Category Archives: Atherosclerosclerotic Cardiovascular Disease

One Question On A Borderline Stress Test and One Comment About Me , Gundry And BIG PHARMA

A reader asks me the following question:

I’m 35 years old male and was positive for myocardial ischemia during stress test. The cardiologist said that my result was borderline. I’m not sure what does he meant by “borderline”. Also does it help if I do CAC score since my stress test already came out with positive MI?

Good questions.

First off, to understand what any stress test means we have to know the pre-test probability of disease. For example, in 35 year old males without chest pain the likelihood of any significantly blocked coronary artery is very low. This means that the vast majority of positive or borderline tests in this group are false positives, meaning the test is abnormal but there is no disease.

Even if we add exertional chest pain into the mix the probability of a tightly blocked coronary in a 35 year year old is incredibly low (but there are some congenital coronary anomalies that occur.)

The accuracy of stress tests varies depending on the type. The standard treadmill stress test with ECG monitoring is about 70% sensitive  and 70% specific. Adding on a nuclear imaging component improves the sensitivity (it makes it more likely we will pick up a blockage if it is present) to about 85% however, in the real world, the specificity (chance of a false positive) is still quite high. Accuracy varies a lot depending on how good the study is and how good the reader is.

Borderline for either the stress ECG the stress nuclear (or stress echo) means that the test wasn’t clearly abnormal but it wasn’t clearly normal. It is in a grey zone of uncertainty.

Given your low pre-test probability of disease it is highly likely your “borderline” test result is a false positive. Whether anything else needs to be done at this point depends on many factors (some from the stress test)  but most importantly, the nature of the symptoms that prompted the investigation in the first place.

If there are no symptoms and  you went for more than 9 minutes on the treadmill likely nothing needs to be done.

Would a coronary calcium scan add anything?

A very high score (>let’s say 100 for age 35) would raise substantial concerns that you have a coronary blockage.

A zero score would be expected in your age group and probably wouldn’t change recommendations .

A score of 1 up to let’s say 100  means you have a built up a lot more plaque than normal and should look at aggressive modification of risk factors but likely wouldn’t change other recommendations.

So the CAC might be helpful but most likely it would be a zero and not helpful.

A Nasty Comment.

The skeptical cardiologist gets lots of nasty comments about his post on the bad science behind Dr. Esselstyn’s diet and another post on the totally bogus Plant Paradox book/diet by Stephen Gundry. I don’t think Esselstyn is a quack but he pretends that there is scientific support for his wacky diet when all he has is anecdotes.

With Gundry, on the other hand, there is a strong smell of quackery.

With this new book he’s developed a line of ridiculous foods that he’s approved.

Gundry will sell you a 75$  piece of chocolate with resveratrol added to it. Despite the multiple health claims for this antioxidant (found in red wine) there are no proven health benefits.

 

Snake oil and supplements abound in all of his presentations and there is much promotion of useless expensive skincare products and  foods that only he sells.

I’m thinking of  adding promotion of special, super-charged olive oil to the red flags of quackery.

There’s no health  reason to get extra-virgin olive oil adulterated with anything. Just make sure you are actually getting EVOO.


Here’s one of Gundry’s supporters comments.

Thank you for your opinion and that’s exactly what it is YOUR OPINION. I suggest you try the Plant Paradox. You sound like someone from a pharmaceutical company. Why don’t you write about how BIG PHARMA is deceiving the public along with how they are keeping people sick.

People who leave nasty comments on my blog typically don’t identify themselves. I can’t tell if this is an authentic comment or someone paid by Gundry’s vast snake oil empire.

They really like using ALL CAPs.

And they like to accuse me of being from BIG PHARMA or in the pay of BIG PHARMA.

BIG PHARMA and I, apparently, have the goal of misleading the populace about the benefits of Gundry’s BS diet and useless supplements so that they will remain sick and require drugs that  gain us huge profits.

I’m still waiting for the checks from BIG PHARMA to roll in. In the meantime I am scrupulously avoiding lunch with pharmaceutical reps and drug/device sponsored boondoggles.

Pharmalargically Yours,

-ACP

N.B. If you’d like to see how much money BIG PHARMA is paying me (or any doctor) you can go to the Dollars for Docs website run by Pro Publica here.

What John Mandrola Learned About Aspirin in Munich

The skeptical cardiologist did not get to travel to Munich to attend the recent European Society of Cardiology meetings but the electrophysiologist, John Mandrola did. He summarized two big trials which showed no benefit of aspirin in the primary prevention of cardiac disease, one in patients with diabetes and one in patients with moderate risk in Ten Things I Learned About Aspirin at ESC

Of note, the lack of benefit in these studies is partially related to a much lower rate of events than predicted from standard risk models.

Why? Mandrola notes:

“societal efforts, such as lower rates of smoking and removal of trans-fats from the food supply, have led to a heart-healthier environment. In addition, greater use of preventive therapies—statins and antihypertensive meds, for instance—have also contributed to lower rates of cardiac disease. These developments increase the difficulty of running trials for primary prevention but are decidedly good news for patients.”

Similar to the ASPREE study, aspirin did not show any benefit in reducing GI cancer in these two large studies.

So aspirin may be less effective than it was decades ago because we have done a good job overall of reducing the risk of heart attack and stroke.

acetylsalicylic ally Yours,

-ACP

h/t Reader Francis

Revisiting Who Should Take Aspirin

Four years ago the skeptical cardiologist wrote the (in his extremely humble  and biased opinion) the definitive post on aspirin and cardiovascular disease.  Entitled “Should I take aspirin to prevent stroke or heart attack“,  it pointed out that although Dr. Oz had recently told almost all middle-aged women to take a baby aspirin and fish oil, there was, in fact no evidence to support that practice.

The publication of the ASPREE (Aspirin in Reducing Events in the Elderly) trial results in the latest issue of the New England Journal of Medicine further strengthens the points I made in 2014.

Between 2010 and 2014 the ASPREE investigators enrolled over 19,000 community-dwelling persons in Australia and the United States who were 70 years of age or older (or ≥65 years of age among blacks and Hispanics in the United States) and did not have cardiovascular disease, dementia, or disability.

(It’s important to look closely at the precise inclusion and exclusion criteria in randomized studies  to understand fully the implications of the results (for example, what qualified as cardiovascular disease) and I’ve listed them at the end of this post.)

Study participants were randomly assigned to receive 100 mg of enteric-coated aspirin or placebo. At the end of the study about 2/3 of participants in both groups were still taking their pills.

When I wrote about aspirin in 2014 I focused on cardiovascular disease. At that time, there was some reasonable evidence that aspirin might lower the risk of colorectal cancer. But when we look at outcomes the bottom line is how the drug influences the overall mix of diseases and deaths.

The ASPREE researchers chose disability-free survival, defined as survival free from dementia or persistent physical disability (inability to perform or severe difficulty in performing at least one of the six basic activities of daily living that had persisted for at least 6 monthas their primary end-point which makes a lot of sense-patients don’t want to just live longer, they want to live longer with a good quality of life. If aspirin, to take a totally hypothetical example) is stopping people from dying from heart attacks but making them demented it’s not benefiting them overall.

After 5 years there was no difference in the rate of death, dementia or permanent physical disability between the aspirin group (21.5 events per 1000 person-years) and placebo group (21.2 per 1000).

However those taking aspirin had a significantly higher rate of major bleeding (3.8%) than those taking placebo (2.8%).

The risk of death from any cause was 12.7 events per 1000 person-years in the aspirin group and 11.1 events per 1000 person-years in the placebo group.. Cancer was the major contributor to the higher mortality in the aspirin group, accounting for 1.6 excess deaths per 1000 person-years.

Screen Shot 2018-09-19 at 9.26.41 AM

And, despite prior analyses suggesting aspirin reduces colorectal cancer the opposite was found in this study. Aspirin takers were 1.8 times more likely to die from colorectal cancer and 2.2 times more likely to die from breast cancer.nejmoa1803955_t2

 

Did Aspirin Reduce Cardiovascular Events?

No. It did not.

A separate paper analyzed cardiovascular outcomes

After a median of 4.7 years of follow-up, the rate of cardiovascular disease was 10.7 events per 1000 person-years in the aspirin group and 11.3 events per 1000 person-years in the placebo group (hazard ratio, 0.95; 95% confidence interval [CI], 0.83 to 1.08). The rate of major hemorrhage was 8.6 events per 1000 person-years and 6.2 events per 1000 person-years, respectively (hazard ratio, 1.38; 95% CI, 1.18 to 1.62; P<0.001).

The ASPREE study confirms what I advised in 2014 and hopefully will further reduce the inappropriate consumption of aspirin among low risk individuals.

I’ve taken more patients off aspirin since 2014 than I’ve started on and what I wrote then remains relevant and reflects my current practice. Especially in light of the increase cancer risk noted in ASPREE patients should only take aspirin for good reasons.

Below is my 2014 post entitled “Should I Take Aspirin To Prevent Heart Attack or Stroke.”

Aspirin is a unique drug, the prototypical  two-edged sword of pharmaceuticals. It t has the capability of stopping platelets, the sticky elements in our blood, from forming clots that cause strokes and heart attacks when arterial plaques rupture, but it increases the risk of serious bleeding into the brain or from the GI tract. Despite these powerful properties, aspirin is available over the counter and is very cheap, thus anyone can take it in any dosage they want. 

Who Should Take Aspirin?

For the last five years I’ve been advising my patients who have no evidence of atherosclerotic vascular disease against taking aspirin to prevent heart attack and stroke. Several comprehensive reviews of all the randomized trials of aspirin had concluded by 2011 that

The current totality of evidence provides only modest support for a benefit of aspirin in patients without clinical cardiovascular disease, which is offset by its risk. For every 1,000 subjects treated with aspirin over a 5-year period, aspirin would prevent 2.9 MCE and cause 2.8 major bleeds.

(MCE=major cardiovascular events, e.g. stroke, heart attack, death from cardiovascular disease)

Dr. Oz, on the other hand, came to St. Louis in 2011 to have  lunch with five hundred women and advised them all to take a baby aspirin daily (and fish oil, which is not indicated for primary prevention as I have discussed here). When I saw these women subsequently in my office I had to spend a fair amount of our visit explaining why they didn’t need to take aspirin and fish oil.

After reviewing available data, the FDA this week issued a statementrecommending against aspirin use for the prevention of a first heart attack or stroke in patients with no history of cardiovascular disease (i.e. for primary prevention). The FDA pointed out that aspirin use is associated with “serious risks,” including increased risk of bleeding in the stomach and brain. As for secondary prevention for people with cardiovascular disease or those who have had a previous heart attack or stroke (secondary prevention), the available evidence continues to support aspirin use.

Subclinical Atherosclerosis and Aspirin usage

As I’ve discussed previously, however, many individuals who have not had a stroke or heart attack are walking around with a substantial burden of atherosclerosis in their arteries. Fatty plaques can become quite advanced in the arteries to the brain and heart before they obstruct blood flow and cause symptoms. In such individuals with subclinical atherosclerosis aspirin is going to be much more beneficial.

 

Guided Use of Aspirin

zerilloplaque
Large, complex atherosclerotic plaque in the carotid artery found by vascular screening in an individual with no history of stroke, heart attack, or vascular disease. This patient will definitely benefit from daily aspirin to prevent stroke or heart attack

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.

Coronary calcium is another, which I’ve written extensively about.

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 significant 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).

There are no randomized trials testing this approach but in the next few years several large aspirin trials will be completed and hopefully we will get a better understanding of who benefits most from aspirin for primary prevention.

Until then remember that aspirin is a powerful drug with potential for good and bad effects on your body. Only take it if you and your health care provider have decided the benefits outweigh the risks after careful consideration of your particular situation

Acetylsalicylically Yours,

-ACP

 

The inclusion criteria for ASPREE define significant cardiovascular disease as follows

a past history of cardiovascular or cerebrovascular event or established CVD, defined as myocardial infarction (MI), heart failure, angina pectoris, stroke, transient ischemic attack, >50% carotid stenosis or previous carotid endarterectomy or stenting, coronary artery angioplasty or stenting, coronary artery bypass grafting, abdominal aortic aneurysm

Heart Attacks and E-cigarettes: Are America’s Teens Putting Themselves At Risk?

Many of the skeptical cardiologist’s patients managed to quit cigarette smoking by using e-cigarettes . They often continue to vape, prolonging their addiction to nicotine but overall I felt they were probably better off than smoking cigarettes. However,  a couple of recent articles have me very concerned about the overall effect of e-cigarettes on public health.

The first article came from the PR department at  UCSF with the headline:

Smoking E-Cigarettes Daily, Doubles Risk Of Heart Attacks”

It focused on an abstract presented in Baltimore in February 2018 by Stanton Glantz, UCSF professor of medicine and director of the UCSF Center for Tobacco Control Research and Education. The abstract (paper yet to be published) was an observational study of about 70,000 individuals. Since it was observational the causality implied by the headline is not justified but the findings are still worrisome:

When adjusted for other risk factors, daily e-cigarette use was associated with significantly increased odds (Odds Ratio: 1.79) of having had a heart attack (myocardial infarction), as was daily conventional cigarette smoking (OR: 2.72). Former and occasional e-cigarette use were not associated with significant changes in the odds of having had a heart attack, while the same categories of cigarette smoking were associated with smaller increases in risk than for current smokers.

So e-cigarettes might be safer than real cigarettes but if you don’t quit smoking you are worse off:

“E-cigarettes are widely promoted as a smoking cessation aid, but for most people, they actually make it harder to quit smoking, so most people end up as so-called ‘dual users’ who keep smoking while using e-cigarettes,” said Glantz. “The new study shows that the risks compound. Someone who continues to smoke daily while using e-cigarettes daily has an increased risk of a heart attack by a factor of five.

Juul and The Rise In Teenage Vaping

The second article was from The New Yorker and is fascinating. Entitled “The Promise of Vaping and the Rise of Juul.” ,  it details an alarming rise in teenage vaping which often involves a particular brand of e-cigarette, Juul,  which resembles a flash drive.

Screen Shot 2018-05-22 at 12.13.01 PM
“Smoking is gross,” a high schooler said. “Juuling is really what’s up.”Photograph by Elizabeth Renstrom for The New Yorker

To Juul (the brand has become a verb) is to inhale nicotine free from the seductively disgusting accoutrements of a cigarette: the tar, the carbon monoxide, the garbage mouth, the smell. It’s an uncanny simulacrum of smoking. An analyst at Wells Fargo projects that this year the American vaporizer market will grow to five and a half billion dollars, an increase of more than twenty-five per cent from 2017. In the latest data, sixty per cent of that market belongs to Juul.

Scientists Warn of E-cigarette Health Risks 

In March, a congressionally mandated report on the health effects of e-cigarettes  from the National Academies of Sciences, Engineering, and Medicine concluded:

Evidence suggests that while e-cigarettes are not without health risks, they are likely to be far less harmful than conventional cigarettes, the report says. They contain fewer numbers and lower levels of toxic substances than conventional cigarettes, and using e-cigarettes may help adults who smoke conventional cigarettes quit smoking.

With respect to cardiovascular diseases, their conclusions were:

  1. We don’t currently have evidence that e-cigarettes increase risk of stroke or heart attack or subclinical atherosclerosis
  2. There is good evidence that in the short term the nicotine in e-cigarettes raises systolic and diastolic blood pressure and heart rate
  3. There is limited evidence that e-cigarettes increase biomarkers of oxidative stress, increase endothelial dysfunction and arterial stiffness. All of these factors are known to contribute to the development of atherosclerosis.

Long term, it is anyone’s guess what the consequences of vaping on the cardiovascular system will be.

As the New Yorker article makes abundantly clear, however, the youth of America are taking up vaping and Juuling increasingly and the National Academies are appropriately worried:

However, their long-term health effects are not yet clear. Among youth — who use e-cigarettes at higher rates than adults do — there is substantial evidence that e-cigarette use increases the risk of transitioning to smoking conventional cigarettes

Are Your Kids Vaping?

In 2015 there was a 40% chance your middle school or high school child had used e-cigarettes. The chart below from the CDC shows how rapidly rates are climbing.

The surgeon general/CDC issued a warning in 2016, writing:

E-cigarette use among U.S. youth and young adults is now a major public health concern. E-cigarette use has increased considerably in recent years, growing an astounding 900% among high school students from 2011 to 2015. These products are now the most commonly used form of tobacco among youth in the United States, surpassing conventional tobacco products, including cigarettes, cigars, chewing tobacco, and hookahs. Most e-cigarettes contain nicotine, which can cause addiction and can harm the developing adolescent brain.

Compared with older adults, the brain of youth and young adults is more vulnerable to the nega- tive consequences of nicotine exposure. The effects include addiction, priming for use of other addic- tive substances, reduced impulse control, deficits in attention and cognition, and mood disorders. Furthermore, fetal exposure to nicotine during pregnancy can result in multiple adverse consequences, including sudden infant death syndrome, altered corpus callosum, auditory processing deficits, effects on behaviors and obesity, and deficits in attention and cognition. Ingestion of e-cigarette liquids con- taining nicotine can also cause acute toxicity and possibly death if the contents of refill cartridges or bottles containing nicotine are consumed.

Stealth Vaping Devices

Vaping devices no longer clearly look like cigarettes. Here are some examples from the CDC report.

 

 

 

 

 

 

 

 

Note, however, that the Juul is not depicted.

By Mylesclark96 [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)%5D, from Wikimedia Commons
It doesn’t look like a cigarette or a device that would be facilitating your child’s addiction to nicotine. And it has a USB port so it can be recharged from a laptop.

 

 

This wasn’t an issue as far as I can tell when my children were teens but I’m pretty sure if I had teenagers I would ban vaping and would confiscate anything that resembled an e-cigarette including  flash or thumb drives that aren’t flash or thumb drives.

Skeptically Yours,

-ACP

What You Should Know About Lipoprotein(a) And Heart Attack Risk

If you have had a heart attack at an early age or one of your parents did but your standard risk factors for coronary heart disease are normal you should consider getting tested for Lipoprotein(a) or Lp(a).

The standard lipid profile that most patients get checks LDL (bad) HDL (good) and total cholesterol along with  triglycerides. While these are useful, I have many patients who have normal standard values but have developed advanced coronary heart disease at an early age despite following a perfect lifestyle (not smoking, regular aerobic exercise, healthy diet.)

The skeptical cardiologist tests such patients for Lp(a) (pronounced LP little a)  and it is quite frequently elevated.

For patients, these are the facts to know about Lp(a)

  1. It is the strongest single inherited (monogenetic) risk factor for the early development of coronary artery disease, heart attacks and strokes.
  2. In addition to increasing risk of atherosclerosis, high Lp(a) is strongly associated with the development of calcific aortic valve disease which can result in narrowing of the aortic valve and aortic stenosis.
  3. Depending on the cut-off used  up to one in five individuals may have elevated Lp(a)
  4. Levels of Lp(a) can be measured with a simple blood test that should cost no more than 50 to 100$. This is not included in standard lipid or cholesterol testing.
  5. Risk for heart attack starts to rise with levels above 30 mg/dl and Canadian guidelines from 2016 (see here)) consider >30 mg/dl to be a risk factor and they recommend measuring Lp(a) in those with a family history of premature CAD or those at intermediate risk.
  6. The European Atherosclerosis Society (EAS, 2010), suggested levels of <50 mg/dl as optimal. The EAS advised measuring Lp(a) once in all patients with premature CVD.
  7. As levels get even higher risk also rises as these graphs show

 

 

 

 

Treatment For High Lp(a)

The lifestyle changes (both exercise and diet) that improve bad and good cholesterol levels have no effect on Lp(a). Our best drugs, the statins, for reducing risk of heart attack and stroke also don’t lower Lp(a) levels.

Only niacin has been shown to reduce Lp(a) across broad populations but there is no evidence that Lp(a) lowering by niacin lowers cardiovascular risk so it cannot be recommended for treatment.(In the AIM-HIGH study niacin did not reduce cardiovascular events in patients with Lp(a) with levels>50 mg/dl, despite achieving a mean Lp(a) reduction of 39%.)

Cholesteryl ester transfer protein inhibitors which raise HDL levels also reduce lipoprotein(a) concentrations, but three such inhibitors have not shown a clinical benefit.

In fact, currently there are no studies showing that lowering Lp(a) with any drug will effectively lower the associated risk of heart attack, stroke and aortic stenosis.

In the not too distant future, effective therapies may emerge. There are promising newer agents (antisense oligonucleotides or ASOs) currently in clinical trials and in limited populations the PCSK9 inhbitors, mipomersen and estrogen have lowered Lp(a) levels.

Why Test For Lp(a)?

If we have no effective therapies that work by lowering Lp(a) why recommend testing for it?

I test Lp(a) for  two reasons.

First, since it is inherited, patients with high levels should consider having first degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.

Second, I tend to recommend  more aggressive cholesterol lowering in patients who have evidence for early plaque build up for atherosclerotic events early in life than I otherwise would be.     I tend to agree with the approach diagrammed below:

 

With this approach for patients who have had events related to atherosclerosis or advanced CAC for age we work super aggressively on optimizing all risk factors. I try to lower LDL to <70 with statins and with the addition of ezetimibe or PCSK9 inhbitors if needed.

If the patient has more problems with atherosclerotic events despite optimizing risk factors and Lp(a) >60 mg/dl, some experts recommend using apheresis a technique which runs the patient’s blood through a filter which removes LDL and Lp(a). Personally, I have not sent any patients for apheresis and await better studies proving its benefit.

Antiproatherogenically Yours,

-ACP

For those patients seeking more detailed information and references I recommend Dr. Siggurdson’s excellent post on Lp(a)

There is a Lipoprotein(a) Foundation with reasonably informative and accurate website you can peruse here for more information.

Finally, if you want to delve deeply into the data check out this recent JACC review here.

The graphs above and this figure
showing the proposed pro-inflammatory, pro-atherogenic and pro-thrombotic pathways of Lp(a) are from that article.

 

Thoughts On Prolonged Bleeding Whilst Taking Baby Aspirin

I was hurriedly shaving the other day and felt a sharp stinging sensation in my philtrum.  Shortly thereafter, blood began pouring forth from the area and dribbling into my mouth.

I don’t typically name-check the area between the nose and the margin of the upper lip, but if one cuts the area (and wants to write about the experience), it is useful to have a single noun that describes it precisely.

This is not my philtrum but the graphic nicely demonstrates why the area is often called “cupid’s bow”. Courtesy of Wkipedia

The human philtrum is apparently vestigial; per Wikipedia

The philtrum (Latin: philtrum, Greek: φίλτρονphiltron, lit. “love charm”[2]), or medial cleft, is a vertical groove in the middle area of the upper lip, common to many mammals, extending in humans from the nasal septum to the tubercle of the upper lip. Together with a glandular rhinarium and slit-like nostrils, it is believed[by whom?] to constitute the primitive condition for mammals in general.

Although lacking function, it does cause a protrusion in the otherwise smooth facade of the face, and as a consequence, is at an increased risk for cuts.

Despite holding pressure on the cut for many minutes and daubing it with toilet paper, it continued to bleed. The bleeding continued on for much longer than I am use to, and after a while I realized that my bleeding was prolonged due to the aspirin I have been taking.

I’ve been following my own advice to those with documented significant atherosclerotic plaque, and have been taking 81mg aspirin daily. I began chewing daily my chewable aspirin after writing my post on the best form of baby aspirin to take. Prior to that it was only intermittently.

BARCing Up the Willow Tree

As a cardiologist I commonly hear patients complain about the nuisance of bruising and bleeding caused by the aspirin and other blood thinners I have prescribed them. Now I had joined their ranks.

Doctors mostly worry about major bleeding caused by aspirin; things like bleeding from the gastrointestinal (GI) tract, or into the head. A recent review found that baby aspirin doubles the risk of bleeding from the upper GI tract, and increases the risk of intracranial hemorrhage by a factor of 1.4.

There is relatively little concern about the type of minor bleeding I experienced. However, beginning in 2010, the Bleeding Academic Research Consortium (BARC) investigators came up with a more precise way of categorizing bleeding events, the BARC bleeding types.

By far, the most common bleeding on aspirin is the kind I had: Type 1 BARC.

Type 1: bleeding that is not actionable and does not cause the patient to seek unscheduled performance of studies, hospitalization, or treatment by a healthcare professional. Examples include, but are not limited to, bruising, hematoma, nosebleeds, or hemorrhoidal bleeding for which the patient does not seek medical attention. Type 1 bleeding may include episodes that lead to discontinuation of medications by the patient because of bleeding without visiting a healthcare provider.

Indeed, my Type 1 bleeding prompted me to skip my aspirin doses for the next few days.

Many patients do the same thing. Just this morning a patient told she had stopped taking her aspirin because she thought it was causing “little red spots” on her arms.

Does Prolonged Bleeding Mean You Are Taking Too Much Aspirin?

My philtrum persisted in bleeding, and as I felt the need to use my hands for something other than holding pressure, I put a band-aid on the area (actually a Nexcare), which temporarily stemmed the bleeding tide: I began pondering if I was taking too much aspirin.

Since aspirin is so widely used to prevent heart attacks and strokes caused by sticky platelets, why isn’t there a way to see how effective it is at making sticky platelets less sticky?  We have such methods for blood pressure meds (blood pressure levels) and cholesterol lowering drugs (cholesterol levels).

And for the older blood thinner warfarin, we have a blood test which helps us make sure the dosage of medication is keeping the blood thinning in a range that maximizes  effectiveness and minimizes bleeding risk.

It turns out there are lots of ways to measure how effective aspirin is in an individual, but no consensus on which particular method should be used, and authorities don’t recommend we make such measurements.

This article on platelet function tests lists 13 different platelet function tests, ranging from the mostly historical “bleeding time” to sophisticated tests of platelet aggregation.

The  Verify Now test (not available in the US) of platelet reactivity predicted in one study which patients would have BARC type I bleeding like mine.  The test did not predict major bleeding complications, things like GI bleeding and intracranial hemorrhage.

Those patients who had minor bleeding problems were more likely to be noncompliant, stopping their aspirin therapy.

I could easily visualize the following  scenario as the blood began pooling underneath my band-aid and progressing down my philtrum.

Let’s say I’ve just had a heart attack and had a drug-eluting stent placed in one of my coronary arteries. I’ve been started on aspirin and another anti-platelet drug. I cut myself and bleed excessively and prolongedly. I decide that the aspirin is the reason, and start skipping doses. The lower aspirin levels subsequently allow my platelets to become sticky again. As a result a clot forms in my coronary stent and a heart attack ensues.

Thus, prolonged bleeding from a cut, considered a minor side effect of aspirin therapy, could increase heart attack risk.

There is a clinically available test for aspirin effect called AspirinWorks.

The AspirinWorks Test Kit is an enzyme-linked immunoassay (ELISA) to determine levels of 11-dehydrothromboxane B2 (11dhTxB2) in human urine, which aids in the qualitative detection of aspirin effect in apparently healthy individuals post ingestion. Unlike platelet aggregation tests, which require freshly drawn blood that must be evaluated within at least four hours, the AspirinWorks Test is performed on a random urine sample that can easily be obtained in any doctor’s office.

AspirinWorks points out the putative benefits of testing for aspirin effect:

An increasing body of evidence in the medical literature overwhelmingly supports clinically significant variability in aspirin effect, which has been well-established in findings from trials, including the Heart Outcomes Prevention Evaluation (HOPE) Study and the CHARISMA trial published in Circulation (Journal) (2002 and 2008). These trials have demonstrated that:

  1. Increased levels of urinary 11dhTxB2 are associated with as much as a four fold increased risk for adverse cardiovascular events or death.
  2. Statin treatment is associated with lower concentrations of 11dhTxB2
  3. 11dhTxB2 is an independent, modifiable predictor of risk for stroke, heart attack and cardiac death (CHARISMA).

I have never ordered this test and am unaware of any other physicians ordering it on their patients.

Doctors don’t test for aspirin effect in individual patients because it is expensive and it won’t change our approach in most cases.
Taking  81 mg aspirin daily might be too high a dose to optimize the balance between bleeding and clotting in me.  If I took it every other day I might have less Type I BARC episodes. However, we don’t have any good evidence that adjusting the dosage based on aspirin effectiveness testing will improve my outcomes.
Thus, we bleeders on baby aspirin (the BOBA) of the world must find better ways of dealing with minor bleeding.
When I changed the band-aid on my philtrum several hours after the initial cut, I began actively bleeding again. This time I decided to apply ice to the area to vasoconstrict the arteries. This, plus more pressure and time, almost completely stopped the bleeding.
Another Nexcare was applied to the area, and when it was removed the next morning, the bleeding did not resume.
There are a variety of other measures that can be tried with varying degrees of success, as described here (deodorant, lip balm, listerine, Visine) and here (styptic pencils and powders, cayenne pepper, tea bag, sugar, alum-ironically this article mentions making a paste out of aspirin and applying it to the cut).
There also appears to be a thriving industry devoted to commercial  products for stopping bleeding from minor cuts outlined here.
Should We Worry About Minor Bleeding?
Ultimately, the seemingly excessive bleeding one experiences upon incidentally cutting oneself while taking aspirin is best viewed as a reassuring sign that the drug is doing its job: Your platelets are less sticky, less likely to cause bad clots that cause strokes and heart attacks.
Platelets don’t know bad from good clots, they just react indiscriminately.
The small amount of blood that exudes from superficial cuts can be scary but it can be controlled with fairly simple measures.
The little red dots my patient experiences, although unattractive, are benign.
Styptically Yours,
-ACP

Do The Zen Diaries of Garry Shandling Yield Insight Into The Cause of His Death?

The skeptical cardiologist watched a little bit of the Judd Apatow HBO Documentary on Garry Shandling last night. For fans of the comedian like me, it is fascinating. As I watched I was reminded of two posts I had written about the cause of his death and the physician detective in me searched for clues to his ultimate demise.

Right after his sudden death at the age of 66, media sources reported that he had died of a massive heart attack “according to insiders.”

At the time, TMZ reported that  “Sources familiar with the situation tell TMZ Shandling died from a massive heart attack, with no prior warning whatsoever”

In a post I wrote entitled “Do You Know What is on Garry Shandling’s and Your Parent’s Death certificate?” I pointed out that his cause of death was unknown and that:

Although a heart attack resulting in ventricular fibrillation is the most common cause of a sudden, unexpected death in individuals over the age of 40, it is not the only one.

In fact, People  magazine reported that Sanders experienced shortness of breath and pain in his legs just a day before his death, and that he spoke to a doctor friend about his symptoms, who stopped by that night to check on him,

Shortness of breath and pain in the legs raise the possibility of a clot or DVT in the leg, which can break loose and embolize into the pulmonary arteries. Such a pulmonary embolism, if massive, can result in swift and sudden death.

I wrote another post on this after his autopsy was released.

His autopsy revealed that he  died from a pulmonary embolism, the disease I had raised as a likely  alternative cause of his sudden death in my post in April, 2016. The actual death certificate can be viewed here.

The medical report on his death reveals that Shandling had a prior
history of clots in the leg (s) (DVT) and that previously he had had an IVC filter implanted.

An IVC filter is an umbrella shaped device that is inserted into the major vein draining blood from the the lower half of the body (the inferior vena cava) to physically obstruct the vein and thereby prevent clots from reaching the pulmonary artery. These are used in cases where the normal medical treatment for blood clots (anticoagulants or blood thinners) can’t be utilized due to bleeding risk or have proven ineffective.

Although effective 95% of the time in preventing legs clots from migrating to the pulmonary artery there are reported failures and Shandling was clearly one.

Risk factors for DVT and PE include cancer, surgery and immobility. Shandling, it appears, was recently in Hawaii and long plane flights like the one he must have taken back to LA are notorious causes of immobility that can lead to DVT.

What Can We Learn From Shandling’s Death

Some take home points

-When some one dies suddenly and unexpectedly  it is not automatically due to a massive heart attack. Do not assume your family member or spouse who  was found dead in bed suffered a myocardial infarction.

-Unless the victim was quite old or had advanced cancer consider asking for an autopsy to find out the true cause of death. Whatever disease caused the death could be  inherited by the victim’s offspring.

-Pulmonary embolism can be a rapidly lethal disease. Consider a medical evaluation for it if you are experiencing leg pain/swelling, sudden, unexplained shortness of breath or chest pain which worsens upon taking a breath. If you have risk factors for leg clots or prior leg clots be even more vigilant.

 

Watching the Zen Diaries of Garry Shandling gave me no further insights into his death. Sudden death typically happens without warning to the victim and even those who are closest to him/her.

Antithrombotically Yours

-ACP

 

N.B. In the second post I talked about Carrie Fisher’s death (also widely reported falsely as due to a “massive heart attack”) and speculated that we might never know the cause of her death because I anticipated that her autopsy (with toxicology) would not be released.

I was right about her not dying of a “massive heart attack” .

Her cause of death was listed as sleep apnea with other factors.

The other factors appear to be LOTS of drugs:

“Fisher’s toxicology review found evidence of cocaine, methadone, MDMA (better known as ecstasy), alcohol and opiates when she was rushed to Ronald Reagan UCLA Hospital on Dec. 23, a toxicology report showed.”

No autopsy was done per family request but CT scanning was performed.

Still More Evidence That Fish Oil Supplements Do Not Prevent Cardiovascular Disease

Avid readers of the skeptical cardiologist know that he is not an advocate of fish oil supplements.

One of my first posts (1/2013) was devoted to taking down the mammoth OTC fish oil industry because recent scientific evidence was clearly showing no benefit for fish oil pills.

I concluded:

", the bottom line on fish oil supplements is that  the most 
recent scientific evidence does not support any role for them  inpreventing heart attack, stroke, or death. There are potential 
down sides to taking them, including contaminants and the impact on the marine ecosystem. I don’t take them and I advise my
patients to avoid them (unless they have triglyceride levels 
over 500.)"

Despite a lack of evidence supporting taking them, the fish oil business continues to grow,  buttressed by multiple internet sites promoting various types of fish oil (and more recently krill oil)  for any and all ailments and a belief in the power of “omega-3 fatty acids”.

Another Meta-Analysis Concludes No Benefit To Fish Oil Supplements

A publication this month evaluated the 10 randomized controlled trials involving 77 917 thousand individuals that have studied fish oil supplements in preventing heart disease. The writers concluded that fish oil supplements do not significantly prevent any cardiovascular outcomes under any scenario.

It was written by a group with the ominous title of “The Omega-3 Treatment Trialists’ Collaboration.”

The Omega-3 Treatment Trialists’ Collaboration was established to conduct a collaborative meta-analysis based on aggregated study-level data obtained from the principal investigators of all large randomized clinical trials of omega-3 FA supplements for the prevention of cardiovascular disease, using a prespecified protocol and analysis plan. The aims of this meta-analysis were to assess the associations of supplementation with omega-3 FAs on (1) fatal CHD, nonfatal MI, stroke, major vascular events, and all-cause mortality and (2) major vascular events in prespecified subgroups.

The authors conclusions:

. Randomization to omega-3 fatty acid supplementation (eicosapentaenoic acid dose range, 226-1800 mg/d) had no significant associations with coronary heart disease death (rate ratio [RR], 0.93; 99% CI, 0.83-1.03; P = .05), nonfatal myocardial infarction (RR, 0.97; 99% CI, 0.87-1.08; P = .43) or any coronary heart disease events (RR, 0.96; 95% CI, 0.90-1.01; P = .12). Neither did randomization to omega-3 fatty acid supplementation have any significant associations with major vascular events (RR, 0.97; 95% CI, 0.93-1.01; P = .10), overall or in any subgroups, including subgroups composed of persons with prior coronary heart disease, diabetes, lipid levels greater than a given cutoff level, or statin use.

Nothing. Nada. No benefit.

There is clearly no reason to take fish oil supplements to prevent cardiovascular disease!

American Heart Association Sheepishly Recommends Fish Oil Supplements

If the science was conclusive on this in 2013 why did the American Heart Association (AHA) issue an “advisory” in 2017  suggesting that the use of omega-3 FAs for prevention of coronary heart disease (CHD) is probably justified in individuals with prior CHD and those with heart failure and reduced ejection fractions?

The AHA advisory is clearly misguided and relies heavily in its discussion on a 2012 meta-analysis from Rizos, et al. published in 2012.

Oddly, this is the study that prompted me to write my first fish oil post in 2013

The AHA advisory totally distorts the completely negative conclusions of the Rizos meta-analysis, writing:

A meta-analysis published in 2012 examined the effects of omega-3 PUFA supplementation and dietary intake in 20 RCTs that enrolled patients at high CVD risk or prevalent CHD and patients with an implantable cardioverter-defibrillator (total n=68 680). That meta-analysis demonstrated a reduction in CHD death (RR, 0.91; 95% CI, 0.85–0.98), possibly as the result of a lower risk of SCD (RR, 0.87; 95% CI, 0.75–1.01).11

Strangely enough, if you look at the conclusions of Rizos, et al. they are

No statistically significant association was observed with all-cause mortality (RR, 0.96; 95% CI, 0.91 to 1.02; risk reduction [RD] -0.004, 95% CI, -0.01 to 0.02), cardiac death (RR, 0.91; 95% CI, 0.85 to 0.98; RD, -0.01; 95% CI, -0.02 to 0.00), sudden death (RR, 0.87; 95% CI, 0.75 to 1.01; RD, -0.003; 95% CI, -0.012 to 0.006), myocardial infarction (RR, 0.89; 95% CI, 0.76 to 1.04; RD, -0.002; 95% CI, -0.007 to 0.002), and stroke (RR, 1.05; 95% CI, 0.93 to 1.18; RD, 0.001; 95% CI, -0.002 to 0.004) when all supplement studies were considered.

Nothing. Nada. No significant benefit!

The AHA was so confused by their own advisory that in the AHA news release on the article they quote Dr. Robert Eckel, a past AHA president as saying he remains “underwhelmed” by the current clinical trials.

“In the present environment of evidence-based risk reduction, I don’t think the data really indicate that fish oil supplementation is needed under most  circumstances.”

The end of the AHA news article goes on to quote Eckel as indicating he doesn’t prescribe fish oil supplements and the science advisory won’t change his practice:

Eckel said he doesn’t prescribe fish oil supplements to people who have had coronary events, and the new science advisory won’t change that. “It’s reasonable, but reasonable isn’t a solid take-home message that you should do it,” he said.

AHA: Wrong On Coconut Oil and Fish Oil

It’s hard for me to understand why the AHA gets so many things wrong in their scientific advisories. In the case of the recent misguided attack on coconut oil , their ongoing vilification of all saturated fats, and their support for fish oil supplements I don’t see evidence for industry influence. The authors of the fish oil supplement advisory do not report any financial conflicts of interest.

There is, however, one bias that is very hard to measure which could be playing a role: that is the bias to agree with what one has previously recommended.  The AHA issued an advisory in 2002 recommending that people take fish oil. Changing that recommendation would mean admitting that they were wrong and that they had contributed to the growth of a 12 billion dollar industry serving no purpose.

Personally, I am aware of this kind of bias in my own writing and strive to be open to new data and publications that challenge what I personally believe or have publicly recommended.

In the case of fish oil supplements for preventing cardiovascular disease, however, the most recent data supports strongly what I wrote in 2013:

Don’t take fish oil supplements to prevent heart disease.

Americans want a “magic-bullet” type pill to take to ward off aging and the diseases associated with it. There isn’t one. Instead of buying pills and foods manipulated and processed by the food industry which promise better health, eat real food (including fish) eat a lot of plants and don’t eat too much.

Piscinely Yours,

-ACP

N.B. I have no patients on the two prescription fish oil supplements available, Lovaza and Vascepa. I wrote about Vascepa here

Below is an excerpt:

Like the first prescription fish oil available in the US, Lovaza, VASCEPA is only approved by the FDA for treatment of very high triglycerides (>500 mg/dl).

This is a very small market compared to the millions of individuals taking fish oil thinking that  it is preventing heart disease.

The company that makes Vascepa (Amrin;$AMRN)would also like to have physicians prescribe it to their patients who have mildly or moderatelyelevated triglycerides between 200 and 500 which some estimate as up to 1/3 of the population.

The company has a study that shows that Vascepa lowers triglycerides in patients with such mildly to moderately elevated triglycerides but the FDA did not approve it for that indication.

Given the huge numbers of patients with trigs slightly above normal, before approving an expensive new drug, the FDA thought, it would be nice to know that the drug is actually helping prevent heart attacks and strokes or prolonging life.

After all, we don’t really care about high triglycerides unless they are causing problems and we don’t care about lowering them unless we can show we are reducing the frequency of those problems.

Data do not exist to say that lowering triglycerides in the mild to moderate range  by any drug lowers heart attack risk.

In the past if a company promoted their drug for off-label usage they could be fined by the FDA but Amarin went to court and obtained the right to promote Vascepa to physicians for triglycerides between 200 and 500.

Consequently, you may find your doctor prescribing this drug to you. If you do, I suggest you ask him if he recently had a free lunch or dinner provided by Amarin, has stock in the company (Vascepa is the sole drug made by Amrin and its stock price fluctuates wildly depending on sales and news about Vascepa) or gives talks for Amarin.

If he answers no to all of the above then, hopefully, your triglycerides are over 500.

.

 

 

 

 

Which Kind of Baby Aspirin Should I Take To Prevent Heart Attack? Chewable Versus Enteric Coated Versus Regular

The skeptical cardiologist recently asked his Eternal Fiancée to grab a bottle of baby aspirin  while she was at the local Walgreen’s. Aspirin or acetyl salicylic acid (ASA) comes in either a 325 mg dose or in a low dose which can be between 75 to 100 mg and is often called “baby” aspirin.

However, since a link between aspirin use and a potentially lethal disease called Reye’s syndrome was identified in the 1980s, no authorities recommend aspirin in children or babies, and the low dose ASA (LDASA) is primarily marketed and used for prevention of cardiovascular disease.

Although Bayer and Dr. Oz would have us believe that all individuals over the age of 55 should be taking LDASA, as I pointed out here in 2014, the FDA no longer recommends it for prevention of cardiovascular disease.

The US Preventive Services Task Force, on the other hand, recognizes certain individuals without heart disease who benefit from LDASA:

The USPSTF recommends initiating low-dose aspirin use for the primary prevention of cardiovascular disease (CVD) and colorectal cancer (CRC) in adults aged 50 to 59 years who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years.
I’m 63  years old, so the USPTF recommendation for me to take LDASA is a little less enthusiastic:
The decision to initiate low-dose aspirin use for the primary prevention of CVD and CRC in adults aged 60 to 69 years who have a 10% or greater 10-year CVD risk should be an individual one. Persons who are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit. Persons who place a higher value on the potential benefits than the potential harms may choose to initiate low-dose aspirin.
Following my own advice (see here), I have started taking 81mg of aspirin regularly (well, when I remember) in order to prevent stroke and heart attack. I do have subclinical atherosclerosis with a plaque in my LAD, and I think the aspirin will make my platelets less sticky and less likely to form clots if my plaque ruptures, thereby reducing my chances of an acute heart attack.
I am willing to accept the increased risk of bleeding from the gastrointestinal tract and hemorrhagic stroke associated with LDASA use.

Previous to this I had been taking ASA from little sample bottles that Bayer sends to my office. These bottles are quite annoying as they are stuffed with cotton and contain very few pills making extrication of the tiny pills an exercise in futility (I am using this as an excuse for my lack of regularity in taking them).

There’s no reason to pay the premium for Bayer ASA despite the company’s advertising attempts to link inextricably their name with ASA.  Aspirin is aspirin, whether Bayer made it or Walgreens. In Bayer’s defense, their website has reasonable information on heart attacks and they appear to be giving aspirin away to people named Smith.

But what type of aspirin should you get? Enteric-coated, safety-coated, delayed release, chewable?

Chewable Aspirin

I asked the Eternal Fiancée to buy the cheapest baby aspirin possible.

She ended up buying a chewable formulation with orange flavoring, presumably aimed at children:

When I put one of these in my mouth I tasted the sickly sweet taste of an artificial sweetener. The ingredients are listed as: Dextrates, Ethyl Cellulose, FD&C Yellow 6 Aluminum Lake, Orange Flavor, Sodium Saccharin, Starch. Saccharine! Yikes!

The only reason to chew ASA is if you are having an acute heart attack.

In this situation, chew 4 of the LDASA or one regular 325 mg aspirin.  Chewing the aspirin makes the levels rise faster in your blood stream and can help dissolve the clot causing your heart attack more rapidly.

How do you know if you are having a heart attack? This is actually a very difficult question to answer with certainty. See here for a reasonable discussion.

Low Dose Aspirin: Enteric-Coated versus Non-coated

It is very difficult (perhaps impossible) to find low dose, non-chewable ASA that has not been “safety-coated” or “enteric-coated.” These formulations have become popular by promoting the idea that they are less likely to cause stomach pain or bleeding.

The concept is that the coating leads to delaying the aborption of the ASA until it reaches the small intestines where, presumably, it will do less damage. However, there is no good evidence to support lower bleeding risk with enteric-coasted (EC) ASA.

There is, on the other hand, very good evidence that therapeutic levels of aspirin in the bloodstream, and therefore the speed and efficacy of ASA in preventing heart attacks, is reduced by these “safety” formulations.

The most recent study showing this was published in 2017.

Volunteers were given either 325mg regular ASA or 325mg EC ASA and researchers looked at how each formulation effected platelet activity.  The onset of antiplatelet activity was determined by the rate and extent of inhibition of serum thromboxane B2(TXB2) generation.

The EC ASA took longer and was less effective at blocking platelet activity than plain ASA. Presumably, this translates into lower efficacy in preventing heart attacks and strokes.

Therefore,  if you feel like you are having a heart attack, chew ASA which is not enteric or safety-coated. Yes, you can chew a regular 325 mg ASA pill. Or you can chew 4 of the LDASA, preferably uncoated but still helpful if coated.

If it turns out you weren’t having a heart attack there is no down side to having chewed 325 mg ASA.

I just spent a fair amount of time trying to find non EC, non-chewable LDASA online and failed.

For the time being I will be swallowing daily the orange chewable LDASA and I will carry a bottle around in my satchel for emergency use.

Salicylically Yours,

-ACP

N.B. Aspirin is generally recommended in secondary prevention of cardiovascular disease, ie. for those who have had heart attacks, stents or bypass surgery . For a good review of the evidence for this see here.

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.

I pointed out that his previous  score was average for white men his age and his repeat score is also similar to the average white male of 71 years.

Entering Trump’s numbers into the MESA coronary calculator shows us he is at the 46th percentile, meaning that 46% of white men his age have less calcium.We can also calculate Trump’s 10 year risk of heart attack and stroke using the app from the ACC (the ASCVD calculator) and entering in the following information obtained from the White House press briefing:

Total Cholesterol          223

LDL Cholesterol            143

HDL Cholesterol              67

Systolic Blood Pressure 122

Never Smoked Cigarettes

Taking aspirin 81 mg and rosuvastatin (Crestor) 10 mg.

His 10 year risk of heart attack or stroke is 16.7%.

Given that his calcium score is average it doesn’t change his predicted risk and the conclusion is that his risk is identical to the average 71 year old white man-moderate.

We also know that Trump had an exercise stress echocardiogram which was totally normal and therefore can be reasonably certain that the moderate plaque build up in his arteries is not restricting the blood flow to his heart.

Here is what Dr. Jackson said about the stress echo:

He had an exercise stress echocardiogram done, which demonstrated above-average exercise capacity based on age and sex, and a normal heart rate, blood pressure, and cardiac output response to exercise.  He had no evidence of ischemia, and his wall motion was normal in all images. the stress echo:

The New York Times article on this issue, entitled “Trump’s Physical Revealed Serious Heart Concerns, Outside Experts Say”  however, presents a dramatically worrisome and misleading narrative.

It quotes several cardiologists who were very concerned about Trump’s high LDL level, weight and diet.

It’s interesting that some of the experts quoted in the NY Times piece feel that Trump’s Crestor dose should be increased in light of the recent NY  Times piece questioning whether the elderly should take statins at all.

If we have serious concerns about Trump’s heart then we should have the same concerns about every 71 year old white man because he is totally average with regard to cardiac risk. In addition he is on a statin and on aspirin, the appropriate drugs to reduce risk.

In contrast to the average 71 year old male he has had a battery of cardiac tests which show exactly where he stands cardiac wise.

Most of these cardiac tests we would not recommend to an asymptomatic individual of any age. Jackson revealed that Trump had an EKG and an echocardiogram.

His ECG, or commonly EKG, was normal sinus rhythm with a rate of 71, had a normal axis, and no other significant findings.

He had a transthoracic echocardiogram done, which demonstrated normal left ventricular systolic function, an ejected fraction of 60 to 65 percent, normal left ventricular chamber size and wall thickness, no wall motion abnormalities, his right ventricle was normal, his atria were grossly normal, and all valves were normal.

So our President has a normal heart for a 71 year old white male. This automatically puts him at moderate risk for heart attack and stroke over the next 10 years but he is being closely monitored and appropriately treated and should do well.

Nonalarmingly Yours,

-ACP

N.B. I see that Trump’s LDL was reported previously as 93. The current LDL of 143 suggests to me that he has not been taking his Crestor.

N.B. Below is an excerpt from my prior post which explains coronary calcium

Regular readers of the skeptical cardiologist should be familiar with the coronary calcium scan or score (CAC) by now.  I’ve written about it a lot (here, here, and here) and use it frequently in my patients, advocating its use to help better assess certain  patient’s risk of sudden death and heart attacks.

coronary calcium
Image from a patient with a large amount of calcium in the widowmaker or LAD coronary artery (LAD CA).

The CAC scan utilizes computed tomography (CT)  X-rays, without the need for intravenous contrast, to generate a three-dimensional picture of the heart. Because calcium is very apparent on CT scans, and because we can visualize the arteries on the surface of the heart that supply blood to the heart (the coronary arteries), the CAC scan can detect and quantify calcium in the coronary arteries with great accuracy and reproducibility.

Calcium only develops in the coronary arteries when there is atherosclerotic plaque. The more plaque in the arteries, the more calcium. Thus, the more calcium, the more plaque and the greater the risk of heart attack and death from heart attack.

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

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