Category Archives: heart attack

Top Skeptical Cardiology Stories of 2017

Science continued to progress in the field of cardiology in 2017. Some cardiology interventions were proven to be more beneficial (TAVR) and some less (coronary stents). A class of cholesterol lowering drugs had a big winner and a big loser. A supplement that many thought, based on observational studies, was crucial to prevent heart disease, turned out to be unhelpful. More evidence emerged that saturated fat is not a dietary villain.

From the skeptical cardiologist’s viewpoint, the following were the major scientific studies relevant to cardiology:

1.  “Thousands of heart patients get stents that may do more harm than good”

Thus read the Vox headline for the ORBITA study which was published in November.

Indeed this was an earth-shattering study for interventional cardiologists, many of whom agreed with the NY Times headline “Unbelievable: Heart Stents Fail To Ease Chest Pain.”

Cardiologists have known for a decade (since the landmark  COURAGE study) that outside the setting of an acute heart attack (acute coronary syndrome or ACS), stents don’t save lives and that they don’t prevent heart attacks.

Current guidelines reflect this knowledge, and indicate that stents in stable patients with coronary artery disease should be placed only after a failure of  “guideline-directed medical therapy.”  Despite these recommendations, published in 2012, half of the thousands of stents implanted annually in the US continued to be employed in patients with either no symptoms or an inadequate trial of medical therapy.

Yes, lots of stents are placed in asymptomatic patients.  And lots of patients who have stents placed outside the setting of ACS are convinced that their stents saved their lives, prevented future heart attacks and “fixed” their coronary artery disease. It is very easy to make the case to the uneducated patient that a dramatic intervention to “cure” a blocked artery is going to be more beneficial than merely giving medications that dilate the artery or slow the heart’s pumping to reduce myocardial oxygen demands.

Stent procedures are costly  in the US (average charge around $30,000, range $11,000 to $40,000) and there are significant risks including death, stroke and heart attack. After placement, patients must take powerful antiplatelet drugs which increase their risk of bleeding. There should be compelling reasons to place stents if we are not saving lives.

I, along with the vast majority of cardiologists, still recommended stents for those patients with tightly blocked coronary arteries and stable symptoms, which were not sufficiently helped by medications. ORBITA calls into question even this indication for stenting.

The ORBITA study investigators recruited 230 patients to whom most American cardiologists would have recommended stenting. These patients appeared to have a single tightly blocked coronary artery and had chest pain (angina) that limited their physical activity.

They treated the patients for 6 weeks with aspirin/statins/ and medications that reduce anginal symptoms such as beta-blockers, calcium-channel blockers or long-acting nitrates. At this point patients were randomized to receive either a stent or to undergo a catheteriation procedure which did not result in a stent, a so-called sham procedure.

The performance of a sham procedure was a courageous move that made the study truly double-blinded; neither the patients nor the investigators knew which patients had actually received a stent. Thus, the powerful placebo effects of having a procedure were neutralized.

Surprisingly, the study found that those patients receiving stents had no more improvement in their treadmill exercise time, angina severity or frequency or in their peak oxygen uptake on exercise.

ORBITA hopefully will cause more cardiologists to avoid the “oculo-stenotic” reflex wherein coronary artery blockages are stented without either sufficient evidence that the blockage is causing symptoms or that a medical trial has failed.

Although this was a small study with a very narrowly defined subset of patients, it raises substantial questions about the efficacy of coronary stenting. If ORBITA causes more patients and doctors to question the need for catheterization or stenting, this will be a  very good thing.

2. Vitamin D Supplementation Doesn’t Reduce Cardiovascular Disease (or fractures, or help anything really).

One of my recurring themes in this blog is the gullibility of Americans who keep buying and using useless vitamins, supplements and nutraceuticals, thereby feeding a $20 billion industry that provides no benefits to consumers (see here and here).

Vitamin D is a prime player in the useless supplement market based on observational studies suggesting low levels were associated with increased mortality and cardiovascular disease

Despite well done studies showing a lack of benefit of Vitamin D supplementation, the proportion of people taking more than 1,000 IU daily of Vitamin D surged from just 0.3 percent  in 1999-2000 to 18 percent in  2013-2014.

I’ve written previously (calcium supplements: would you rather a hip fracture or a heart attack) on the increased risk of heart attack with calcium supplementation.

Most recently a nicely done study showed that Vitamin D supplementation doesn’t reduce the risk of heart disease.

In a randomized clinical trial that included 5108 participants from the community, the cumulative incidence of cardiovascular disease for a median follow-up period of 3.3 years was 11.8% among participants given 100 000 IU of vitamin D3 monthly, and 11.5% among those given placebo.

Aaron Carroll does a good job of summarizing the data showing Vitamin D is useless in multiple other areas in a JAMA forum piece:

Last October, JAMA Internal Medicine published a randomized, controlled trial of vitamin D examining its effects on musculoskeletal health. Postmenopausal women were given either the supplement or placebo for one year. Measurements included total fractional calcium absorption, bone mineral density, muscle mass, fitness tests, functional status, and physical activity. On almost no measures did vitamin D make a difference.

The accompanying editor’s note observed that the data provided no support for the use of any dose of vitamin D for bone or muscle health.

Last year, also in JAMA Internal Medicine, a randomized controlled trial examined whether exercise and vitamin D supplementation might reduce falls and falls resulting in injury among elderly women. Its robust factorial design allowed for the examination of the independent and joined effectiveness of these 2 interventions. Exercise reduced the rate of injuries, but vitamin D did nothing to reduce either falls or injuries from falls.

In the same issue, a systematic review and meta-analysis looked at whether evidence supports the contention that vitamin D can improve hypertension. A total of 46 randomized, placebo controlled trials were included in the analysis. At the trial level, at the individual patient level, and even in subgroup analyses, vitamin D was ineffective in lowering blood pressure.

Finally, if the Vitamin D coffin needs any more nails, let us add the findings of this recent meta-analysis:

calcium, calcium plus vitamin D, and vitamin D supplementation alone were not significantly associated with a lower incidence of hip, nonvertebral, vertebral, or total fractures in community-dwelling older adults.

3. PCSK9 Inhibitors: Really low cholesterol levels are safe and reduce cardiac events

I reported the very positive results for evolocumab and disappointing results for bosocizumab on the physician social media site SERMO in March but never put this in my blog.

As a practicing cardiologist I’ve been struggling with how to utilize the two available PCSK9 inhibitors (Amgen’s Repatha (evolocumab) and Sanofi’s Praluent (alirocumab) in my clinical practice.  I would love to use them for my high risk statin-intolerant patients but the high cost and limited insurance coverage has resulted in only a few of my patients utilizing it.

The lack of outcomes data has also restrained my and most insurance companies enthusiasm for using them.

The opening session at this year’s American College of Cardiology Scientific Sessions in DC I think has significantly changed the calculus in this area with two presentations: the first showing  Amgen’s “fully humanized” evolocumab significantly lowers CV risk in high risk patients on optimal statin therapy and the second showing that Pfizer’s “mostly humanized” bococizumab loses efficacy over time and will likely never reach the market.

The FOURIER study of evolocumab randomized  27, 564 high risk but stable patients who had LDL>70 with prior MI, prior stroke or symptomatic PAD to receive evolocumab or placebo on top of optimized lipid therapy. 69% of patients were recieving high intensity statin therapy and the baseline LDL was 92. LDL was reduced by 59% to average level of 30 in the treated patients. The reduction in LDL was consistent through the duration of the study.

IN 1/4 of the patients LDL was <20! These are unprecedented low levels of LDL.

Active treatment significantly reduced the primary endpoint by 15% and reduced the secondary endpoinf  of CV death, MI, stroke by 20%. absolute difference 2% by 3 years. 

There was no difference in adverse effects between placebo and Evo. 

The next presentation featured data using Pfizer’s candidate in the PCSK9 wars and the acronym SPIRE (Studies of PCSK9 Inhibition and the Reduction in vascular Events (SPIRE) Bococizumab Development Program).

Paul Ridker presented the outcomes data for bococizumab which was actually similar to evolocumab data but given the declining efficacy and development of antibodies to the Pfizer drug over time these were very disappointing for Pfizer and I would presume their drug will never reach the market.

How will these results impact clinical practice?

I am now more inclined to prescribe evolocumab to my very high risk patients who have not achieved LDL< 70. I’m willing to do what I can to jump through insurance company hoops and try to make these drugs affordable to my patients.

I am less worried about extremely low LDL levels and have more faith in the LDL hypothesis: the lower the LDL the lower the risk of CV disease.

Cost is still going to be an issue for most of my patients I fear and the need for shared decision-making becomes even more important.

 

4. “Pure Shakes Up Nutritional Field: Finds High Fat Intake Beneficial.”

As one headline put it.

I recorded my full observations on this observational international study here

Here is a brief excerpt:

The Prospective Urban Rural Epidemiology (PURE) study, involved more than 200 investigators who collected data on more than 135000 individuals from 18 countries across five continents for over 7 years.

There were three high-income (Canada, Sweden, and United Arab Emirates), 11 middle-income (Argentina, Brazil, Chile, China, Colombia, Iran, Malaysia, occupied Palestinian territory, Poland, South Africa, and Turkey) and four low-income countries (Bangladesh, India, Pakistan, and Zimbabwe)

This was the largest prospective observational study to assess the association of nutrients (estimated by food frequency questionnaires) with cardiovascular disease and mortality in low-income and middle-income populations,

The PURE team reported that:

-Higher carbohydrate intake was associated with an increased risk of total mortality but not with CV disease or CV disease mortality.

This finding meshes well with one of my oft-repeated themes here, that added sugar is the major toxin in our diet (see here and here.)

I particular liked what the editorial for this paper wrote:

Initial PURE findings challenge conventional diet–disease tenets that are largely based on observational associations in European and North American populations, adding to the uncertainty about what constitutes a healthy diet. This uncertainty is likely to prevail until well designed randomised controlled trials are done. Until then, the best medicine for the nutrition field is a healthy dose of humility

I wish for all those following science-based medicine a healthy dose of humility. As science marches on, it’s always possible that a procedure we’ve been using might turn out to be useless (or at least much less beneficial than we thought), and it is highly likely that weak associations turn out to be causally nonsignificant. Such is the scientific process. We must continually pay attention, learn and evolve in the medical field.

Happy New Year to Be from the Skeptical Cardiologist the EFOSC!

The skeptical cardiologist and his Eternal Fiancee marveling at the total eclipse of the sun (very accurately predicted by science) in St. Genevieve, Missouri

-ACP

 

Two Three Letter Words For Saving Lives: CPR and AED

Every two years the skeptical cardiologist has to get recertified in Basic Life Support for medical personnel. This involves a review of what, the American Heart Association has decided, are important changes in guidelines for Emergency Cardiac Care and cardiopulmonary resuscitation (CPR).

I highly recommend all of you undergo such training. Although the survival rate of patients with “out of hospital cardiac arrests” is very low, your appropriate actions could be crucial in saving the life of a stranger or a loved one.

About a year ago one of my patients suddenly, and without any warning symptoms, collapsed at work. Fortunately for him, a co-worker had undergone CPR training and initiated chest compressions right away. When paramedics arrived 15 minutes later he was defibrillated from ventricular fibrillation and taken to a nearby hospital.

Our best information on cardiac arrest suggests that without CPR, irreversible brain damage (due to lack of oxygen) develops in about four minutes after the heart stops beating. Even with good CPR, the longer the time interval from arrest to defibrillation, the less likely the patient is to survive with good brain function.

Thus, the two keys to helping someone who drops dead next to you are beginning effective CPR (and compression only is OK) and defibrillating a fibrillating heart as soon as possible.

My patient was comatose on arrival to the hospital and was put into a hypothermic state, a process which has been shown to improve neurological outcome in cardiac arrest victims. Doctors informed his wife that they thought his prognosis was bad-less than 5% chance of surviving with intact brain function.  After three days he awoke from his coma and was transferred to my hospital.

I visited him in the ICU and other than a sore chest and an inability to remember the events surrounding his cardiac arrest, he was mentally normal and felt great. He continues to do very well to this day, but without the bystander CPR that he received (followed by the defibrillation) he would be one of the 350,000 who die of cardiac arrest in the US each year.

If the co-worker had not initiated CPR for the many minutes it took for EMRs to arrive, my patient’s brain would have been dying from lack of oxygen and it is most likely he would have suffered severe encephalopathy or brain death.

Recognizing Cardiac Arrest

Recognizing when someone needs CPR is a critical first step in the chain of events that can improve survival in cardiac arrest.

You are looking for two things before starting CPR:

  1. Unresponsiveness. The victim  does not move and does not respond at all to either verbal or physical stimulation.
  2. Breathing is absent or atonal (meaning ineffective , intermittent gasps).

Agonal respirations have also been described as “snoring, snorting, gurgling, or moaning or as barely, labored, noisy, or heavy breathing.”  Studies have shown that agonal respirations are common in the early minutes after cardiac arrest and are associated with good outcomes.

Two Steps To Save A Life

The two key components of resuscitation are CPR and defibrillation.

Performing these steps is simple and straightforward.

The earlier they are started, the more likely the victim is to survive.

If someone collapses near you and they are unresponsive and not breathing, they need CPR and an AED. Call for help as you are starting CPR.

images

 

Cardiopulmonary Resuscitation (CPR)

CPR consists of repeated compressions of a victim’s chest.

img_7451
I came across this machine recently. You can learn and practice hands-only CPR using it.

Everyone has seen dramatizations of CPR and it is quite simple to do even without training. Basically, you want to “push hard and fast in the center of the chest.”

CPR training undergoes some tweaking over time as more scientific data is obtained but the fundamentals remain the same. The changes that the AHA is emphasizing in their current CPR courses are:

-depress the chest at least 2 inches

-depress the chest 100-120 times per minuCPR-Certificationte (as opposed to just >100 time per minute).

Of note, the recommended sequence has changed from A, B, C, to C, A, B. Compressions right away followed by assessment of airway and then mouth-to-mouth breathing.  In fact, because compressions without breaths have been shown to be as effective as with breaths, if you are uncomfortable giving breaths, recommendations now are to just do CPR.

 

Initiating CPR and calling 911 are the greatest initial things you can do for the person who collapses next to you.

However, the earlier you can defibrillate that person from ventricular fibrillation, the better their chance of survival.

Ambulatory electronic defibrillators or AEDS , if available, are very easy to use devices that can shorten the time to defibrillation and are the second key to successful resuscitation of cardiac arrest victims in the community.

I’ll talk about using them in a subsequent post.

antimortatorially yours

-ACP

 

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.

Screen Shot 2016-07-03 at 7.04.14 AM

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.”

Screen Shot 2016-03-12 at 2.28.26 PM

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

 

I’m Having Chest Pain: Is It a Heart Attack?

IMG_4219I can tell you exactly when the pain started. I was riding  my bike in Forest Park, the great urban park of St. Louis. Ordinarily, I cycle from my house to the park, cutting across the  ivy-covered semi-Ivy league campus of nearby Washington University and circling its beautiful acres on a recently refinished bike path.

As I started the slow incline that parallels Skinker Avenue just West of Forest Park, a cyclist flashed past me. I could swear he said “Oh dear, oh dear. I shall be late.”

Instead of continuing straight along the bike path, the late cyclist suddenly veered to the left, following a heretofore untraveled spur that led up into the dark, impenetrable forests of the park.

At this point, the sensible, sixty-something portion of my psyche should have taken over and had me continue on the relatively straight, flat and well-traveled road that I had grown accustomed to. Alas, it was the teenage boy who took control and insisted on us taking the road less traveled.

The spur of the bike path had not been regularly maintained and there were numerous rough spots: ridges and chasms emerged with disconcerting frequency as I progressed.

The lure of exploration pulled me on. I kept my speed up as I descended a hill with the path turning sharply to the right. Suddenly an even sharper right turn emerged with a particularly uneven section of path. I lost control of the bike and landed heavily on my left side.

I felt a sudden sharp pain just to the left of my breastbone about midway in my chest.

As a cardiologist I spend a lot of time talking to people about chest pain and thinking about what is causing it.

The heart is in the chest and it is natural to believe that pain that comes from this area could be a manifestation of the dreaded heart attack. Since heart attacks are the #1 killer of both men and women  and they can very quickly lead to life-threatening arrhythmias it is wise to take seriously  any pain in the chest.

Three Types of Chest Pain

I was trained to sort what patient’s described to me about their chest pain  into three bins: Typical anginal pain, atypical anginal pain and non cardiac pain.

Angina is doctor-speak for chest pain that is due to the heart muscle not getting enough blood (usually due to a blocked coronary artery)

Cardiologists consider any discomfort from the lower ribs up to the bottom of the neck as chest pain although patients often don’t perceive it as a pain.

Heart attack pain often feels like a pressure, a heaviness or a burning and in addition to somewhere in the anterior chest region it can manifest in the neck or jaw or one or both of the upper arms.

My chest pain was  worse  when I took a deep breath (pleuritic) and this almost always indicates a lung cause or inflammation in the muscle/bones/joints that are related to breathing. Furthermore, pushing on the ribs  made it worse making it virtually certain that it was musculoskeletal.

A brief (well done) history and physical exam therefore would assign my chest pain to the “non cardiac” bin.

Typical anginal pain is brought on by exertion, lasts 3-15 minutes and is relieved by nitroglycerin or rest.

pretest likelikhood cadThe probability of a patient with non cardiac chest pain having significantly blocked coronary arteries is generally lower than that of a patient with typical anginal pain. However, as this chart demonstrates, patients (generally those with significant risk factors) can have severely blocked coronary arteries and have non cardiac chest pain.

For example, I have risk factors of age (>55 years), being male, hyperlipidemia and hypertension. A cardiac catheterization done on me at the time of my non cardiac chest pain might well show significantly blocked coronary arteries. Of course, these blocked arteries would have absolutely nothing to do with my pain.

This fundamental paradox is the source of a lot of the overtesting and over treatment that occurs in cardiology. Most of the time, chest pain that prompts a patient to come to the ER or doctor’s office does not fall easily into the non cardiac category or the typical anginal category: these are the atypical anginal patients.

Additional testing is required , progressing from EKGS and cardiac enzymes to stress testing to cardiac catheterization. If there are elevation of the cardiac enzymes or abnormalities of the EKG that indicate a recent or active heart attack then a cardiac catheterization is warranted because it is very highly likely that a tightly blocked coronary artery is the cause and opening that artery will be beneficial.

However, most patients have normal cardiac enzymes and unremarkable EKGS and can end up getting catheterizations (due to either  inaccurate stress tests or cardiologist’s recommendation) that they don’t need.

Once a catheterization is done, patients may then get a stenting procedure on a blocked coronary artery that wasn’t causing any problems. Not uncommonly, multiple blocked coronary arteries are found and the patient is rushed off to have a bypass operation. If the blocked arteries weren’t the cause of the patient’s chest pain (i.e. the pain was non cardiac) these procedures are likely doing more harm than good.

When To Go To ER With Chest Pain

I’ve spent thirty years fielding after hours telephone calls from patients who are having  chest pain.

It is not easy to make a reliable determination of who is likely having a heart attack or other potentially dangerous cardiac problem and who is not just based on the history.

If a patient called me describing what I described above I would likely advise him to go to the ER for evaluation (although I would be pretty sure it wasn’t a heart attack: sometimes rib fractures are associated with collapsed lungs or hemorrhage into the pleural space and sometimes trauma to the chest can cause heart damage). It’s always better to err on the side of caution when were’ dealing with potentially life-threatening problems.

After office hours, the only way to get an electrocardiogram and cardiac enzymes to be sure that the chest pain is or is not a heart attack is to go to an ER. Generally, if the patient has escalated the level of concern to calling the on call cardiologist, the symptoms are worrisome.

The bottom line for me is that you only get one chance to die (You only die once (YODO)

If you’re having a heart attack at any second your heart can go into ventricular tachycardia or ventricular fibrillation and you will die within minutes.

Thus, I have to have a very low threshold for advising trips to the ER. If I’m wrong, the patient  could die.

I didn’t go to the ER because I was 100% certain that my chest  pain was non cardiac. I’m also a doctor and therefore a very bad patient. I survived, however, and over several weeks the pain gradually subsided.

As a result of this fall (and several other bike falls I’ve had in the last few years) I’ve re-evaluated my cycling. I’m going to stay on very well-maintained paths and slow way down when the going gets rough.

Hopefully, this will allow me to continue the cycling which I’m convinced is helping to prevent me from visiting the ER with a true heart attack!

Skeptically Yours

-ACP