Tag Archives: myocardial infarction

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

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.

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“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)], 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.

 

Do You Know What’s On Garry Shandling’s And Your Parent’s Death Certificate?

0324-garry-shandling-twitter-4
Better Call Saul’s Bob Odenkirk and Kathy Griffin “hanging” with an apparently healthy Larry Sanders on March 20. These two appeared on Shandling’s brilliant Larry Sanders TV show.

When someone who had appeared to be healthy dies suddenly, it is often assumed that he/she died of “a massive heart attack.” Certainly, this was the case in the recent unexpected sudden death of Garry Shandling, the actor and comedian.  Shandling, aged 66, died March 24 of this year.

ET online reported:

“His publicist Alan Nierob told the ET that Shandling had no history of heart problems, but that doctors believe he died as the result of a heart attack.”

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.

The LA Coroner’s office could not get Sanders’ physician to sign his death certificate and the cause of death has still apparently not been determined, pending toxicology testing which typically takes 6 weeks.

What’s On Your Parent’s Death Certificate

More important than what is on Garry Shandling’s death certificate is what is on your parent’s death certificate, and whether it is accurate. If one of your parents died prematurely and suddenly, it is  important to know with precision what caused it. If the cause was an heritable cardiovascular condition, hopefully, appropriate testing can determine if you have that condition, and steps can be taken to prevent your premature demise.

Examples of inherited cardiovascular conditions (in addition to heart attack (myocardial infarction) or pulmonary embolism) that can cause sudden and unexpected death include aortic aneurysm dissection, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasis, and long QT syndrome.

Unfortunately I find that, at least in my patients, uncertainty about the cause of death of one’s parents is the norm.

Many of my patients, for example, tell me one of their parents died of a “massive heart attack” and they assume that they are at increased risk of the same fate. When I press for details, typically no autopsy was performed.  Mom or dad may have been found dead at home, or they may have suddenly keeled over but not survived to make it to the hospital for a definitive diagnosis.

Without an autopsy in such circumstances, it is not possible to be sure of the cause of death.

Even if you have a cause of death listed on your parent’s death certificate, there is no guarantee that it is accurate.  The doctor that filled it out, without an autopsy in many circumstances, is just speculating on the cause based on what he/she knew about prior medical conditions and the circumstances surrounding the death.

I was recently asked to fill out the death certificate of an elderly patient of mine who had atrial fibrillation and congestive heart failure and was living in a nursing home.

One night she was noted by the staff to be very short of breath and was taken to a local  emergency room where she was pronounced dead.

Based on the information available to me, I had no idea what caused her death. Although she had quite signifiant cardiac problems, when I last saw her she was stable and I have numerous patients with the same conditions who live for decades.

I filled out the death certificate, listing all of her conditions, and entered in that the cause of death was unknown.

Although the CDC guide for physicians filling out death certificates clearly states that this is acceptable, I was subsequently informed that the funeral home did not accept unknown cause of death and that they had found another doctor to fill in a cause  of death.

I guarantee you, whatever he put on as the cause of death was total speculation.

Jerry Seinfeld was good friends with Garry Shandling and, oddly enough, not too long ago, featured him in an episode of his internet series “Comedians in Cars Getting Coffee” entitled “It’s Great That Garry Shandling Is Still Alive.

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Shandling mentions “I had hyperparathyroidism,” making a joke that “the symptoms are so much like being an older Jewish man, no one noticed!”

James Fallows, the excellent The Atlantic writer, highlights his own experience with hyperparathyroidism (a disease that leads to high calcium levels and is easily treated with surgery), in a recent Atlantic article. The subtitle of this article, “a rare and under-publicized condition that can sometimes be fatal,” suggests that hyperhyperparathyroidism might have led to Shandling’s death.

I don’t think this is likely because Shandling suggests that the disease is in the past tense (i.e. he has already had the surgery), and sudden death from hyperparathyroidism would be extremely unlikely.

Fortunately, Shandling is getting a full examination and autopsy to fully determine the cause of his death. If he has offspring, this will be extremely helpful to them in understanding what medical conditions they can expect later in life.

If he was not a celebrity, his death, like many of your parents’, most likely would have been ascribed to a “massive heart attack.”

 

 

Are We Springing Forward to Death?: Daylight savings time and myocardial infarction

Tonight we will lose an hour of our lives when we observe Daylight Savings Time (DST).

Media reports suggest that DST, beyond robbing of us that nocturnal hour in the spring are also increasing our risk of heart attack (myocardial infarction or MI) and death.

Is this a valid concern or just media hype on a slow news day?

Scientific studies on this topic are mixed.

A recent study from Finland found MI rates increased 16% on the Wednesday after spring DST time change and dropped by 15% on the Monday after fall DST time change.

A 2015 German study found no difference in MI rate in the 3days or 1 week after spring or fall DST transitions.

However, some American studies have detected a bump in MI rate on the day after DST transition in the spring and a similar drop in MI rate on the day after the fall DST change.

A study of 42000 patients undergoing acute PCI for MI in Michigan found that

“The Monday following spring time changes was associated with a 24% increase in daily AMI counts (p=0.011), and the Tuesday following fall changes was conversely associated with a 21% reduction (p=0.044). No significant difference in total weekly counts or for any other individual weekdays in the weeks following DST changes was observed.”

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They concluded:

Our data argue that DST could potentially accelerate events that were likely to occur in particularly vulnerable patients and does not impact overall incidence. There is considerable controversy over the health and economic benefits of DST, and some authorities have argued that this practice should be abandoned.17 Although we are unable to comment on the merits of these arguments, our data suggest that while such a move might change the temporal fluctuations in AMI, it is unlikely to impact the total number of MIs in the broader population.

Mondays, in general, are the days of the week on which most MIs occur. This has been attributed to an abrupt change in the sleep–wake cycle and increased stress in relation to the start of a new work week

Manipulations of the sleep–wake cycle have been linked to imbalance of the autonomic nervous system, rise in proinflammatory cytokines and depression so presumably the additional disruption created by DST adds to this effect.

However, the data suggest that this very weak effect means only that if you were going to have an MI in the next week, after DST it is more likely to occur on the Monday of that week than on another day. Your overall risk of MI is not changed.

From a public health standpoint the major conclusion is that emergency rooms and cath labs should consider increasing staffing by 24% on the Monday after the spring DST time change.

I don’t think this is a significant factor for my patients. We have to deal with events and stressors that influence our sleep-wake cycle constantly. Good planning and sleep hygiene are the keys to success and reducing stress.

So, fear not the grim reaper as you set your clocks forward tonight.

Circadianly yours,

-ACP

PHOTO: PAVEL ŠEVELA/WIKIMEDIA COMMONS