Meaningful treatments in the battle against coronary disease

I saw a patient in my office this week who had received a stent from one of my partners last month.  The man was highly satisfied with his experience—the procedure was tolerable, the recovery short, and the nurses were pretty (he specifically made a point of this, presumably because the post-hospitalization customer surveys don’t include what seemed to him to be the most important feedback metric)—but his wife had a different opinion.  She was upset (and not about the nurses).

“Why did he get only one stent?”

The cardiac catheterization had apparently revealed the presence of at least a couple of blockages.  The 99% narrowing—the one that was stented—was the clear cause of his chest tightness, and fixing this one had dramatically improved the patient’s ability to get from the couch to the refrigerator without gasping for breath and clutching his chest.  Another coronary vessel tapered to 70%, the cardiologist estimated, but that artery received no stent.  I pulled up the images from the procedure and saw that other minor disease was present but none that impinged on the vessel by more than 20 or 30%.

The concern from the patient’s wife is valid.  Why not put a stent in the 70% vessel while you’re in there?  The question implies the underlying logic that a 70% blockage, while perhaps not yet critical, will progress over time and eventually cause a heart attack: Let’s just put in a stent now and prevent future problems.  This same line of reasoning applies to so many other things we deal with.  Take cars, for example.  If three of my tires are bald and the fourth is 70% bald, wouldn’t it make sense to replace them all?  I know for a fact that my own mechanic has squeezed me for plenty of cash by successfully applying this logic to brake pads, filters, belts, etc.

Recently I read an article in the New York Times about this very topic (well, maybe not this exact topic—my mind tends to tie together lots of loose connections).  For years now, it appears, some dentists have made a pretty healthy income by drilling and filling small “pre-cavities” that would not progress to full blown erosions and which, if left untreated, might even resolve on their own (the author cites “mineral-containing saliva” that possesses some sort of salutary effect—and to think I’ve lived with my spit for four decades and never realized how magically healthy it is).  The concept behind a more conservative approach to cavity treatment is not without detractors, as evidenced by one dentist’s comments:

Dr. Douglas Young, a dental diagnostician at the University of the Pacific, thinks that “watchful waiting” doesn’t make sense.

“If you were to go to a physician and he were to diagnose risk factors for heart disease, the physician would take action and treat the early signs of disease and try to prevent future disease,” said Dr. Young, who helped develop a standardized cavity risk assessment adopted by the dental association.

I have a feeling from his comments that Dr. Young would join my patient’s wife in her dissatisfaction over our apparent disregard for moderate coronary obstructions.  Watchful waiting, in the words of Dr. Young, is an approach that any medical professional worth his or her salt—especially those that deal with heart disease—would never deign to recommend.

But here we are—my partners and I—suggesting nothing more than watchful waiting.  Why?

The answer lies in an understanding of how coronary atherosclerosis actually causes problems.  Here I cite a paragraph I penned in a blog post titled “The Paradox of Stenting” from February, 2009:

Despite our fervent desires to the contrary we know that intervening on a coronary blockage in an individual with little or no symptoms does nothing to decrease the future risk of heart attack.  We have numerous trials and procedure registries that attest to this.  Why is this?

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.

My patient had symptoms of coronary narrowing—chest tightness with exertion—that resolved completely once the 99% blockage was fixed.  The remaining cholesterol plaque in the range of 20-70% resulted in no adverse symptoms.  If a 70% blockage never worsens over time, it’ll never cause problems.

It is well established that drilling through an otherwise stable obstruction provides no benefit to quality or length of life, although this wasn’t always known.  When catheter-based coronary plumbing was first developed the early operators gleefully attacked every blockage in the belief that they were saving the patient from heart attack and death.  The so-called “oculostenotic reflex” led stent specialists to engage in aggressive vascular arts-and-crafts that produced gorgeous appearing vessels on the video monitor, but did little to make the patient healthier.

Thankfully, we’ve learned from our mistakes.  Opening blocked vessels is useful in really only two general areas:

  1. Heart attack, where the rule of thumb is to open the tightest blockage (we refer to it as the “infarct-related artery”) and leave the rest as is.
  2. Symptomatic blockages such as the 99% plug that caused my patient his troubles.  If, on the other hand, a person has no chest pain or breathing difficulty associated with the disease, we provide no benefit by uncorking it—even if the blockage is 100%.

Does that mean we do nothing?  Of course not.  On the contrary we eagerly provide the really meaningful therapy in the battle against coronary disease: medications and lifestyle modification.  Sure, it’s not particularly sexy—not like thousand-dollar stents in high-tech cath labs, at least.  But it’s effective.  As I pointed out in another post, the really meaningful impact on a person’s risk of future heart attack and stroke comes in the form of diet, exercise, smoking cessation, and the right prescriptions.

As for my patient and his wife, they left my office with that skeptical look on their faces you get when someone tells you something that you’re sure is untrue.  I had done my best to walk them through the logic behind our conservative approach but it wouldn’t surprise me if she immediately hit the Yellow Pages when she got home, looking for another cardiologist who isn’t so incompetent.  I don’t know who I’d recommend for a second opinion in the matter—most cardiologists recognize the limitations of performing unneeded procedures—but I sure know a dentist who’ll gladly take her side in the argument.

Eric Van De Graaff is a cardiologist at Alegent Health who blogs at the Alegent Health Cardiology Blog.

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  • katellington

    It’s tough to convince patients on this evidence-based approach medicine because most need more education on how the cardiovascular system works.  It would help to have more public health messages about this and to push patients into healthier lifestyle approaches after such interventions.  The KevinMD post on “what heart disease can learn from cancer patients offers some insight.   Interventional cardiology patients should go through some cardiac rehabilitation to help, yet there are so few programs.

    Link
    http://www.kevinmd.com/blog/2011/11/patients-heart-disease-learn-cancer-patients.html

  • Anonymous

    First off thank you for being honest about the now well publicized limits of PCI. PCI can save lives or at least reduce permanent damage to the heart in those whose plaques have ruptured and in the midst of an MI. But PCI (and to a lesser extent angiography) damages the endothelium and may well speed up atherosclerosis and/or increase the risk of plaque rupture  and no one ever seems to talk about this. Having seen hundreds of people who have passed up angioplasty and even bypass surgery over the past 25+ years and gotten rid of their stable angina with diet and exercise and more recently with greater ease with statins also I am less than sure that PCI is optimal medical therapy even for those with stable angina. Yes it can be palliative but one could argue taking away a patient’s only symptom of their disease may well make it easier for them to return more comfortably to a diet and lifestylke that will in the end likely shorten their life – most likely from an MI (possibly in the middle of that “pretty” stent).

    At best PCI in patients with stable angina is palliative and at worst it allows the patient to slip back into the all too comfortable denial process that allows far to much time on the couch and far too little time devoted to learning about what they should be eating to slow, stop and even reverse the atherosclerotic process and really cut their risk of a futute MI. Am I wrong?

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