Warning: This is a long and tedious post that many of you will find boring (I actually fell asleep briefly while writing it) but it contains good information that I believe is useful. If you’re the type of reader who’s looking for something lighter and wittier please skip this week’s post and look to my other inane blog articles (Better yet, turn off your computer and go out to enjoy the nice weather . . . sorry, forgot this is Nebraska. Read on).

Quiz. Which of the following statements are true?

1. A normal stress test means you won’t have a heart attack.
2. An abnormal stress test means you have coronary artery disease.
3. If you have coronary artery disease you need an annual stress test.

A stress test in the cardiology world is an indirect way to assess the flow of blood through the coronary arteries that feed the heart muscle. My group’s web site has some good general information on treadmill, echo and nuclear stress testing so I won’t go into detail here.

Stress testing is not a terribly complicated subject but it can be a bit confusing and suffers from a few misconceptions. The idea is pretty simple. First, we find some way to assess whether heart muscle is getting enough oxygen (so-called ischemia), some marker that we can follow through the course of testing. When doing the plain treadmill test we watch one particular segment of the EKG that changes in the presence of ischemia. With stress echocardiogram we examine the motion of the left ventricular wall. If the ventricle struggles for oxygen to any degree the affected area becomes flaccid and fails to contract appropriately. With the nuclear medicine study we observe where the muscle tissue absorbs the isotope (the nuclear dye) and where it doesn’t. This gives us an idea about blood flow to each region of the heart.

Then we find a way to exert stress on the heart. The treadmill raises the heart rate and blood pressure as well as the contractile force of the ventricle. The healthy heart has enormous functional reserve and can increase its output over a dozen-fold. If the patient can’t walk on the treadmill we can stress the heart with chemical infusions. Dobutamine more or less mimics exercise by revving up the heart and adenosine (and the newer Lexiscan) causes temporary expansion of healthy arteries with effective shunting of flow away from diseased areas.

We assess the heart at rest and then repeat the assessment at peak stress. If blood flow is good we should see good function at both points. If a major coronary vessel is blocked more than about 70% we’ll see normal function at rest but abnormal results at peak stress. The next test ordered will likely be a cardiac catheterization for definitive diagnosis and treatment of the affected artery.

With stress testing we are able to determine—with reasonable reliability—if the patient has any major coronary artery blocked to more than 70%.

Now let’s review how a heart attack happens. Heart attacks occur because a cholesterol-rich “plaque” in the wall of the artery becomes unstable, ruptures, and the body tries to seal the damage with proteins and cells that form a clot. The clot occludes the flow in the vessel and all downstream muscle is starved for oxygen. We’ve known for several years that the physical dimensions of a stenosis (ie. how narrow the blockage) don’t determine its risk of plaque rupture and complete vessel closure—a 50% blockage may be just as likely to result in a heart attack as a 90% blockage. A more important indicator of whether the artery will develop plaque rupture is the microscopic structure of the plaque: how much cholesterol is built up in the vessel wall and how stable the thin lining of fibrous tissue is that separates the cholesterol from the flowing blood.

While we have several tests that can evaluate the degree of narrowing caused by the plaque, there is currently no test available that can see the coronary arteries in enough detail to assess the stability of the plaque. Even cardiac catheterization can’t tell us which 60% blockage will become unstable and trigger a heart attack.

It’s for this reason that a normal stress test can’t insure against the future possibility of a heart attack. Furthermore, since stress testing is sensitive enough to detect only the worst of the blockages we can’t declare a patient free of coronary disease based on a normal test. A patient could have a handful of 30-50% blockages in their coronary tree and still pass a stress test with flying colors.

So what good is stress testing? Here are some situations where it’s helpful.

1. It’s most useful in patients with exertional symptoms since those are easiest to reproduce on the treadmill. If chest pain arises from a coronary blockage then we’d expect to see the abnormalities show up reliably on our testing. Exertional chest pain in the face of a normal test is a pretty good argument for a noncardiac source of symptoms.
2. Stress testing prior to major surgery is often helpful to rule out high-risk, dangerous blockage in persons who don’t regularly exert themselves to a great degree. We use it to prove that the heart can tolerate the physical demands of the surgery (which is generally equivalent to briskly climbing a couple flights of stairs).
3. As part of the hospital evaluation for chest pain. Please see my recent post on CT angiography for a summary of how this is used. As with the pre-operative testing, we are mainly looking for dangerous blockages in critical locations of the heart.

The downside to stress testing is the moderate false positive rate (the likelihood that someone with normal arteries is erroneously found to have an abnormal test result) that accompanies this screening test. It’s this reason that our current expert guidelines don’t recommend using stress testing to screen asymptomatic patients, even if they a history of stable coronary artery disease (in fairness, many cardiologists order routine stress tests for patients with previous stents or bypass surgery—the utility of this is debatable).

So, here are the answers to the questions I pose above:

1. A normal stress test means you won’t have a heart attack. False. We do a better job of predicting a heart attack by looking at your risk factors and lifestyle (see the more useful Framingham Risk Calculator).
   
2. An abnormal stress test means you have coronary artery disease.  False.  All we can say is that you might have blockage in the 80-99% range, but the false-positive rate of the study requires more definitive testing.
   
3. If you have coronary artery disease you need an annual stress test. False, although some cardiologists will have a different opinion.

There you have it. For those of you who actually made it through this post you can now move on to reading War and Peace or the IRS tax code.

I can’t tell you how many times I’ve had patients timidly admit that they’d researched some aspect of their medical condition online. That confession is usually followed by “You probably hate it when your patients get their information on the internet” spoken in the same tone of voice they use in their visits to the confessional.

I don’t really know where the perception comes from that doctors don’t want their patients researching their own health ailments on the computer. I, for one, am immensely relieved when I don’t have to educate patients about complicated conditions starting from square one—it’s nice when they have already looked into the basics of the disease and explored the possible treatment options even before they come to me for an opinion.

I think it’s fair to say that most patients and doctors find the internet a valuable source of medical information and are eager to make use of it. In that spirit I’d like to share with you my favorite web-based medical resources:

1. WebMD. I list this one first not because it’s my favorite but because it is so commonly referenced. I like the patient-based information that is available on a wide variety of subjects, but I don’t much care for the distracting gauntlet of advertisements and sponsored links you have to navigate to find your subject. Those of you who make use of my (sometimes overused) hyperlinks will note that I frequently cite WebMD for background information.
   
2. WrongDiagnosis. This site allows you to enter your symptoms and let the computer take a crack at the diagnosis. I have to admit this didn’t work so well for me. I tried to diagnose a heart attack by entering “chest pain, sweating, shortness of breath” and came up with 396 different possibilities (including “acute leukaemia of ambiguous lineage”). Still it’s good for providing you with a long and exhaustive list of possible ailments to account for any given symptom.
   
3. Centers for Disease Control. The CDC sponsors a great website that allows you to quickly find very reliable information about infectious diseases and public health concerns. Want to cut through the myths and half-truths about the H1N1 vaccine? It’s all there with extensive referencing. Need the final word on insect repellents? Rodent-borne diseases? Black mold? This is the place.
   
4. Merck Manual. I’ve long been a fan of the Merck Manual, the 110-year-old medical encyclopedia, now in its 18th edition, and have had a copy on my shelf ever since I started medical school. The Merck Manual site is a great resource if you need more information that you can find at places like WebMD. You can even download podcasts on a huge number of subjects, written and narrated by medical specialists (see chest pain podcast).
   
5. UpToDate. For the medical professionals, this one is hard to beat. It is by far the most exhaustive and current resource of medical reviews available. The downside? It costs a fortune to subscribe. Since mortgaging my house to gain access to this valuable resource I’ve turned to it frequently to supplement my knowledge base. I recommend it only if you like to read a lot and have a rich uncle in poor health. UpToDate does offer a valuable trove of patient information that is free to the public.
   
6. Quackwatch. This is a wonderful non-profit site aimed at providing peer-reviewed scientific information to debunk unproven or ineffective alternative medicine remedies. I like it because I can quickly educate myself on various new products and therapies my patients ask me about. So, before you let grandma invest her life savings into that diet of blue-green algae she heard about on the shopping channel make sure she takes a look at this website.
   
7. theheart.org. This resource is most useful for cardiologists but also contains great information for all professionals. It summarizes and editorializes the latest breakthroughs in my field with direct access to the experts on the front lines of research. It also offers an enormous library of professional slide presentations on every cardiac subject imaginable.
   
8. Medscape. This is a nice all-around site for both patients and providers that I’ve turned to for years for information on medications and as a search engine for the MEDLINE database. It’s also a great resource for online continuing medical education.
   
9. Wikipedia. Okay, I’ll admit it—this is my guilty pleasure. I love turning to Wikipedia for medical information, especially when I need only a superficial but broad perspective. It’s also a great resource for information relating to the history of medicine.
   
10. Alegent Cardiology Blog. A valuable source of dubious wisdom, questionable medical punditry, and sorry attempts at humor. I turn to it at least weekly.

That’s my list. I’d love to hear from you. What do you think of the use of the internet as a resource for patients? What are your most trusted sites? The comment button (below) is so rarely used it has collected web dust. Give it a try and let us know what you think.

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.

Let’s say you come to the emergency room with chest pain.  Pretend you are a 40-something-year-old male with a history of high blood pressure but no previous heart problems.  After a few tests the doctor comes into the room to tell you that your EKG and lab work are normal but that you’ll be staying in the hospital overnight anyway.

The next morning, with your repeat EKG and blood work showing no abnormality, you are ushered to the treadmill room for a test called a stress echocardiogram.  You walk, then run, on the treadmill until your pulse reaches about 85% of your maximum rate and the echocardiogram technician takes pictures of your rapidly beating heart.  The doctor supervising the test interprets the pictures and declares you free of significant blockage in the arteries of the heart.  A few hours later you’re discharged—about 24 hours after you arrive—without a firm diagnosis and with the hopeful anticipation that your hospital bill won’t be too big.

This scenario describes the way we go about evaluating most patients who come through the ER with chest pain.  I say “most” patients because there are often exceptions.  Someone with an abnormal EKG, elevated cardiac enzymes, or features to their chest pain that we consider “high risk” would likely bypass the above evaluation and proceed directly to the cath lab.  Other patients whose symptoms are so clearly noncardiac might get dismissed with instructions to seek out their primary physician’s guidance for further evaluation.

The vast majority are admitted and treated as described above.  In the business we refer to this method as a “rule-out,” as in “we’ll rule out a heart attack (with the enzyme tests) and then do a stress test.”  Doctors are quite comfortable with this for good reason.  For many years it has been a safe and effective way to figure out who is really having heart problems and who is just still trying to digest last night’s Mexican dinner.

You can turn to demographic studies to get a sense of what might be happening with the people who fall into this category (we call them “moderate risk”).  Out of every hundred people admitted for a “rule out” only a handful—five or ten—will end up having coronary disease as the cause for their symptoms.  If you were to take all 100 of them to the cath lab and look at their arteries you would find absolutely no narrowing in the majority.  Using the current method described above we admit an overwhelming preponderance of patients with normal coronary arteries just to find those few with blockage.  Most patients coming in with chest pain can plan on at least a few meals of hospital food before they get their answer.

What we really need is a test that can reliably exclude those patients with clearly normal coronary arteries and that can do it quickly with minimal risk and expense.  When you come in the ER with chest pain you need a test that can tell you with as much certainly as scientifically possible whether your coronary arteries are normal or not.  If your test is normal you can be discharged with the knowledge that your chest pain is not your heart.  If the test is abnormal you can then come into the hospital for further testing.

In statistical parlance what you need is a test with an extremely high negative predictive value.

A little primer on medical tests is in order.  The screening tests we use (such as stress tests, mammograms, blood PSA, etc) are not perfect.  Each test has various limitations that make it so we cannot conclude that an abnormal test definitively signifies the presence of disease (or that a normal test predicts that absence of disease).  We rate the accuracy of a test using complex principles called sensitivity and specificity.  These values (which are not particularly intuitive and continually vex new medical students and residents) can be translated into the more useful terms positive (PPV) and negative predictive value (NPV) by incorporating into the equation the prevalence of a particular disease in the population being tested.

PPV  is defined as the likelihood that a positive (or abnormal) test correctly identifies the presence of disease (if a stress test has a PPV of 80%, then you, as a patient, have an 80% chance of actually having significant coronary blockage with an abnormal stress test).  Just the opposite, the NPV is the likelihood that a normal test will prove the absence of disease (a NPV of 90% means that you have a 90% chance of being normal if you have a normal test).

This may alarm some people.  We are accustomed to believing that our medical tests are precise all the time, but most are not, and we doctors have to, in effect, decode the test results (interpret the interpretation, if you will) based on the individual patient’s clinical profile.

At least one test is changing that, and if you plan to head to an ER anytime soon with chest pain you should know about it.  The technology has now advanced so far that we are now able to use computed tomography (CT, or “CAT” scans) to obtain beautiful images of the heart and its arteries—images good enough to be able to immediately determine if a patient with chest pain has normal coronary arteries or not.

The coronary CT angiogram, or CCTA, is a study where the patient undergoes a chest CT scan with intravenous contrast injection.  The test is noninvasive (only an IV line is needed), low risk and quick, and it produces beautiful picture (see linked images).

Best of all CCTA has an astoundingly high sensitivity for the presence of coronary disease.  In the moderate-risk population referred to above, this translates to a near-perfect NPV.  Two recent papers (in Circulation and JACC) assessed CCTA in the ER and determined that the sensitivity and NPV for this test is 100%.

There are downsides to CCTA.  It involves radiation (about the same amount you’d get with a nuclear stress test) and so we obviously don’t want to do this in anyone who might be pregnant.  It also doesn’t do as good a job of proving the presence of significant coronary disease as it does the absence thereof, and you might need more testing if the study is not normal.

So, if you’re planning to come to the ER with chest pain you may find that we are able use CCTA to get you in and out a little more quickly than we used to.  That’s good news for all involved (unless you were hoping to enjoy a few more hospital meals).

Thank goodness.  Thank goodness I’ve finally got a little leverage I can use to convince my patients to get tested and treated.

I’m talking about the ubiquitous problem of obstructive sleep apnea, or OSA.  This is a disorder where the affected person erupts into a chorus of snoring and breath holding as they drift off to sleep.  If you’ve ever witnessed these apneic episodes you’ll never forget them.  The patient starts with loud snoring but reaches a point where it seems as if he’s sucked something into the back of his throat and can’t get another breath in.  He lies there, struggling against the obstruction for what seems like an eternity, until he wakes up and gasps for air.  To the alarmed onlooker (most often a spouse, although night-shift nurses can regale you with stories of breath holding that would impress Filipino pearl divers) it looks for all the world like the patient has sucked in his own pillow and will give up the ghost if he’s not awakened with a restorative kick.

The problem is not with an inhaled pillow but with collapse of the patient’s own tissue in the back of the throat.  When supine and somnolent, the patient relaxes the muscles that normally hoist the excess weight off the pharynx and the airway closes.  Breathing out works just fine—it’s the breathing in part that doesn’t go so well.  During inhalation the airway collapses like a flimsy straw used to suck up a milkshake.  The first time I witnessed this I found myself desperately chanting “breathe, breathe, breathe!”   Of course the patient doesn’t realize any of this is happening.

If you were to put a pulse oximeter (a device that measures oxygen level in the blood) on the finger of an OSA sufferer and watch him sleep you’d see something remarkable.  He’ll start off the evening near 100% but drop as low as 70% during a period of breath-holding lasting as long as a minute or more.  In classic cases this can happen literally dozens of time each night, each occurring during the most restorative phase of sleep.  As the concentration of carbon dioxide rises (normally exhaled during respiration) the patient begins to suffocate to the point that the brain kicks him back into semi-consciousness and triggers normal breathing.

As you can imagine the quality of sleep with OSA is terrible.  Morning headaches are common and daytime sleepiness is a hallmark of the disorder.   The long-term effects of untreated OSA are more insidious.  The recurrent low oxygen levels in the lungs leads to a scarring and stiffening of the blood vessels exiting the right ventricle of the heart.  The normally low pressure of this chamber rises two- and three-fold over time and it subsequently fails to cycle blood effectively, especially blood from the legs, which already has a tough enough time overcoming the force of gravity to get back up to the heart.  Severe, intractable swelling ensues that no amount of diuretic medication can cure.  For complicated reasons OSA also leads to high blood pressure that is very difficult to treat.  Also more frequent in this population are arrhythmias and sudden cardiac death.

While not limited to the overweight crowd, this disorder afflicts mostly those with extra pounds and is therefore rising in prevalence in parallel with the burgeoning obesity epidemic.  It’s now estimated that at least one in ten Americans suffer from OSA.

To diagnose the problem the patient has to undergo a sleep study.  This is where they come to a strange room, have every imaginable type of electrode attached to their head and body, and are monitored during the night under the watchful eye of a camera. At this point it’s actually fortunate that OSA patients are perpetually exhausted and drowsy—it’s the only way a person could be expected to sleep under these conditions.  If their oxygen levels drop sufficiently and frequently during the night the diagnosis is secured and treatment recommended.

While sufficient weight loss and exercise can effectively cure the problem in some people, therapy comes mainly in the form of a continuous positive airway pressure (CPAP) mask that the patient straps to their face with the same gusto as a creature from the movie Alien.  The mask forces air down the trachea of the patient with a slight pressure that is just enough to keep the airway from collapsing during inspiration.  A patient once told me the first time he strapped on the mask and went to bed he felt a little like Hannibal Lecter in a Serta commercial.

I hear it takes some getting used to.

For those who can tolerate the therapy it’s a life changing experience.  All of a sudden they feel more rested, have more energy, enjoy lower blood pressure, and gradually their swelling dissipates.  Now that they are no longer living life in the haze of perpetual drowsiness some patients even find the motivation to exercise more and lose the weight responsible for the OSA in the first place.

Unfortunately it has been a bit of a hard sell for us doctors.  Between the inconvenience of the sleep study and the threat of the CPAP mask many patients don’t want to have anything to do with getting to the bottom of their symptoms.  Up until now I’ve relied on the futile application of logic and reason.  Don’t like the fatigue and swelling?  Go get tested.  Want to feel better during the day?  Get back on your CPAP therapy.

Now back to the leverage.  It turns out some clever researchers decided to look at the effect that nasal positive airway pressure (NPAP) treatment for OSA has on that most important clinical marker of physiological function: the golf game.  Apparently, being compliant with NPAP improves a golfer’s game by as many as 3 strokes (the researchers didn’t comment on whether the therapy improves a golfer’s ability to accessorize with plaid):

"As any golfer knows," stated study co-author Dr. Marc L. Benton, "when your ability to think clearly or make good decisions is compromised, the likelihood of playing your best is greatly diminished. Through treatment with NPAP, we can improve many cognitive metrics, such as attention span, memory, decision-making abilities, and frustration management, which may, in turn, positively affect a person's golf game."

No more futile application of logic and reason for me.  I can now offer my recalcitrant patients not only the guarantee of better health and more fitful sleep, but also the promise of a few more birdies if they just give therapy a chance.