I was a medical student when I made my first medication error.  Most doctors wait until they’re out of training and can actually write prescriptions and give orders before they screw things up.  Not me.

It was the very first clinical rotation of my third year and we had admitted a lady to our service who had chest pain and high blood pressure.  All of the testing had come back normal and it was looking less likely that she was actually experiencing a heart attack or aortic dissection (much to the dismay of us medical students, who desperately wanted to witness our first real medical disaster).  While looking through her records I hit upon the idea that this lady might be suffering a panic attack and suggested to the attending physician that we try treating her for this.  He gave my suggestion a moment’s consideration and shooed me away by telling me to ask the intern write for the sedative Klonopin.

Somehow, as the message spun through my cerebral cortex on its way to being translated into a request for the team’s intern, I got a little confused and passed on the wrong bit of information.  “The attending wants you to try some clonidine.”  The intern dutifully wrote the order and the nurse administered the medication.

In the end the patient faired just fine despite my error.  Clonidine—the somewhat homophonous counterpart to Klonopin—is actually a blood pressure pill and was a reasonable addition to her medication regimen.

It was then that I became conscious of the multiple layers of difficulty surrounding the names of drugs.  Clonidine and Klonopin.  Zantac and Xanax.  Inderal and Adderall.  Take one look at the complete list of “sound-alike” drugs and you’ll begin to understand how a young medical student could make such an error.

To make matters worse, every drug has to have not one, but two separate names.  Clonidine is also Catapres and Klonopin is also clonazepam (you’ll notice that I stick with the convention of capitalizing the trade name of the compound).  Some have even more: diltiazem can be Cardizem, Cartia, Dilacor, Diltiaz, Tiazac, Viazem, Dilzem, and Dilatrate.  This sort of chaos would be appropriate only if diltiazem treated multiple personality disorder rather than hypertension.

We study drugs for hours and hours in medical school but don’t even come close to learning all the different names for them until we have to start dispensing them as interns and residents.  I’m pretty sure I wasn’t passably fluent in drug nomenclature until I graduated internal medicine residency, a full seven years after I started med school.

I bring all this up as a preface for the subject of this week’s blog post: “Drug names are confusing” with subtitle “How can you expect an eighty-year-old patient to know his entire medication list if his own doctor struggles with it?” with sub-subtitle “The drug naming system is a clever plot by a vast pharmaceutical conspiracy to enslave the human race in mindless confusion” with sub-sub-subtitle “How I learned to stop worrying and love the bomb.”  Sorry, wrong subtitle.

Here are my gripes (and for the purpose of my argument I’ll stick mainly to the drugs I know best):

1. All drugs have at least two names (as outlined above).  Some are similar (digoxin and Lanoxin, niacin and Niaspan) and others not (verapamil and Calan), but all are confusing.  Why not just stick with just one name (say, Zocor) and add the suffix “generic” or “branded” as indicated?  Is it really necessary that patients learn both Zocor and simvastatin?

2. Drug names are rarely descriptive.  Here’s a game: take out your copy of the PDR (you know, the one you keep on your bedstand), scan the list of medications and just try to guess what each drug is meant for based on the name.  Ranexa, Inspra, Keppra, Zyprexa, Celexa.  Meaningless, all of them.  At least car companies come close to conveying some sense of meaning with their names (Viper, Cobra, Firebird, Pacer).  Years ago we had drugs like Hytrin and Minipress—with monikers that invoked some blood pressure-ishness—until we discovered that they’re actually lousy blood pressure pills and relegated them to the domain of the prostate.  Lopressor alone remains a blood pressure pill that actually sounds like one.

   You’ve got the diabetic drug Januvia that sounds like a new-age face cream (“Eliminate unsightly wrinkles with Januvia”); the antiarrhythmic Tambocor that sounds like something from band camp (“My son’s singing with so off-key that his music teacher made him play the Tambocor”); and Exubera, the insulin formulation that sounds like a street name for speed (“Dude, where can I score some of that Exubera?”).

3. Drug names are often unpronounceable.  I remember when the clot-busting drug ReoPro came out, with the alphabetically-random generic abciximab.  It took me weeks before I could spit that one out without giving my tongue a hernia.

   Then there are some simple ones that just beg to be pronounced incorrectly.  Write down the following names and hand them one of your patients: atenolol, diltiazem, simvastatin, lisinopril, and amiodarone.Odds are pretty good that what you’ll hear will be something like this: AT-en-all, DILT-i-zem, sim-VAST-in, LIS-prel, and AM-a-RI-dee-an. 

   Even the medical professionals can’t get Cardizem right.  The makers of this drug came up with a fiendishly slick way to get us all messed up on this one.  The generic, diltiazem, has the “ia” sound in the middle, but they conveniently left that out when they came up with the trade version, Cardizem.  Hence, half the time you hear someone refer to this medication they’ll call it car-DEE-a-zem rather than CAR-di-zem.

4. Drug names are often unspellable.  Need something to control your rhythm?  Try Rythmol (but where did the “rh” go?).  What was that new med my doctor put me on?  Multack, Multak, Multaque?  No, Multaq.  Why do half of all new drugs have to start with X or Z?  And what’s with the fixation on using the letter Y as a vowel (Zyrtec, Lyrica, Zyvox, Bystolic)?  What ever happened to “a, e, i, o, u and sometimes (only sometimes) y”?  The name Xyzal (levocetirizine) looks more like an algebra equation than an allergy drug.  Taking the cake in this category has got to be Pristiq (generic desvenlafaxine): it’s unspellable in both brand and generic, unpronounceable, and has a trade name that in no way relates to its purpose (antidepressant).  The only way it could be worse is if they had spelled it Prystyq.

Can you really blame the medical student who can’t tell the difference between a sedative and an antihypertensive whose names are separated by a solitary consonant?  Or the geriatric patient who stares at you in confusion when you tell him you’re putting him on Zaroxolyn (metolazone) or hydrochlorothiazide?

All I know is I want first dibs on the naming of the next batch of high blood pressure medications that come on the market.  You’ll love them: Normopress*, High-no-more, and Strokeblocker—catchy names, without resorting to a single X, Y, or Z.

* Note: I thought I was being pretty clever when I came up with the fictional name “normopress.”  Just as I was about to submit this post to my hardcore and unforgiving editors I decided to Google the name.  It turns out that Normopress is the trade name for methyldopa in South Africa, atenolol/indapemide in Europe, and losartan in Pakistan—all blood pressure pills.  Guess I’m not the only one eager to prescribe medications that sound more intuitive than Ranexa and Exforge.

Let’s say you develop some heart problem and get sent to me for an evaluation. You show up to the office, check in, get ushered into an exam room, then you wait and wait and wait. When I finally come into the room I seem terse, impatient and rushed, and you end up visiting with me for less than 5 minutes. I provide you with a diagnosis, order a couple of tests and dash off a prescription.

What’s your impression of me? What’s your opinion of me as a doctor, or of my medical skills? If you were asked to rate the quality of care you receive what kind of score would you give me?

Now let’s add some more information to the mix. Would it change your mind to learn that I was late seeing you because I was in the emergency department providing lifesaving care to Sister Margaret Mary, an elderly nun who is the sole caregiver for a dozen homeless orphans? And I cut my visit short because I had to get back to the cath lab to open her critically blocked heart artery so that she can survive to continue her motherly care and what seemed like impatience was actually my anxiety about the welfare of the poor orphaned children.

Would your opinion of me be any different?

And what if you see me for a follow-up visit on a day when I am not busy saving nuns or orphans, have all the time in the world for you, and yet I indifferently rush through my appointment just so I can get back to my office to surf the internet and update my Facebook profile? Are you now back to your original opinion of me?

My real question for you is this: Given the limited interaction you’ve experienced, are you in a good position to pass judgement on my skills as a doctor?

According to many websites on the Internet, you are.

Go to your favorite search engine and type in “rate your doctor” and you’ll find a dozen sites that allow you to grade your doctor on knowledge, timeliness, professionalism, competency, and even compassion. The rise of these sites mirrors other service industries—hotels, restaurants, home repairpersons, etc.—that have had to begin to factor open, anonymous, internet-based feedback into their management strategies. One area where this has become amazingly popular is education, where students can now seek revenge on boring instructors who were not insightful enough to reward the student’s languid brilliance with anything more than a C-.

In order to come to some understanding of this trend I spent a little time browsing my own entry on various doctor rating websites and have come to the conclusion that they tend to be inaccurate, dated, and sparsely applied.

I learned from RateMDs.com that my name is actually Dr. Van and that I practice in Lincoln (my office used to be headquartered there). No one has provided any feedback on Dr. Van, although one person gave a glowing report to my brother, Dr. Van De Graaff, a dermatologist in Omaha (whom I easily found): “Staff was super nice as was he, and he didn't waste my time. He isn't out for the money as he even recommended the least expensive option which worked great. I would totally recommend him.” This anonymous rater, who thought my big brother was “super nice,” obviously didn’t grow up with him.

Vitals.com also believes I practice in Lincoln but at least they got my last name right. In addition to the usual demographic information they provide about me they also go to the trouble to rate my medical school (3 stars) and my residency training program (4 stars).

DrScore doesn’t even know who I am, but did identify another sibling of mine as a head and neck surgeon in Lincoln (unfortunately, he moved to Idaho over two years ago). He hasn’t had anyone rate him yet, although I was tempted to grade him on his competence as a little brother.

DoctorScorecard and Healthcare Reviews advertise themselves as rating sites but are pretty shoddy. To be fair, though, they seemed to target an international audience by providing ratings for physicians in India and the U.K. Needless to say I couldn’t find my name on these sites.

The very popular Angie’s List has come to doctor rating a little late in the game. This is the only site that requires you to pay a subscription to search for your doctor (the other sites will give you basic information for free but you’ll have to pay a small fee to learn if your doctor has malpractice suits or is wanted by the police). I can’t give you any feedback about Angie’s List since I’m too much of a cheapskate to sign up for service.

The most popular site for doctor rating appears to be HealthGrades (another site, PhysicianReports, links straight into HealthGrades). I was able to find my name along with current addresses for our Alegent offices, although I had to search under “Lincoln” to locate myself. Miraculously I learned that one patient went to the trouble to locate me on this site and provide a rating (I got 5 stars in all categories, which makes me suspicious of my 8-year-old daughter and her precocious internet skills).

Thinking that perhaps my patients are less internet-savvy (or perhaps more indifferent to the care I provide) I browsed HealthGrades to see if other doctors in Omaha have more patient feedback that I have. Of the 84 cardiologists listed, only 36 showed any rating at all, with most of those having only a solitary patient who went to the trouble to find and grade them. Only one cardiologist had ratings from 3 patients.

Our experience in Omaha doesn’t differ significantly from the trend nationwide.

A study in last month’s Journal of General Internal Medicine showed that Boston-area practitioners were as rarely reviewed as my colleagues and I are. Additionally, almost all the reviews given where overwhelmingly glowing—not much help if you want to weed out the doctors you want to avoid. A commentary in the LA Times summed up the overall impact of these sites:

Patients just don't appear too interested in providing feedback on their doctors, the authors noted, despite the fact that consumers generally love and use ratings systems. In contrast to the scarcity of doctor reviews, a search of restaurants in Boston's Beacon Hill area "turned up 38 narrative reviews for a single Lebanese restaurant," the authors pointed out.

The sites have the potential to empower patients. And, to be sure, consumers today are encouraged to be smarter and more discriminating shoppers of healthcare services and products in order to reduce costs. But this is one Internet function that doesn't seem to do patients much good or doctors much harm.

From a statistical perspective it makes sense that these ratings sites have yet to achieve prime-time utility. Just one or two reviews on a doctor are not enough to be able to provide a representative opinion on the overall care of the provider. A single, heavily biased review (whether good or bad) would impart an inordinate influence on the overall score. In order for such a system to really provide useful feedback it would have to include reviews from hundreds of patients (such as is the case with consumer websites such as Amazon), a scenario we’re not likely to see anytime soon.

My verdict is that the idea as a whole is sound but that the execution thus far is lacking. I feel comfortable that my value as a service provider could be accurately scored and quantified if it were based on the feedback of hundreds of my patients—if I’m a lousy doctor the truth will undoubtedly come out in the overall tally. Just one perfect score (like I currently have on HealthGrades) doesn’t give my prospective patients any useful information about what they might expect when they come to see me. Someday this system might be an excellent way for patients to have more control over what sort of provider interaction they can expect, but as it stands they still have to rely on old-fashioned word-of mouth and hope for the best.

Now, if you’ll excuse me, I’ve got to get back to caring for nuns and orphans.

Just when you thought it couldn’t get any worse.  As if it weren’t bad enough already that you spent your school years being picked dead last for basketball teams and that you always had to crane your neck upward to look into the eyes of your prom dance partner, or that you had to put up with that diabolically catchy Short People song getting stuck in your head, the world now comes along and deals one more injustice to those of you who of challenged vertical stature.  Just last week the Associated Press reported the findings of a study out of Finland that allegedly demonstrates a 50% higher risk of death from heart disease among short people as compared to their lengthier counterparts.

That’s right: not only are you short, but you’re short and doomed.

The researchers reviewed and pooled the findings of 52 previous demographic studies and were able to show that persons under 5’3” are one-and-a-half times more likely to keel over from a heart attack than those over 5’9”.  It wasn’t a bit reassuring that the authors of the study had absolutely no explanation for why diminutive people tend to have hearts with limited warranties.  The best they could do was to smugly remind short people to go out and engage in some form of (presumably non-basketball) exercise.

Tuula Paajanen, the study's lead author, of Tempere University Hospital in Finland, said short people shouldn't be alarmed about the findings.

"Height is only one factor (among many) that may contribute to heart disease risk," she said. Paajanen recommended people focus on other things like not smoking, eating a balanced diet and exercise. "Those are easier to change than your height."

Another European expert (not associated with the study) provided similarly helpful advice:

"We don't want to scare short people, but perhaps they should be extra cautious about their lifestyle," said Borge Nordestgaard, a professor of genetic epidemiology at the University of Copenhagen.

Those among you who will never hope to have a clear view at a movie theater or change a light bulb without a stool have already suffered enough injustice.  You’ve been told that tall people are happier, wealthier, more popular, and are even more likely to win an Academy Award.  Now, to make matters worse, the tall crowd doesn’t have to watch their diet or exercise as much as you do in order to stave off a visit the cardiac ward.

What’s the link between stature and risk of cardiac death?  I don’t know, but here are a few possibilities:

• In the history of humankind, height among various populations has been an indicator of nutrition.  We’re taller these days than were our ancestors of the Victorian age, mainly because we do a better job of getting three square meals a day and eating our leafy greens.  Good nutrition generally means a better chance of survival.  But does this really apply to our present world where my shorter friends have the same access to Whole Foods that I have?
• Perhaps evolution has played a part.  Tall cavemen enjoyed a diet of apples, peaches, and other healthy foods that come suspended in the treetops, while their more compact counterparts had to subsist on starchy subterranean tubers and the atherogenic red meat of a downed mammoth.
• Do tall people give their hearts a better daily workout by simply standing up?  The heart of a Yao Ming has to work harder to circulate blood the full length of his 7’6” towering frame than does the heart of a Hervé Villechaize (who, despite his diminutive stature, seemed to be the only one on the island capable of reliably spotting the plane).
• What if it has more to do with the care the patient receives after he has his heart attack?  A tall person clutching his chest and collapsing in a crowd is more likely to attract the attention of a CPR-trained bystander than is a tiny person.

A more plausible scenario is that this whole line of logic is flawed.  The science of statistics can be easily twisted into a world of smoke and mirrors.  Retrospective analysis of the sort described above can come up with some pretty murky findings and if you spin the data just right you can pull almost anything you want out of a large enough data pool.  If you creatively churn the numbers in any sizable database you’ll find that persons with the last name starting with the letter V are more likely to die of food poisoning, karaoke mishaps, leprosy, accidents involving livestock, toenail fungus, infected paper cuts, or errant golf ball shots.  Does that mean anything?

Another possibility is that short people indeed have more heart disease, but that the reasons for this are so multifactorial as to render the relationship entirely unhelpful.  Can we truly cut the risk of cardiac death among smaller people by simply making them run more and eat less?  Perhaps the relationship resides entirely elsewhere and following the recommendation of more vigorous diet and exercise would have no more impact in this population than in any other.

Besides, in the end it all equals out anyway.  Taller people are more likely to die from breast and prostate cancer, injuries, and endocrine abnormalities.  Short people tend to survive periods of hardship better than taller individuals.  And, of course, don’t forget the whole issue of lightning strikes.

So, short people everywhere: while you may still harbor resentment about sitting the bench during basketball games, don’t lose too much sleep about this supposed predestined failure of your cardiovascular system.  After all, you know what lack of sleep will do to your heart.

There is no class of medications in the history of the world that has been better studied that statins.  This class of drugs is more properly termed HMG CoA reductase (3-hydroxy-3-methyl-glutaryl co-enzyme A reductase) inhibitors, but with a name like that a terser nickname is almost mandatory (the name statin comes from the suffix of the members of this class: lovastatin, pravastatin, etc.).  Simply speaking, this chemical blocks the metabolic pathway that produces cholesterol, which, of course, is known* to be a chief culprit in the formation of arterial blockages and is a direct risk factor for heart attacks and stroke.  Following are statins currently available in the U.S.:

• Lovastatin (Mevacor)
• Pravastatin (Pravachol)
• Simvastatin (Zocor)
• Atorvastatin (Lipitor)
• Rosuvastatin (Crestor)

Since the development of the first widely used statin in 1976 (lovastatin, originally isolated from penicillin fungus) thousands of patients have participated in major research studies assessing the safety and effectiveness of this class of medications and more than 3 billion prescriptions have been filled in the U.S. alone.

The theoretical benefit of widespread statin use has translated into a real effect among the current population of patients at risk for heart disease and stroke.  At present, the prevalence of coronary heart disease is at its lowest in decades, despite an ongoing epidemic of tobacco abuse and obesity.  Many experts in the field of epidemiology feel this is a direct result of the generalized application of the knowledge that has come from these many research studies.  I personally agree that the extensive use of lipid-lowering drugs has actually cut into my cardiology business, and I’m quite pleased with that.

You would think that all this information and scientific certainty would settle any potential controversy surrounding the safety of the statins. You might imagine that doctors and patients alike would feel comfortable using a class of medications for which there is study after study demonstrating the benefit of this type of cholesterol blockade. 

Not so.

Virtually every patient who has ever gone on a statin medication has heard stories from family, friends, neighbors, and acquaintances about the dangers this class of drugs harbors: muscle and joint pain, weakness, paralysis, memory loss, depression, cancer, chronic pain, liver and kidney failure.  If you go on the internet and type “truth about statins” into virtually any search engine you will come up with thousands of sites that provide you with nearly everything except the truth.  I tried this last week and was astounded at the misinformation that is heaped upon anyone trying to come to an unbiased opinion on the matter (I also found that for most of these sites the damaging assertions about statins serve as nothing more than a gateway to advertise some other product).

Before I proffer my opinion on the matter, let’s detour for a moment to review the hierarchy of patient-based research.  Medical studies come in a myriad of different designs and span the gamut of quality and reliability.  At one end of the spectrum are anecdotal reports (“As a doctor I observed that Mr. X had adverse reaction to the drug Y”) that are unquestionably the least reliable of all scientific methods in that they involve only few patients, often only one doctor, and are fraught with heavy personal bias.

At the opposite end sits the gold standard research protocol: the prospective, randomized, controlled, double-blinded study.  Definitions:

Prospective: All data are collected after the study is designed.  The opposite of this is the retrospective study which collects data about events that have already happened.

Randomized: Each patient to enter the study is randomly assigned to one of two (sometimes more) therapies.  This differs from some studies where the clinician picks the therapy the patient will receive.

Controlled: More than one therapy is represented in the study.  Generally you compare the treatment in question (such as a new drug) to another treatment that is either placebo (sugar pills that reportedly have no true effect) or the established standard of care (therapy that patients are already receiving).

Double-blinded: A radiologist once told me this means to two orthopedists trying to read a chest x-ray.  It actually refers to a deliberate concealment from both the patient and the doctor/nurse/study coordinator so that neither entity can know whether the patient is receiving the therapy being tested or the control.  With many medications this is relatively easy to do.  With other therapies, such as surgeries, it’s very difficult.

The point of each of these provisions is to remove the effect of bias—on the part of the patient, the doctor, and the study designers—to the greatest degree possible.  Unfortunately this type of study is also the most difficult to run and extremely expensive, but it yields the most reliable information we can obtain.  A researcher who could successfully run such a study with a few hundred participants would be guaranteed a publication in a highly reputable medical journal.

How many patients have been enrolled in statin studies?  At this point over 120,000 patients have participated in prospective, randomized, controlled, double-blinded trials specifically looking at the statin class of medications.  And in every one of these studies the side effects of both the statin and the placebo have been documented with the precision of a Swiss watchmaker with obsessive-compulsive disorder.  Every ache and pain, each rise and fall of dozens of lab markers, and all doctor and hospital visits are painstakingly recorded, tracked, and dissected using a mind numbing array of statistical analyses.

Modern medical science has never (and may never again) so thoroughly dissected the effect—and possible adverse effects—of a class of medication as has been the case with statins.  Here’s what the research teaches us:

• If you’ve had a heart attack already, or have coronary artery disease, you are at relatively high risk for heart attack, stroke and death.  Those with diabetes or atherosclerosis elsewhere in their circulation (carotid or peripheral) are at similarly high risk.  This group of patients has at least a 20% risk of death or severe cardiac problem over the course of 10 years.  A general rule holds true about risk and therapy: the higher your risk, the greater the magnitude of benefit you get from a therapy.
• If you average all the studies you will find that you can reduce the risk of cardiac-related death by about 20% among individuals at higher risk.
• Statins reduce the risk of stroke by about 20-30%.
• Statins are known to raise liver enzymes in a dose-dependent fashion in around 5 percent of people
• Statins very rarely lead to dangerous muscle damage (myopathy).
• Side effects were reported only slightly more commonly in patients randomized to receive the statin drugs (when compared to those on placebo), but the rate of drug discontinuance was similar between both groups. 

This last finding is critical.  It means that regardless what you may hear from neighbors and family about the dangerous side effects of statins, the truth of the matter is that among the 120,000 patients studied the side effects of the statins were no different than those of the placebo pill.  Sure, muscle aches occurred, but they were no more prominent among patients randomized to receive the statin.

At least one caveat exists to all this research, however.  There is one form of prominent bias that cannot be excluded from prospective studies such as these, and is in fact inherent in the design of the trial.  This bias occurs when the investigator decides what type of patient should be enrolled in the research and who should be excluded.  A good example is the mammoth Heart Protection Study (HPS), a research endeavor that randomized over 20,000 patients to statin versus placebo.  The enrollment criteria required patients to have some form of vascular disease present (coronary, cerebral or peripheral vascular disease) and therefore excluded patients with no established history of atherosclerosis.  Since healthy individuals weren’t enrolled it stands to reason that the findings of the HPS cannot be applied to the general population. 

Also excluded were patients with certain medical problems.  Since muscle aches and liver enzyme abnormalities are a known possible side effect of statins, HPS kept patients with preexisting muscle and liver ailments from enrollment in order to limit the confusion. 

Research coordinators are free to exclude these individuals from receiving statin therapy but we clinicians aren’t.  Patients with liver and muscle problems come in with heart attacks as often as anyone else does and we are left trying to decide how safe and advisable it is to start these people on statins.  It’s not known whether people with other complicated medical problems (or complex drug regimens) are at higher risk for statin side effects.

Now, having bored you with my lengthy sermon on the scientific literature supporting statin safety and tolerability, let’s look at real world experience.  Most every physician you talk to will tell you that the rate of statin intolerability among their patients is higher than 5%,  I, too, have seen a higher than expected proportion of patients come back to my office complaining of muscle aches and fatigue after initiating this cholesterol therapy.

What to make of this?  I don’t really know.  I have to believe that statins in the general population result in side effects at a rate not seen in the study groups.  For me to deny this would be ignoring my personal experience with patients whose symptoms improve once they stop the medication and recur if it is restarted.

That said, I also believe that the specter of statin toxicity has so suffused the general population that it has affected the way patients and doctors react such possible side effects arise.  When a person who is not on a statin has joint or muscle aches or fatigue, those complaints are attributed to nothing more than old age, obesity, arthritis, or what have you.  But, these days, when a patient on a statin reports the same symptoms, the statin becomes the culprit and is quickly discontinued.  An example: I saw a patient this week who complained to his pharmacist of muscle aches associated with a cold and was told to stop his Crestor because “it might be killing him.”  Thankfully, the patient—an elderly gentleman at great risk of repeat heart attack—was open to hearing a second opinion.

In summary, if you are unfortunate enough to have had a heart attack, stroke, vascular disease, or diabetes, you are at immense risk of suffering some vascular complication down the road.  Pharmaceutical research has provided us an enormously potent tool to cut the risk of heart attack, stroke and death in such individuals, and more than a hundred-thousand patients donated their bodies to help prove the safety of this therapy.  Each of you has to make your own choice about every medication you introduce into your body, but I would encourage you to put a little faith in the best science that modern medicine has to offer and submit to letting your doctor help you control your cholesterol.

* Remarkably, there are numerous so-called experts who call into question the linkage between cholesterol and heart disease and their websites can be easily found.  The research that implicates cholesterol in vascular disease—starting with the seminal Framingham Heart Study in the 1950s—is about as ironclad as any concept we have in modern medicine.  Those who can’t get on board with the lipid hypothesis would likely have been the same ones to reject the earth-is-round theory.

Prior to a few weeks ago I had never heard of Bret Michaels.  I’ve now learned he’s a musician in the “glam metal” band Poison and has had some health difficulty recently.  While most of my readers are probably avid fans of hair bands and need no primer on Poison’s rise to stardom in the 80’s (you may even have their classic rock ballad “Every Rose Has Its Thorn” as your cell phone ring tone) I am somewhat more sheltered and had to look up his information on the internet prior to writing this blog post.

While I take no pleasure in the suffering of others, I have to confess that I find it useful when a celebrity suffers from some heart related problem.   For a few days or weeks the issue of heart health rises to public discourse and gives everyone an opportunity to become more educated.  Also, since I have to come up with a different topic to write on every week, I am relieved when something interesting falls into my lap.  When a famous person launches a heart problem into the public spotlight it makes my job that much easier.

Such was the case recently with Mr. Michaels, who is also apparently a recent winner of the reality TV show The Apprentice and a multi-talented fellow, with screen-writing and acting credits to his name.  At the age of 6 (according to his entry on Wikipedia) he was diagnosed with type 1 diabetes and for years has used his fame to advocate on behalf people with this illness.  Comments from adoring fans on his website attest to his likeable character.

Earlier this year Mr. Michaels was admitted to the hospital for an excruciating headache only two weeks after undergoing emergency appendectomy.  Tests showed a subarachnoid hemorrhage—a bleed in the brain—that appears to have required no urgent therapy.  Just one month later he returned to the hospital after suffering temporary numbness to the left side of his body and was diagnosed with a transient ischemic attack (TIA), or ministroke.  Evaluation of his heart revealed that Mr. Michaels was born with a patent foramen ovale (PFO) and that this had been the apparent cause of his brief stroke symptoms.  His doctors maintain that Mr. Michael’s recent ailments—the appendicitis, the brain bleed, his underlying diabetes, and his TIA—are all unrelated to each other.  What this means, of course, is that Bret Michaels is one really unlucky fellow and is on pace to match reputations with the Biblical, boil-plagued Job (although for his sake I hope Mr. Michaels is not actually the subject of a wager between God and the devil).

One relationship worth exploring, however, is the connection between a PFO and his stroke symptoms.  To understand this relationship you need to learn more about a PFO, and to do that we need to go back, back, back . . .  (cue the flashback music) . . .

Back to when you were an embryo.  As you rested in the warm embrace of your mother’s womb your lungs sat dormant, bathed in amniotic fluid and serving no purpose other than to prepare for the moment the doctor spanked your bottom and you took your first breath of air.  Before your birthday, oxygen entered your body not through your mouth but through a constant flow of blood coming from your umbilical cord.

(These days your blood reenters your heart through the right atrium, is passed into the right ventricle, and is then squeezed out to the lungs.  In the lungs it dumps off the unwanted stuff (carbon dioxide), picks up the good stuff (oxygen), then returns to the left atrium and ventricle to be pumped out to the body.)

Back when you were the source of morning sickness for your longsuffering mother the blood took something of a detour after it entered your heart through the right atrium.  Since passage through the wet lungs was not necessary the blood was shunted through a hole in the heart and was pumped directly out to the body.  The hole in the heart, called a foramen ovale (literally, oval hole) was a normal and necessary part of your cardiac anatomy.  According to your body’s owner’s manual this hole was supposed to seal shut the moment you popped out into the labor and delivery ward and belted out your first scream.  From that point on, the blood dutifully passed through the lungs to be loaded with oxygen prior to heading out to the body.

Unfortunately, somewhere between 15 and 25 percent of all people continue to have a persistent hole where the foramen ovale existed (this is, of course, the PFO), and Bret Michaels is one of them.  In most people this PFO never represents any problem.  In a rare minority, however, various issues can arise.

In the case of Mr. Michaels an embolic stroke seems to be the problem.  As he recovered from his other health problems he likely developed a small clot in one of the veins of his legs that dislodged and headed toward his heart.  In the “non-PFO” patient such a clot would end up in the small capillaries of the lungs where it would quietly dissolve and result in no untoward effect.  The PFO in Mr. Michaels allowed the clot to bypass the filtration system of the lungs and proceed directly to the brain where it briefly choked off blood flow to his valuable neural tissue (possibly the region of the brain responsible for an appreciation of power chords and spandex pants).  Luckily he suffered no long-term effects.

Stroke is not the only problem associated with a PFO.  There is increasing evidence to suggest that patients with a PFO are more likely to suffer routine migraine headaches and there are ongoing research trials meant to better explain this relationship (including a study being done here in Omaha—see below).  Deep sea divers with PFOs are at particular risk of neurological problems as they deal with pressure changes and nitrogen gas bubbles.

Surgeons used to repair the PFO by cracking the chest and sewing a patch over the opening.  We are fortunate these days to have a less invasive, slick approach to the problem that can plug the PFO with minimal risk and discomfort.  In my practice we have an expert in the area of PFO closure, Dr. Himanshu Agarwal, and I turned to him for a couple of questions regarding this issue:

Question: How successful is PFO closure?

Dr. Agarwal: Catheter-based closure is more than 99% successful in plugging the PFO and in preventing recurrence of cryptogenic stroke.  Our team at Bergan Mercy has completed approximately 30 cases in the last 3 years with a 100% technical success rate.

Question: As a patient, how tough would it be to undergo this procedure?

Dr. Agarwal: The risks are similar to those associated with a cardiac catheterization and include less than a 1% risk of any major neurovascular or cardiac trauma. Operating time is only 10 to 30 minutes.  Since the procedure requires vascular access through the vein (rather than the artery, as with the cardiac catheterization), the patient can get up and walk after only a couple of hours.

Question: As a doctor, how would you rate the technical difficulty of this procedure (scale of 1-10, one being the Dutch kid sticking his finger in the dike, and 10 being BP successfully plugging the oil leak in the Gulf of Mexico)?

Dr. Agarwal: 2 or 3

Question: What do you think of the link between PFO and migraine headaches?

Dr. Agarwal: There is a strong correlation between PFO and migraine headaches, as well as between closure of the PFO and improvement in the headache syndrome. You can read more on the subject in a publication from the American Headache Society.

Question: What’s your role in researching this link?

Dr. Agarwal: We are part of the ongoing PREMIUM Migraine Clinical Trial and are actively enrolling subjects with migraine headaches (for more information, call Alegent Research at 402-343-8511).

Question: Who should be screened for a PFO?

Dr. Agarwal: Patients less than 55 who have cryptogenic stroke or those with recurrent stroke; deep sea divers or those who frequently suffer from high altitude hypoxemia; patients planning to undergo posterior fossa surgery (a type of brain surgery usually performed in a sitting position—the presence of a PFO would necessitate a supine positioning during surgery); and patients with frequent, unexplained hypoxemia.

Question: You didn’t include migraine sufferers?

Dr. Agarwal: That’s what the research is for.

Well put.  Thanks to Dr. Agarwal for sharing his expertise with us.

It appears PFO closure is in the stars for Bret Michaels.  According to his website, the musician has recovered and is now back to performing rock ballads to sold-out stadiums.  I wish him well and thank him for helping to educate us on the subject of PFO and for giving me a topic for this week’s blog post.  Hopefully his streak of bizarre health woes won’t continue—I don’t want to have to rely on his bad luck for too many more articles.