram. One of the key pieces of information that would come from this same echocardiogram is the ejection fraction. Why doesn’t he mention the EF?

Several 24-hour recordings of your heart electrical activity indicated no significant heat rhythm abnormality.

So Senator Sanders had at least two Holter monitors. This is not the norm post MI and I have to think he must have had some significant arrhythmias on telemetry while hospitalized to prompt these investigations. What rhythm abnormalities prompted multilple Holter monitor studies?

Sanders also underwent a treadmill stress test in December which is the norm post MI. Findings were  summarized by Monahana

a successful graded exercise treadmill examination monitoring your heart function, muscular exertion, and oxygen consumption that indicated a maximal level of exertion to 92% of your predicted heart rate without any evidence of reduced blood flow to your heart or symptoms limiting your exercise performance. Your overall test performance was rated above average compared to a reference population of the same age. The cardiac exercise physiologist who evaluated your results determined that you are fit to resume vigorous activity without limitation.

A  letter from Dr. Phillip Ades indicates this was a cardiopulmonary exercise test and it appears maximal aerobic capacity was measured directly but this number is not revealed.

However, this type of stress test is not capable of monitoring “heart function” and Monahan’s statement that there was no “evidence of reduced blood flow to your heart” can only mean there were no EKG changes as blood flow to the heart was not directly measured.

Fitness To Continue Campaigning And Serve As President

Senator Sanders’ doctors conclude based on all the evidence they have that he is fit and able.

In addition to the letters referenced above, Mr. Sanders’s personal cardiologist, Martin LeWinter wrote a letter (which I can’t locate) which states that Mr. Sanders had experienced “modest heart muscle damage” but that his heart function was now “stable and well-preserved.”

Once more, the two things I would like to know are not being precisely described.

Heart muscle damage would be precisely assessed by the maximal troponin level during his MI. Modest is defined as “not large” in the Cambridge English dictionary.

Heart function would be precisely assessed by the ejection fraction. Well-preserved is most frequently used to describe older things or people that are in good condition or don’t appear as old as they really are. It’s often used to describe left ventricular function but is vague. Why not just state the ejection fraction?

It would also be nice to know what coronary artery was stented and what was the status of the other coronary arteries that weren’t stented.

Dr. LeWinter concludes

“At this point, I see no reason he cannot continue campaigning without limitation and, should he be elected, I am confident he has the mental and physical stamina to fully undertake the rigors of the presidency,”

I have a lot of confidence in Dr. LeWinter’s (see below) integrity and judgement and therefore would agree with his conclusions. I’d feel even more confident if I had access to all of Senator Sanders’ relevant data.

Skeptically Yours,

-ACP

N.B. I recognized Dr. LeWinter’s name as he has been a prominent figure in the area of pericardial disease and heart failure research.

His CV is very impressive.

Dr. LeWinter is Professor of Medicine and Molecular Physiology and Biophysics and Director of the Heart Failure and Cardiomyopathy Program at the University of Vermont. He received his undergraduate degree from Columbia University, his M.D. from New York University and sub-specialty training in Cardiovascular Disease at University of California, San Diego.  In addition to heart failure, cardiac hypertrophy and myocardial dysfunction Dr. LeWinter has had a longstanding interest in pericardial disease. Dr. LeWinter has received continuous research support from the NIH for over 35 years and is the author of over 190 original research papers, over 60 book chapters and review articles, and the Editor of two books. He is a Fellow of the American Heart Association, the American College of Cardiology, the Cardiovascular Section of the American Physiological Society and the International Academy of Cardiovascular Sciences, and a member of the Association of University Cardiologists. Dr. LeWinter has served on numerous Editorial Boards and research review committees and is an Associate Editor of the journals Circulation and Coronary Artery 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

Taking Blood Pressure Medication At Bedtime Lowers Risk Of Death, Stroke And Heart Attack

When should you take your once daily BP meds?

Increasingly, the skeptical cardiologist has been recommending to patients that they take BP meds at bedtime as evidence has mounted  that this does a better job of normalizing asleep blood pressure and minimizing daytime side effects.

Now a study published in European Heart Journal in October has demonstrated that routine ingestion of BP meds at bedtime as opposed to waking results in improved 24 hour BP control with enhanced decrease in asleep BP and increased sleep-time relative BP decline (known as BP dipping.)

More importantly, bedtime BP med ingestion in this randomized trial of over 19 thousand hypertensive Spaniards resulted in highly significant reductions in cardiovascular events including death, heart attack, heart failure and stroke over a 6 year median follow-up

The so-called Hygia Chronotherapy Trial was extremely well done and the results are powerful and should modify clinical practice immediately.

This figure demonstrates the dramatic and highly significant 45% reduction in all types of cardiovascular events measured. Note that stroke rate was halved!

Screen Shot 2019-11-05 at 7.56.12 AM

Here are the Kaplan-Meier curves showing early and progressive separation of the treatment curves.

Screen Shot 2019-11-05 at 7.50.10 AM

There was no difference side effects or compliance between the two groups.

The remarkable aspect of this intervention is that it costs nothing, introduces no new medications and has no increased side effects.

This study is practice-changing for me. We will be advising all hypertensive patients to take their once daily BP meds at bedtime.

Chronotherapically Yours,

-ACP

h/t Reader Lee Sacry for bringing this study to my attention

 

 

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

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

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

Are You Doing Enough Push Ups To Save Your Life?

The skeptical cardiologist has always had a fondness for push-ups. Therefore I read with interest a recent study published in JAMAOpen which looked at how many push-ups a group of 30 and 40-something male firefighters from Indiana could do and how that related to cardiovascular outcomes over the next ten years.

The article was published in the peer-reviewed journal JAMA Network Open, and is freely available to access online.

The British National Health Service pointed out that “The UK media has rather over exaggerated these findings:”

Both the Metro and the Daily Mirror highlighted the result of 40 push-ups being “the magic number” for preventing heart disease, but in fact being able to do 10 or more push-ups was also associated with lower heart disease risk.

What Was Studied?

The study involved 1,104 male firefighters (average age 39.6) from 10 fire departments in Indiana who underwent regular medical checks between 2000 and 2010. 

At baseline the participants underwent a physical fitness assessment which included push-up capacity (hereafter referred to as the push-up number (PUN))and treadmill exercise tolerance tests conducted per standardized protocols.

For push-ups, the firefighter was instructed to begin push-ups in time with a metronome set at 80 beats per minute. Clinic staff counted the number of push-ups completed until the participant reached 80, missed 3 or more beats of the metronome, or stopped owing to exhaustion or other symptoms (dizziness, lightheadedness, chest pain, or shortness of breath). Numbers of push-ups were arbitrarily divided into 5 categories in increments of 10 push-ups for each category. Exercise tolerance tests were performed on a treadmill using a modified Bruce protocol until participants reached at least 85% of their maximal predicted heart rates, requested early termination, or experienced a clinical indication for early termination according to the American College of Sports Medicine Guidelines (maximum oxygen consumption [V̇ O2max]).

The main outcomes assessed were new diagnoses of heart disease from enrollment up to 2010. 

Cardiovascular events were verified by periodic examinations at the same clinic or by clinically verified return-to-work forms. Cardiovascular disease–related events (CVD) were defined as incident diagnosis of coronary artery disease or other major CVD event (eg, heart failure, sudden cardiac death)

Here’s the graph of the probability of being free of a CVD event on the y-axis with time on x-axis.

The black line represents those 75 firefighters who couldn’t make it into double digits, the green those 155 who did more than 40 pushups.

Participants able to complete more than 40 push-ups had a significant 96% lower rate of CVD events compared with those completing fewer than 10 push-ups.

It is surprising that the push up number seemed a better predictor of outcomes than the exercise test, This should be taken with a grain of salt because although the investigators report out “VO2 max” the stress tests were not maximal tests.

The firefighters with lower push up numbers were fatter, more likely to smoke and had higher blood pressure, glucose and cholesterol levels.

What useful information can one take from this study?

You definitely cannot say that being able to do more than 40 pushups will somehow prevent heart disease. The PUN is neither causing nor preventing anything.

The PUN is a marker for the overall physical shape of these firefighters. It’s a marker for how these men were taking care of themselves. If you are a 39 year old fireman from Indiana and can’t do 11 push-ups you are in very sorry condition and it is likely evident in numerous other ways.

The <11 PUN crew were a bunch of fat, diabetic, insulin resistant, hyperlipidemic, out-of-shape hypertensives who were heart attacks in the waiting.

Push-ups Are A Great Exercise

Despite the meaningless of this study you should consider adding push-ups to your exercise routine. Doing them won’t save your life but it will contribute to mitigating the weakness and frailty of aging. Don’t obsess about your PUN.

I’ve always liked push-ups and highly recommend them. They require no special equipment or preparation. It’s a quick exercise that builds upper body muscle strength, adds to my core strength and gets my heart rate up a bit. For some reason my office in O’Fallon is always cold so several times during the day when I’m there I’ll do 100 jumping jacks and drop on the carpet and do some push-ups in an effort to get warm.

I don’t do them every day but the last time I tried I could do 50 in less than a minute and that has me convinced I will live forever!

Calisthenically Yours,

-ACP

N.B. In my post on mitigating sarcopenia in the elderly I talked about the importance of resistance exercise:

Americans spend billions on useless supplements and vitamins in their search for better health but exercise is a superior drug, being free  and without drug-related side effects

I’ve spent a lot of time on this blog emphasizing the importance of aerobic exercise for cardiovascular health but I also am a believer in strength and flexibility training for overall health and longevity.

As we age we suffer more and more from sarcopenia-a gradual decrease in muscle mass.

Scientific reviews note that loss of muscle mass and muscle strengh is quite common in individuals over age 65 and is associated with increased dependence, frailty and mortality

Push-ups are a great resistance exercise. For a description of the perfect form for a push up see here.

Prevention of Heart Attack and Stroke-Early Detection Of Risk Using Coronary Artery Calcium Scans In The Youngish

Since 1/3 of Americans die from atherosclerotic cardiovascular disease (ASCVD, mostly heart attacks and strokes) and dropping dead is often the first symptom of ASCVD it’s incredibly important to identify early, “subclinical” ASCVD and begin measures to reduce risk.

How early to begin that process is open to debate. The recent sudden death of the 41-year old son of a patient of mine, however, has reinforced to me how crucial it is to begin risk assessment and potential treatments as early as possible, especially in individuals with a strong family history of premature ASCVD.

We use standard risk factors like lipids, smoking, age, gender and diabetes to stratify individuals according to their 10 year risk of ASCVD (using this online risk calculator) but many apparent low risk individuals (often due to inherited familial risk) drop dead from ASCVD and many apparent high risk individuals have no subclinical ASCVD and don’t need preventive therapy.

Recent studies provide compelling support for the early utilization of cardiac imaging in to identify high risk individuals.

Heart attacks and most sudden cases of sudden death are due to rupture of atherosclerotic plaques. Thus, it makes sense to seek out  such plaques, a process I call searching for subclinical atherosclerosis. There are a number of ways to search for sublinical plaques but the two most widely studied are carotid ultrasound screening and coronary artery calcification (CAC) measurement.

I’ve been utilizing CAC (also termed  heart scan, coronary calcium score, or cardioscan) to help assess my patient’s risk of ASCVD for years although the procedure is not covered by insurance and until recently was not strongly endorsed by major guidelines. (For a complete description of the test and the risks/benefits see here). As I pointed out here, in November the new ACC/AHA guidelines finally embraced CAC for

adults 40 to 75 years of age without diabetes mellitus and with LDL-C levels ≥70 mg/dL- 189 mg/dL (≥1.8-4.9 mmol/L), at a 10-year ASCVD risk of ≥7.5% to 19.9%, if a decision about statin therapy is uncertain

Typically, if we have calculated (using the ASCVD risk estimator) a 10 year risk >7.5% we have a discussion with the patient about beginning drug treatment to reduce risk.

To inform the decision and help us “get off the fence” I usually recommend a CAC. To see how this works in a typical sixty something see my posts here and here.

Significant Of CAC Score

As the new ACC/AHA guidelines state:

If CAC is zero, treatment with statin therapy may be withheld or delayed, except in cigarette smokers, those with diabetes mellitus, and those with a strong family history of premature ASCVD.

A duo of studies from Walter Reed Army Hospital have provided more support for the value of the zero CAC for risk prediction and identifying who should get treatment for prevention of both heart attacks and strokes.

Over 10,00 subjects underwent CAC and were assessed for the primary outcomes of all-cause mortality, incident MI, stroke, and the combination of major adverse cardiovascular events (MACE), defined as stroke, MI, or cardiovascular death over an average 11.4 years

Patients were classified on the basis of the presence or absence of calcium and further subdivided into CAC score groups of 0, 1 to 100, 101 to 400, and >400

Patients without a zero CAC had a very low number of events , with a 1.0% rate of mortality and 2.7% rate of MACE over a 10-year period.

On the other hand subjects without any traditional risk factors (n = 6,208; mean age 43.8 years), the presence of any CAC (>0) was associated with a 1.7 fold increased risk of MACE after adjustment for traditional risk factors.

f2.large-3
Patients with CAC who were prescribed a statin had a significantly reduced risk of MACE (aSHR: 0.76; 95% CI: 0.60 to 0.95; p = 0.015), whereas patients without CAC had no associated MACE reduction (aSHR: 1.00; 95% CI: 0.79 to 1.27; p = 0.99). p = 0.097 for interaction between statin treatment and CAC presence. aSHR = adjusted subhazard ratio; CAC = coronary artery calcium; CI = confidence interval; MACE = major adverse cardiovascular event(s)

The red line of the >400 score individuals has a much higher risk of death, stroke and heart attack (myocardial infarction) than the blue (CAC 1-100) or the gray line of the zero CAC scorers.

Furthermore, when these investigators looked at outcomes in those individuals who received statins versus those who didn’t, the zeros didn’t benefit from statin therapy over the 10 year follow-up.

f3.large
Benefit of statin therapy was significantly related to CAC group with benefit in patients with CAC score >100 but not in patients with CAC <100. aSHR = adjusted subhazard ratio; CAC = coronary artery calcium; CI = confidence interval; MACE = major adverse cardiovascular event(s).

But there was a tremendous reduction in bad CV events in those with scores >100 who received statin (red line) versus those who did not (blue line).

Here’s the figure which encapsulates both the risk prediction power of the CAC (and the benefits of statin treatment restricted to those with >0 (blue lines)

f2.large-4

 

Benefits of CAC Testing In The Young

So these new studies provide powerful data supporting the use of CAC in younger individuals to help us refine risk estimates and target the individual at high risk of MI and sudden death. It seems highly appropriate to consider CAC testing beginning at age 40 years as the AHA/ACC guidelines suggest.

But what about the individual who has a strong family history of premature CAD and is age say 35 or 39 years of age. Do we ignore advanced risk assessment? Very few individuals die in their 30s from ASCVD but I have a number of patients who suffered heart attacks in their forties. In addition, the earlier we can start risk modification the better as the process begins very early in life and accumulates over time.

The Coronary Artery Risk Development in Young Adults (CARDIA) Study published in 2017 has demonstrated the early development of nonzero CAC score in the youngish and the predictive value of the high CAC score for mid life ASCVD events.  It was  a prospective community-based study that recruited 5115 black and white participants aged 18 to 30 years from March 25, 1985, to June 7, 1986. The cohort has been under surveillance for 30 years, with CAC measured 15 (n = 3043), 20 (n = 3141), and 25 (n = 3189) years after recruitment. The mean follow-up period for incident events was 12.5 years, from the year 15 computed tomographic scan through August 31, 2014.

The conclusions:

Any CAC in early adult life, even in those with very low scores, indicates significant risk of having and possibly dying of a myocardial infarction during the next decade beyond standard risk factors and identifies an individual at particularly elevated risk for coronary heart disease for whom aggressive prevention is likely warranted.

screen shot 2019-01-19 at 12.36.44 pmI read CAC scans every day and it is not uncommon to see a non-zero scores in individuals in their late 30s or early 40s.

The two sons of another one of my patients both in their late 50s with unremarkable risk factor profiles and both developing anginal type symptoms limiting their activities each underwent multi vessel stent procedures in the last month. If I had seen them  10 to 20 years ago we would have identified the subclinical atherosclerosis building up in their coronaries, started treatment and avoided the need for invasive, expensive procedures.

Other Risk-Enhancing Factors To Consider In The Young

The ACC/AHA guidelines list some “risk-enhancing factors” some of which I find useful.

screen shot 2019-01-19 at 7.33.39 am

Clearly family history of premature ASCVD is important but the devil is in the details. What relatives count? What was the event in the family member? If it was sudden death was an autopsy done?

What about nontraditional lipid/biomarkers?  I consider an assessment of Lp(a) and some more sophisticated measurement of atherogenic dyslipidemia (apoB, LDL-P) and inflammation (CRP) essential.

Interestingly the guidelines include ABI (which I do not find helpful) but not carotid vascular screening which has frequently guided me to earlier therapy in youngish individuals with abnormal biomarkers or strong family history.

Vascular screening in young subjects may detect subclinical atherosclerosis as measured by thickening of the carotid wall (IMT) or early carotid plaque prior to the formation of calcium in the coronary arteries. Advanced IMT precedes the formation of soft plaque in arteries and only later is calcium deposited in the plaque.

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 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.

Skeptically Yours,

-ACP

What Can You Really Learn From Celebrity Bob Harper’s Heart Attack And Near Sudden Death?

Until recently I had never heard of Bob Harper (The Biggest Loser) but apparently he is a celebrity personal trainer and had a heart attack and nearly died.  He  is known “for his contagious energy, ruthless training tactics, and ability to transform contestants’ bodies on The Biggest Loser” (a show I’ve never seen.)

When celebrities die suddenly (see Garry Sanders, Carrie Fischer) or have a heart attack at a youngish age despite an apparent healthy lifestyle this get’s people’s attention.

The media typically pounce on the story which combines the seductive allure of both health and celebrity reporting.

It turns out Harper inherited a high Lipoprotein (a) (see here) which put him at high risk for coronary atherosclerosis (CAD) which ultimately caused the heart attack (MI)  that caused his cardiac arrest.

To his credit, Harper has talked about Lipoprotein (a) and made the public and physicians more aware of this risk factor which does not show up in standard cholesterol testing.

Since his heart attack, Mr. Harper of “The Biggest Loser” has embarked on a newfound mission to raise awareness about heart disease and to urge people to get tested for lp(a).

Harper As Brilinta Shill

Unfortunately , he has also become a shill for Brilinta, an expensive brand name anti platelet drug often prescribed in patients after heart attacks or stents.

At the end of the TV commercial he says “If you’ve had a heart attack ask your doctor if Brilinta is right for you. My heart is worth Brilinta.”

At least this video is clearly an advertisement but patients and physicians are inundated  by infomercials for expensive, profit-driving drugs like Brilinta.

This Healthline article pretends to be a legitimate piece of journalism but is a stealth ad for Brilinta combined with lots of real ads for Brilinta.

Harper As Lifestyle Coach.

Harper also changed his fitness and diet regimens after his MI reasoning that something must have been wrong with his lifestyle and it needed modification.  For the most part he talks about more “balance” in his life which is good advice for everyone. His fitness regimens pre-MI were incredibly intense and have been toned down subsequently.

After his heart attack, Bob abandoned the Paleo lifestyle for the Mediterranean diet, as it’s been proven to improve heart health and reduce the risk of a heart attack, stroke, and heart-disease-related death by about 30 percent. But recently, he’s moved closer to a vegetarian regimen.

Of course, vegans and vegetarians have seized on this change in his diet as somehow proving the superiority of their chosen diets as in this vegan propaganda video:

Unfortunately there is no evidence that changing to a vegan or vegetarian diet will lower his risk of repeat MI.  Those who promote the Esselstyn, Pritikin or Ornish type diets claim to “reverse heart disease” and to be science-based but, as I’ve pointed  out (see here) the science behind these studies is really bad.

In fact, we know that neither diet nor exercise influence lipoprotein(a) levels which Bob inherited.  Some individuals just inherit the risk and must learn to deal with the cardiovascular cards they’ve been dealt.

What Can We Really Learn From Bob Harper’s Experience?

  1. Lipoprotein (a) is a significant risk marker for early CAD/MI/sudden cardiac death. Consider having it measured if you have a a) strong family history of premature deaths/heart attack (b) if you have developed premature subclinical atherosclerosis (see here) or clinical atherosclerosis (heart attack, stroke, peripheral vascular disease) or (c) a family member has been diagnosed with it.
  2. Everyone should learn how to do CPR and how to utilize an AED. (see here for my rant on these two incredibly important 3-letter words). Harper was working out in the gym when he collapsed. Fortunately a nearby medical student had the wherewithal to do CPR on him until he could be defibrillated back to a normal rhythm and transported to a hospital to stop his MI.
  3. Dropping dead suddenly is often the first indicator that you have advanced CAD. If you have a strong family history of sudden death or early CAD consider getting a coronary artery calcium scan to better assess your risk.

Focus on celebrities with heart disease helps bring awareness to the public about important issues but we can only learn so much about best lifestyle or medications from the experience of one individual, no matter how famous.

Brilliantly Yours,

-ACP