I was recently reading an article published in the British Journal of Medicine in 1987 on the history of coronary care units.  As you may know, the coronary (or cardiac) care unit (CCU) is the specialized ward of the hospital where patients with cardiac problems are closely monitored and intensively treated.  They are staffed by experienced nurses and monitored around the clock by technicians trained in recognizing heart rhythm problems.  The concept of the CCU is now so commonplace that it’s hard to imagine a time when it was considered revolutionary.

The CCU was developed in the 1960s in response to a rise in the perceived incidence of coronary artery disease and heart attacks.  Prior to World War II most of our civilian health casualties were victims of infectious diseases such as tuberculosis and pneumonia.  The recognized heart problems were principally those involving congenital abnormalities and acquired valvular problems (acute rheumatic fever).  In the entire year of 1959 only six articles in the British Heart Journal centered on coronary artery disease.  People were simply too busy dying from other things to bother themselves with heart attacks.

The advent of antibiotics, good nutrition, and workplace safety led the way for people to live long enough to develop coronary atherosclerosis.  Unfortunately there wasn’t much anyone could really do about it.  The mainstay therapy for a heart attack in the 1960s was to simply let the disease runs it’s course and offer bypass surgery only if the patient survived long enough to develop chronic chest pain.  Consider this quote cited in the BJM article by the early CCU advocate Gunnar Biörck:

“There are few diseases in the sphere of internal medicine where the average mortality during four to six weeks hospitalization is over 30%, and if the patients with shock are particularly considered, the figure is more than twice as large.”

Imagine that—30% death rate among heart attack patients (over 60% if the patient presents with shock)!  It was out of the recognition of this abysmal survival statistic that the concept of the CCU was born. 

As time progressed the medical community began to recognize the importance of aggressive therapies to restore blood flow to the blocked artery.  In the early 1970s the median time from the onset of symptoms to the initiation of therapy (at the time it was mainly nitroglycerin, oxygen and morphine) was greater than 8 hours.  These days the standard of care dictates that we reestablish blood flow within the first 90 minutes of the patient entering the emergency department.  It’s not unusual to have a patient resting in a CCU bed—having already undergone successful placement of a coronary stent—within an hour after presenting with chest pain.

Bear this historical progression in mind as I relate a conversation I recently had with a young man who came to our hospital with a heart attack.  When I met him in the emergency department he was sweaty and pale, wide-eyed with fear.  His EKG showed abnormalities reflective of a significant heart attack.  Because he came in during the day we were able to whisk him into the catheterization lab with very little delay and open his occluded artery.

The following morning, as I exhorted him to give up his cigarette habit, he interrupted me to share his thoughts on the need for change in his health habits:

“I don’t need to quit smoking.  This heart attack thing was a piece of cake. I figure if this happens again I’ll just come in here and you guys will take care of it just like you did yesterday.  By the way, when can I go home?”

I have to admit I couldn’t fault his logic even if his level of understanding was sorely deficient.  Dr. Biörck in the quote above spoke of a “four to six weeks hospitalization” as the norm for patients with heart attacks.  In the 1950s and 60s the average cardiac patient would lounge around the hospital for weeks with strict instructions to engage in no more exertion than was required to summon the pinafore-clad nurse for his daily constitutional.  The hard-driving business executive laid low by a coronary event would spend months away from the office as he recuperated amid doting family members.  Manual laborers would find themselves permanently disabled and incapable of resuming their usual employment.

Now, as suggested by my impulsive patient, it’s a totally different world.  These days, thanks to advances in coronary reperfusion (angioplasty, stents, bypass surgery), medications (beta-blockers, statins, aspirin), and aggressive early detection and treatment standards, we’ve chopped Dr. Biörck’s 4 to 6 weeks down to a mere 48 hours. 

Of course, this is all a very good thing and we should be nothing short of ecstatic that a heart attack is no longer the death sentence that it was 50 years ago.  I just wish sometimes that a few of my patients would get a little more spooked over the whole ordeal, that they would recognize this experience as a brief introduction to their own mortality and sincerely commit to the changes they need to make.

A number of people have asked my opinion regarding the risk of dying during a marathon. I consider myself qualified to comment on this—not because I am a cardiologist—but since I recently ran a marathon and felt like I was dying at about the 15th mile (and the 16th, and the 17th, and the 18th, etc.). Since this is not a posthumous blog entry you can assume that I survived all 26.2 miles and have recovered enough to write about it.

The same can’t be said of the three unfortunate individuals who made the news in Detroit this week. As many of you may know this year’s Detroit Marathon was marred by the sudden deaths of three participants—all within minutes of each other. This tragedy has people wondering about the advisability of doing something as crazy as running a marathon and speculating that long distance running may actually be harmful for you. I’d like to dispel a number of misconceptions surrounding this notion.

The sport of distance running has been around as long as humans have existed, but the popularity of running among the general population really didn’t take off until the mid-1970s. With his best-selling book, The Complete Book of Running, Jim Fixx jumpstarted the jogging revolution and inspired millions of Americans to pull on their knee-high white socks, lace up their Nike Waffle Trainers and hit the open roads. Only 7 years after the publication of his book Jim Fixx, at the age of 52, became the face of controversy when he dropped dead from a heart attack shortly after a daily jog. Couch potatoes everywhere herald this event as vindication for a sedentary lifestyle (never mind the fact that Mr. Fixx, who took up running only after the age of 35, came from a family where his father was dead from heart disease by the age of 42).

Since Jim Fixx’s demise there have been numerous high-profile deaths related to competitive running. Every couple of years a story will hit the news of a previously healthy athlete who dies suddenly during competitive exercise. As an example, just two years ago, elite runner Ryan Shay collapsed in the U.S marathon trials and died despite efforts at resuscitation (the news later came out that Mr. Shay had a history of an enlarged heart and at one point had been advised to curtail his competitive career). When you add to these stories the tragedy of the 3 runners in Detroit it starts to look like a pattern.

Or does it? Every weekend thousands of runners take to the streets for races of one length or another. While most are not marathons, the races are likely long enough to tax the stamina of the participants (incidentally, the 3 victims of the Detroit race were not actually participating in the full marathon, only the 13.1-mile half marathon). Despite these massive numbers we only rarely hear of race-related deaths. So why do we have 3 die in one race?

In an insightful article in The New Yorker magazine about 10 years ago, surgeon and author Atul Gawande took to task the many people who get worked up over “cancer clusters”—communities in which there seems to be an unusual number of cancers. Despite reports of unusually high rates of malignancy in certain areas, aggressive investigation by epidemiologists only rarely turns up anything more than what can be explained by random variation. The problem, Dr. Gawande says, is that we humans tend to see remarkable—but isolated—episodes and then extrapolate erroneous generalizations:

“Human beings evidently have a deep-seated tendency to see meaning in the ordinary variations that are bound to appear in small samples. For example, most basketball players and fans believe that players have hot and cold streaks in shooting. In a paper entitled “The Hot Hand in Basketball,” Amos Tversky and two colleagues painstakingly analyzed the shooting of individual players in more than 80 games played by the Philadelphia 76ers, the New Jersey Nets, and the New York Knicks during the 1980-81 season. It turned out that basketball players—even notorious “streak shooters”—have no more runs of hits or misses than would be expected by chance.”

Another example of this is the Florida shark attack scare of 2001—the so-called “summer of the shark.” East coast beaches went vacant because of the news reports of one shark attack after another. In the end, the rate of shark attacks was only minimally higher that year than usual and within statistically expected variation.

Rather than drawing conclusions from what happened in Detroit let’s look at hard data. A report in the Journal of the American College of Cardiology assessed the risk of death in over 200,000 marathon runners and concluded that the risk of suffering cardiac arrest during a marathon was only 0.002% (1 in 50,000). A more recent study put the risk of marathon death at 0.8 in 100,000. To put this in perspective, death from a lightning strike is just slightly more probable at 1 in 79,746.

Now compare this to healthy but sedentary individuals. The best data we have come from a 1984 publication that suggests that the risk of sudden cardiac death is two and a half times higher in sedentary individuals than those who routinely exercise.

A commentary by a physiologist in the Encyclopedia of Sports Medicine and Science puts these recent deaths in perspective:

“On the day James Fixx died, 1000 other Americans would also have died of heart attacks. Few if any would have received nationwide coverage. Yet almost all of those deaths would have occurred in persons who were sedentary, or were smokers, or who had uncontrolled high blood pressure and elevated blood cholesterol concentrations. If only those sudden deaths occurring in athletes are reported in the press, it is understandable why the public acquires a distorted impression of the relationship between exercise and heart disease.”

So, go train for a marathon, but know this: although you may feel like you’re dying, the odds are pretty good that you’ll survive. Just stay out of the lightning storms.

Finally we have some really good news from the world of medical research.  Not just good news, like a drug that cuts the risk of heart attack or a procedure that saves lives.  But really great news.

On September 15th, the New York Times reported on a landmark study involving the salutary effects of a novel therapy on the recovery of patients following a heart attack.  The study, published in the September issue of the Journal of Internal Medicine, assessed the effect of chocolate consumption on the risk of death following a first heart attack.

That’s right: chocolate.

I love to see research like this.  For our entire lives we are lectured on how much fish and legumes we have to consume, what type of food pyramid we have to adhere to, even how many of glasses of water we must imbibe daily.  We are told forego tasty food and snacks and reach for enticing handfuls of celery and carrots when we have the munchies.  I can’t really blame people for believing that we doctors want nothing more for the whole population than to have them run a marathon every day on nothing more than a handful of spinach for calories.

I, of course, am as guilty as the rest of the profession, as my previous blog posts will attest.  We who are responsible for health care delivery want you (who are, in the end, responsible for your own health) to remain fit, and therefore must be the bearers of all the grim news: bad food and poor exercise habits will kill you in the end.  We are obligated to deliver this ominous and unpleasant information because that’s what science provides to us.  It’s really hard to argue against a well-run, double-blinded, placebo-controlled study involving thousands of patients that spits out the conclusion that a diet of vegetables is better for your body than one of Twinkies.

But, at last, we have some really good news we can sink our teeth into (and savor as it melts into warm sweetness in our mouths).  It appears that those who eat chocolate after their heart attack live longer than those who don’t.

The research, done in Sweden (known more for Smörgåsbord and lutfisk than chocolate—I guess not even a Swede could inflict a diet of salted whitefish mixed with lye on patients who’ve already gone through enough with a heart attack), was an observation study rather than a prospective, randomized trial.  This means they polled numerous Svens and Ingmars on their eating habits following the heart attack.  Those who reported higher chocolate consumption were found to live longer.  They also factored in other variables, such as obesity and other dietary habits, to strengthen their conclusion that it was, indeed, the chocolate that imparted the protective effect.  They wisely excluded diabetic patients from their cohort knowing that something as obviously heaven-sent as chocolate simply can’t be good for a diabetic patient.

This isn’t the first time that the link between chocolate and heart health has been studied.  Just this year the esteemed journal Circulation published an expansive review of the cocoa/cardiology literature authored, appropriately, by a team of Swiss cardiologists.  The prevailing theory is that a chemical in cocoa (with the not-so-savory name of epicatechin) exerts an antioxidant effect that protects the heart against the untoward effects of LDL cholesterol.  The dark, least-sweetened, most fat-free variety of chocolate seems to be the healthiest.

Still, all good critics of scientific trials will tell you that we can’t begin to change our clinical practice based on the findings of a solitary observational study.  They’ll explain that rigorous testing must follow before we can translate these findings into general guidelines.  The next step in the process should be the creation and performance of a large prospective study involving thousands of patients to really put the chocolate hypothesis to the test.

This is where we come in.  I propose we launch a massive prospective study to evaluate the effects of chocolate consumption on, well, everything.  We can look at maintenance of heart health, decreasing risk of cancer, prevention of dementia, treatment of depression, etc.  We could seek funding from Hershey or Lindt or  Nestlé and run the study  for four or five years, enrolling ourselves and everyone we know.  Half the group would get rich, dark, delicious chocolate, and the other half would get carob (I’ll make sure you and I get randomized to the good stuff).  We can present the findings to the European Society of Cardiology next time they convene in Zurich.

So next time your sweetheart gives you a box of chocolates for Valentine’s Day, don’t turn up your nose and reach for a celery stick.  Thank them for having your best health in mind as you pick the darkest piece of the bunch and pop it into your mouth with a clean conscience.

In 1982 the National Heart, Lung and Blood Institute (NHLBI) launched the Cardiac Arrhythmia Suppression Trial (CAST) which was completed in 1986 and published in the New England Journal of Medicine in 1989.  I learned about it the year it came out from my medical school professors since it caused quite a stir in the cardiology community.  While I don’t think medical students hear about it anymore (it is 20 years out of date, after all) I think they could still glean a valuable lesson from it.

Let’s go back in time.  If you had a heart attack in 1982 there really wasn’t much that could be done.  Angioplasty, developed in 1977, hadn’t made its way to mainstream hospitals until the mid-80s, and streptokinase, the first thrombolytic, wasn’t in common use until the GISSI trial was published in 1986.  Mostly, you would come into the hospital and receive morphine and nitroglycerin until the affected heart tissue expired and the pain subsided.  Long ago doctors noticed that people who exhibited ventricular electrical irritability in the form of frequent premature ventricular complexes (PVCs) and ventricular tachycardia were at much higher risk of dying from ventricular fibrillation (VF) in the early period after a heart attack.

Several rhythm control drugs were available at that time and appeared to do a good job of decreasing the frequency of PVCs.  It became common practice to empirically start patients on medications such as lidocaine in an effort to decrease the risk of death from ventricular arrhythmia. 

It was during that time that several other antiarrhythmic drugs became available.  Encainide, flecainide, and moricizine were considerably more effective than lidocaine at extinguishing PVCs and became popular among cardiologists.  If lidocaine is good—so the thinking went—these others must be better.

So the logic went like this:

1. More PVCs equals more death from VF
2. Lidocaine decreases the rate of PVCs
3. Ergo, using medications even better than lidocaine will prevent death from VF

Here’s where the lesson comes in.  In medicine we are taught to implement a hypothesized therapy into general use only after it has been rigorously validated.  This last part was bypassed, as lidocaine, encainide, flecainide and moricizine were all used in thousands of patients before any significant research was done to validate the line of logic.

Enter the CAST trial.  When the NHLBI proposed the design of this study (prospective, placebo controlled) some prominent members of the cardiology community were aghast at the possibility of withholding an established therapy from the patients who were randomized to the placebo arm.  They claimed that it was medical malpractice to not give antiarrhythmics to patients with heart attacks and frequent PVCs.

Skip forward to 1989.  The results of the CAST trial settled the debate and retired the routine use of antiarrhythmics in the setting of heart attacks.  It turns out that the empiric use of these medications actually led to a higher rate of death among these patients than the placebo pills.  Apparently this class of medications actually stimulates a more lethal type of ventricular arrhythmia in patients with recently-injured heart muscle.

In the ensuing years encainide and moricizine were pulled from the market, and flecainide is now used only cautiously in younger patients with atrial fibrillation.  We no longer attempt to suppress asymptomatic ventricular activity in people with recent heart attacks and instead focus on restoring blood flow.

The lesson can’t be forgotten.  Even if a course of therapy seems logical we can’t deploy it into general use until the hypothesis is thoroughly tested.  Assumptions and anecdotal evidence are not enough.

What’s the best dose of aspirin to take in order to prevent a heart attack? Which dose do you use to prevent a stroke? What if you’re on low-dose aspirin already and suffer a heart attack? Do you switch to the higher dose? What about after a stent? Or coronary bypass surgery?

Most of you know already that aspirin comes in several doses (according to my PDA-based prescription drug reference it’s available in 5 doses between 81 and 650 milligrams) but in the cardiology world we mainly use the “baby” aspirin at 81mg or the “full-strength” at 325mg.

Years ago aspirin was the mainstay for treatment of arthritis. This was of course before better painkillers and anti-inflammatory drugs came along, like ibuprofen, naproxen and acetaminophen (Tylenol). The doses used back in the day were quite high by today’s standards. It was not uncommon for someone to be on 3000mg a day or more, doses high enough to induce the classic toxic effects of ringing in the ears, hyperventilation and acidosis. The most problematic complication was gastrointestinal bleeding. Aspirin exerts several effects on the protective lining of the stomach that can lead to local erosion, ulceration and even life-threatening perforation.

These days such side effects are far less common, but even when taking lower doses patients are still at higher risk of developing an ulcer on aspirin than they would be otherwise. It is for this reason that physicians and patients frequently try to use the lowest dose of aspirin that is effective.

We use aspirin to inhibit the formation of clots where we don’t want them to occur. Heart attacks and strokes happen when a clot—composed of platelet cells and glue-like proteins—either travels to and lodges in a critical vessel or arises there spontaneously. Blocking platelet function can decrease the chance that a vessel becomes suddenly obstructed.

I have found that many cardiologists, neurologists, internists and family doctors have strong opinions regarding which dose of aspirin a patient should be taking. In order to provide a bit of expert context for this subject I consulted with an old friend of mine, Dr. Steven R. Steinhubl, who just happens to be one of the world’s foremost experts on the subject of arterial clot formation and medications used to block platelets. I reached him in Switzerland and he was kind enough to provide the briefest tutorial on the subject I’ve ever heard:

“Aspirin, the most commonly used drug worldwide for the prevention and treatment of heart disease today, was first shown to be beneficial as a blood thinner less than 30 years ago. However it was 100 years ago when Bayer first introduced a 5-grain (approximately 325 milligrams—today considered an adult dose of aspirin) aspirin pill in response to counterfeiters of aspirin powder. Twenty years later the 81mg “baby” aspirin was developed to be one-quarter the size of the adult strength. It wasn’t until almost fifty years later, following the Nobel Prize-worthy discovery identifying how aspirin inhibited platelets, that it was eventually found that only 30mg to 50mg of aspirin per day is required to fully inhibit platelets. In fact, Sir John Vane, the Nobel Prize-winning scientist, is often credited with saying that it is necessary to only lick an aspirin every day to achieve its full benefit. Despite this, 325mg remains commonly recommended, especially by cardiologists. This appears to be mainly out of habit, as clinical trial data have consistently found no benefit but a higher incidence of stomach problems in patients receiving higher doses of aspirin. Today, for patients in whom it is recommended to take a daily aspirin, an 81mg “baby” aspirin is all that’s needed.”

Dr. Steinhubl also referenced a review article he co-authored in JAMA that expands on his thesis and summarizes all the research data on the subject.

So there you have it from the experts. From now on I guess I can simply say “Lick two aspirin and call me in the morning.”