Dr John M

cardiac electrophysiologist, cyclist, learner

The Case for Opening (some) Pools In COVID19 Pandemic

By

The COVID crisis has decimated water exercise. Can we rethink pool closures?

A significant number of my older patients relied on pools for their fitness. During a pandemic, you can stay active or fit only if you have good legs and joints. Walkers, runners, and cyclists have no problem; they play outside in the Spring weather.

People with bone/joint problems, fitness swimmers, and young children who normally take swim lessons this time of year are out of luck.

Consider the place I swim—the Mary T Meagher Natatorium, named after Mary T, a Louisville native, who won Olympic gold in 1984. The place is an ode to Sparta. The expansive no-frills public facility has tons of space to socially distance. 

Before I tell you my proposal, let’s set out some givens on May 13.

  • Three months into this crisis literally everyone knows the deal: the coronavirus is not going away. It will be as dangerous next year as this year; 
  • Older people are more vulnerable, and they know it;
  • The virus travels via droplets so distance reduces your odds of infection;
  • Other health conditions, such as mental stress, heart disease, obesity, diabetes, immobility and arthritis, do not become less problematic during a pandemic;
  • People differ in their risk tolerance; some people see a 0.5% infection fatality rate as scary as heck, others see a 99.5% chance of survival. 
  • Hand washing reduces transmission. Masks might also reduce transmission.
  • Finally, and this is key, the community-level risk for the virus differs greatly across the US. Policy in New York City or Chicago ought not be the same for rural Kansas or Texas. 

I’ve said before that Americans are not stupid. We can, and we must, rely on people to make good decisions for themselves and their community.

Now to the proposal to open some public pools: 

Start with a big sign in front that says we are open but these are not normal times. 

You place a bunch of hand-sanitizer stations at the entrance.

Tell people to wear a mask and leave it at the poolside. 

Then let them swim, do water aerobics at a distance, and allow teenagers to teach toddlers to swim. 

After the workout, people put their mask on and leave. If they have to use a locker room or shower, that’s fine. I don’t know about women, but in the men’s locker room, social distancing comes naturally whilst being naked.

When schools open in the fall, and they must open, kids should play sports. This includes the swim teams. Teenagers have minimal risk from the virus. If they are mixing in schools, there is no reason not to let them mix on the field and in pools. 

Caveat: I realize that summer scenes of hundreds of children mixed with adults in public pools is more problematic. My proposal applies to opening pools for the purpose of fitness. 

An unintended positive externality: the act of allowing people to exercise in water would be a small step towards making peace with the virus. If people don’t want to risk catching the virus, they can stay away. 

If we let people go to the grocery, walk in crowded parks or shop at gardening stores, we ought to let them enjoy the water. 

JMM 

Conflict of Interest: After fracturing my foot 2 years ago, I rediscovered the joys of swimming. Before the pandemic I often recommended swimming to my patients because there is something soothing about immersion in water.

Questioning Your Doctor is Ok

By

I received a good question(s) from a reader:

In your “Changing the culture” posting there is the comment: “Patients seeking medical treatment should not assume a prescribed therapy is beneficial just because a doctor says it is.”… How then does a patient evaluate a proposed treatment in a way that they aren’t thwarting a doctor from performing what may be a needed course of treatment? … Other writing I’ve seen describes doctors being too accommodative to patients reluctance at a treatment. A bad feedback loop if there was one.

Patients should definitely not assume a treatment (or test) is beneficial just because a doctor says it is. Doctors often practice dogma-based medicine. We get into patterns because that is the way we were trained, or that is the way we have done it for years. One study suggests it takes 17 years for doctors to assimilate evidence into practice.

Take the care of AF patients in the hospital. We, in our hospital and hospitals across the country, are trying to increase the cost-efficiency of caring for patients with AF. The problem is huge variation in care: some docs see a patient, treat her with oral meds, and get her home the same day, while other docs see a similar patient, admit her, put her on IV meds, do many expensive tests and keep her admitted for days.

AF is a variable condition, but one reason there is this much variation in practice is that many doctors don’t keep up. They don’t read the evidence. The other reason for overuse, especially in the US, is that doctors are paid more to do more. Hospitals worry about the latter practice because although they make more money with that approach now, reimbursement will soon favor efficient care rather than more care.

In my last post, I discuss another reason you should not assume a treatment is beneficial even if recommended by a doctor: too often, doctors accept treatments based on weak evidence. Minimally-invasive robot-assisted hysterectomy ended up being 10% worse than traditional surgery. For every 10 women treated with the minimally invasive surgery rather than regular open surgery, one was harmed by having recurrence of cancer.

Doctors–including those who wrote the guidelines–accepted minimally invasive surgery for this indication based on biased weak studies. They thought it was better but when tested in a randomized controlled trial, it was not.

I know questioning a doctor may sound complicated, but it is not. I have written multiple posts (here and here) on the big four questions to ask a doctor about a treatment or a test:

  1. What are the chances it will help me?
  2. What are the chances it will harm me?
  3. What are the alternatives?
  4. What if I do nothing?

Also good news for patients is the democracy of information from the digital age. Take a look at this excellent column the journalist David Epstein wrote for the Atlantic. The title says it all: When the evidence says no, but doctors say yes. Here is a brief quote:

“While he was waiting in the emergency department, the executive took out his phone and searched “treatment of coronary artery disease.”

The point is not that you can be a doctor with a smartphone, but you can look learn basic facts and read guideline statements. For instance, the Cochrane Collaboration, a group of researchers the world over, cull evidence and publish what are called systematic reviews on medical/surgical treatments. Each one of these reviews include plain-language summaries.

Having information helps you get more out of a visit with your doctor. The doctor’s role is changing. More and more, we are becoming advisors rather than prescribers. Good doctors offer the needed context for the information you have learned. They can help you make the best decision for you.

Finally, on the last part of the question: what if having good information leads to patients not taking a treatment?

This is ok. For instance, It happens all the time with clot-blocking drugs to prevent stroke in patients with AF. When people learn how much (or, for some people, how little) the drug reduces the risk of stroke and increases the rate of bleeding, they decide not to take it. Others hear the same statistics and decide to take it.

I say this all the time during lectures on shared decision making and informed consent: doctors may be the experts in medicine, but patients are the experts in what is important to them.

JMM

Cardiology Podcast Every Friday

By

My editors at Medscape warned me years ago that many people, especially younger ones, read a lot less. This saddened me because I’ve spent a great deal of time learning to write.

One of America’s most accomplished writers, Malcolm Gladwell, began his podcast because he worried about not reaching younger people.

Each week, I spend a great deal of time putting together thoughts on the top 4-5 cardiology stories of the week. Most of the ‘stories’ are studies, but not always. I have been doing this podcast for a couple of years now, but haven’t promoted it because I was not sure it would stick. It looks like it has–lots of young doctors have told me they listen.

I call the podcast This Week in Cardiology.

It’s available here on iTunes. https://itunes.apple.com/us/podcast/this-week-in-cardiology/id991125169?mt=2

It lasts about 10-15 minutes. Some of it is technical, but not all of it.

This last two weeks, I discussed the retraction of the PREDIMED trial. Gosh this is a big deal as PREDIMED was a randomized controlled trial (RCT), and most nutrition studies are observational. The differences in the two types of studies are significant.

Observational studies are tough to sort out–because of confounding. Confounding means there are many reasons the two groups could have had different outcomes.

Since PREDIMED was an RCT, the randomization of the two groups balance the confounding factors, and one can tell if the treatments causes a difference. I put causes in italics because good randomization allows one to make causal claims. This differs from observational studies, in which we can only say differences in the two groups associate with each other.

Association does not equal causation.

Specifically, PREDIMED studied use of the Mediterranean diet + Olive oil vs Mediterranean diet + nuts vs low-fat diet. In the original trial, the two versions of the Med diets led to fewer major adverse cardiac events. That was big. The trial was cited more than a thousand times.

But then a single doc, named John Carlisle, working on his own, figured out that there were irregularities in the randomization, not only in PREDIMED but up to 90 major papers.

Carlisle’s revelations prompted PREDIMED authors and the NEJM editors to look further, and indeed, they found irregularities. They republished the paper and the same results stood, but now the trial was considered mostly on observational study.

I discuss these issues on the podcast.

Other topics this week included comments on the massive overuse of tests for heart disease, such as stress tests, and the uncertainties of moderate alcohol intake for healthy and stroke care for the elderly, and the rise of genetic testing.

Perhaps you might find this weekly review useful. If you do, could you give it a rating on iTunes. It helps other find it.

JMM

The Truth on Cancer Screening

By

This week is Cancer Screen Week. It’s a one-sided campaign sponsored by industry and the American Cancer Society that urges people to get screened.

The truth is that the scientific evidence for cancer screening is not convincing. What’s more, screening comes with potential harms.

I know; it’s counter-intuitive, but it’s what the evidence says.

Benjamin Maser is a medical doctor (pathologist) and writer at Yale.

Check out our editorial on WBUR> Does Cancer Screening Save More Lives Overall? Not Necessarily

By the way, you may be thinking: what does a pathologist and a cardiologist know about cancer screening?

My answer is that one need not be a cancer specialist to interpret basic studies. The controlled trials compare a group of people who got screened vs those who do not. These studies, which we cited in the editorial, show that overall mortality is essentially the same in both groups.

That’s not complicated. Nor is understanding the notion of over-diagnosis and over-treatment.

In the article, we favor honesty, balance and informed decisions–not fear and bullying.

JMM

Inflammation, Ablation, Fats, LDL, etc .. My review of ESC 2017

By

The European Cardiology Congress, ESC as it is called, has grown into the largest medical meeting in the world. This year, more than 31,000 attendees from 153 countries came to Barcelona.

I was busy. Here is an update of the big stories:

Inflammation: 

Experts agree that inflammation associates with heart disease. One of the keys to showing inflammation causes heart disease would be to show a reduction of cardiac events with a drug that blocks inflammation.

The CANTOS trial tested the ability of a drug called canukinumab, which is already approved for rare causes of inflammatory diseases, to reduce cardiac events. Canukinumab exerts its anti-inflammation action by blocking a key signaling chemical in the inflammation cascade.

CANTOS turned out positive–well, sort of. Patients who took canukinumab had a 15% reduction of cardiac events. That sounds like a lot but translates to an absolute reduction of 0.64%. Researchers noted two other important observations: one was that blocking inflammation led to a small rise in fatal infections. The other nifty observation was that patients on canukinumab died from cancer at a lower rate than those on placebo. This anti-cancer effect will be explored further.

My post on CANTOS is here: Quick Thoughts on the CANTOS Trial

AF Ablation: 

The CASTLE-AF trial studied the effect of AF ablation in patients with advanced heart failure–patients had low ejection fraction and ICDs. Does ablation in these patients reduce death rates or hospital admissions? The preliminary answer was yes. (Preliminary because the trial has not yet been published.)

Investigators reported a lowering of death rate by 47%. That’s massive. Many drugs and ICDs have been shown to lower death rates in patients with heart failure, but the reductions range from 15-35%.

The published results of this trial will be novel and could change the view of AF ablation. Novel because, to date, AF ablation has only been shown to improve quality of life–not outcomes. One strong warning is that patients included in CASTLE-AF were highly selected, most had previously failed antiarrhythmic drugs and the centers doing the ablation were highly experienced. I worry that irrational exuberance at the time of trial publication will add to the overuse of AF ablation that already exists.

My Post on Castle AF is here:  CASTLE-AF: Does It Change the World of AF Ablation?

New Use of Rivaroxaban (Xarelto):

The drug rivaroxaban (Xarelto) has become well-established for prevention of stroke in patients with AF. At ESC, a huge trial called COMPASS tested lower doses of rivaroxaban for the prevention of cardiac events (heart attack, stroke, death) in patients with established heart disease. We call this secondary prevention.

Showing improvement in secondary prevention in 2017 is hard because we have so many good treatments already.

The COMPASS trial showed that the combination of low-dose rivaroxaban (2.5 mg twice daily) plus aspirin lowered the event rate by a mere 1.3%. And this gain was countered by a 1.2% rise in major bleeding. Though this sounds like a wash, experts from around mainstream cardiology lauded the results. The king of cardiology, Dr. Eugene Braunwald, from Harvard, provided the discussion in the main auditorium after the trial was presented. He embraced the results as a breakthrough.

I was not so embracing. My post on COMPASS is here: The COMPASS Trial: Time for Clear Heads, Not Celebration

Extremely Low Cholesterol Levels:

You may have heard about the new cholesterol-lowering drugs called proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitor drugs. These 14,000$ per year injections cause dramatic drops in LDL–the bad cholesterol. In the previously published FOURIER trial, patients on PCSK9i drugs had a lower rate of cardiac events, but surprisingly, the reduction in nonfatal events did not translate to improved death rates.

At ESC, the authors of FOURIER presented a sub-analysis of the results looking specifically at the association of LDL and cardiac events as well as safety. (Extremely low levels of cholesterol raise concern about other bodily functions.)

Three findings emerged: one is that many patients in the trial achieved crazy-low LDL levels, some in the single digits! The second finding was that the lower the LDL, the lower the event rate. The third finding was that despite crazy-low levels of LDL, the investigators noted no safety issues.

One popular narrative from these observations is that LDL in the blood is toxic and should be removed. In my post, titled, FOURIER: Very Low LDL-C Post Hoc Analysis Doesn’t Move the Needle, I make the case that this evidence is not enough to change our thinking about these expensive drugs. And, since the trial was truncated after only 2 years, it’s hard to say much about safety. Remember, people don’t take cholesterol-drugs for only two years.

The Healthiest Diet? 

The debate on which diet and which percentage of nutrients, say fat, carbohydrates, plants, etc rages on. At ESC, results of massive observational study of more than 130,000 people across Earth, found that carbohydrates to be a villain, and fat intake, even saturated fat, associated with better outcomes. The PURE study, which included not one but three papers, was published in the Lancet.

One aspect of PURE is that it flies in the face of recommendations from our American Heart Association. My colleague Sue Hughes has great coverage of this story here: PURE Shakes Up Nutritional Field: Finds High Fat Intake Beneficial

Sue’s story includes this beautiful quote from senior researcher Dr. Salim Yusuf:

My hope is that our results will stop the whole population from feeling guilty if they eat fat in moderation. While very high fat intake—when it accounts for 40% or more of your dietary intake—may be bad, the average fat intake is about 30% and that’s okay. We’re all afraid of saturated fat, but actually we shouldn’t be. Saturated fat in moderation actually appears good for you.

Miscellaneous: 

I recapped these stories in my weekly podcast called This Week in Cardiology. 

I also gave my Watchman debate. I think I did pretty well as the antagonist. My opponent, Prof Horst Sievert was strong. He made mention that my case against Watchman came from a blog–but I countered that it has, in fact, been peer-reviewed and accepted for publication in a major journal. Stay tuned for more. Readers … stay suspicious of left atrial appendage closure.

Only a week after the terror tragedy, Barcelona felt like the safest city I have been in. If anything, given the tone at the meeting and on the streets, the terror event seemed to create greater cohesiveness of the people.

JMM

The Future of Predicting Heart Disease May Be In Your Genes

By

Three cases first:

A young woman I met recently (outside the hospital) told me her Dad died suddenly a couple of years ago. He was fine, then he was stone cold dead. The wife went outside for a minute and came back to find her husband dead in the chair. There were no warnings. No chest pains, no breathing problems, and no real diseases, except well-controlled high blood pressure.

A middle-aged man came to see me in the office because his brother died suddenly while jogging. The patient wanted to know his risk of heart disease and what he could do to prevent premature death. Both my patient and his dead brother were in decent shape.

Finally, a well-educated patient, who did not have heart disease, asked me about the decision to take statins. His primary care doctor recommended the drug based on his cholesterol level plus his age. This man had read the studies showing only modest benefits for statins in primary prevention.

*****

Gene Risk Scores

My most recent column over at theHeart.org | Medscape Cardiology delves into the use of genetic data to help predict heart disease.

I know; writing and reading about genetics is akin to eating broccoli instead of pizza. Give me leeway for a minute or so, this is nifty stuff. I learned bunches.

First some background: We now know there are many gene locations on our chromosomes that associate with coronary artery disease. At these areas are many single nucleotide changes, called SNPs, or single nucleotide polymorphisms, that may individually or together influence the risk of getting heart disease. SNPs sound tricky but really they are just a single substitutions of say an A for T or G for a C in the DNA.

In recent years, researchers have been able to cull these many SNPs into a composite score, called a GRS, or gene risk score. Companies like 23andMe used to report gene risk scores for heart disease but the FDA asked them to stop. (That’s probably coming back soon.)

My point is that these gene scores are not pie-in-the-sky stuff.

Now to the compelling evidence. In the Medscape Cardiology column (you need to give your email to read), I review the numerous studies of using gene risk scores to predict heart disease. It can be summarized into five main points:

  1. Gene risk scores are not just a fancy family history. The score predicted heart disease independently of self-reported family history. The obvious weakness of a self-reported family history is that people live different lives from their parents.
  2. Gene risk scores can predict different trajectories of heart disease risk. If you plot survival curves of low genetic risk versus high genetic risk people, the people with high risk scores get heart disease at a younger age.
  3. Genetics may help pinpoint those individuals who may benefit most from statins. I cited multiple studies showing that individuals with high genetic risk garnered much greater risk reduction from statins than did those with low genetic risk. This is really cool. The researchers actually used blood from patients in the randomized controlled trials for statins to show these gradients of benefits.
  4. Gene risk scores may influence people to change behavior. I also cited studies showing that people with high genetic risk who pursue healthy behaviors can reduce the chance of a future event.
  5. Gene risk scores have advantages over imaging tests such as coronary artery calcium. For one, CAC depends on age. Gene scores can identify young people at risk. Another advantage is that gene scores are a simple blood test rather than a scan.

I hope you read my column on theheart.org | Medscape Cardiology: Who Needs a Statin? DNA Beats Current Risk Calculators.  The reference list of studies is there.

In the column, I cite work that Dr. Eric Topol and colleagues from Scripps are doing. They are in beta-development of a free-mobile app that takes a person’s 23andMe data and churns out a risk score on your phone. It’s called MyGeneRank.

Your doctor can’t easily order gene risk scores now. Insurance doesn’t cover them. But the tests are not too expensive.  My prediction is that soon enough, knowing your gene risk scores will be like knowing your LDL–only the gene data will be far more useful.

JMM

P.S. I needed a lot of help to learn this stuff. Dr Pradeep Natarajan of Harvard deserves a shout out for taking the time to explain much of this to me. You can follow him and his mentor Dr. Sek Kathiresan on Twitter.

Dr. Eric Topol, who is editor-in-chief of Medscape, a famous cardiologist and now genomics researcher also helped me learn this material.

Statins, Like All Medicines, Are Neither Good Nor Bad

By

We have to talk about drugs.

No, not illicit drugs, but medications used by doctors and patients.

Plaintiff attorneys run ads on TV that fool people into thinking certain meds are bad. The current one I deal with is the clot-blocking drug rivaroxaban (Xarelto.) Before that, it was dabigatran (Pradaxa). If, or when, the makers of rivaroxaban settle a class action suit, you can bet apixaban (Eliquis) will be next.

These ads are a problem because they use fear persuasion (see Scott Adams’ blog), and because they can induce patients to stop taking or not start a beneficial medicine.

Lots of other medications suffer from a “bad” or “toxic” branding. Some people think statins are bad; many people think amiodarone is toxic. Warfarin (Coumadin) still suffers from the branding of rat poison.

I want to be clear: medications are neither bad nor good. Medications are chemicals that act on cells in the body in an attempt to create benefit. All medications can be toxic.

Toxicity turns mostly on dose. (Chance can also play a role in toxicity.)

Warfarin kills rats because the rodents keep eating the pellets and the drug builds up to high doses. In humans, we adjust the dose.

When patients tell me certain medications are toxic, I remind them that too much water, taken by endurance athletes, can cause dangerously low sodium levels that may lead to seizures. Oxygen given at high doses for too long in patients on ventilators can damage the lungs. Life saving-antibiotics can cause life-threatening colon infections.

I would urge doctors and patients to frame medications with the big four questions:

Four Crucial Qustions

As an exercise, let’s apply the four questions to the statin drugs (we exclude from this discussion people with familial hypercholesterolemia):

What are the benefits of taking statins?

There is only one benefit of statins: to reduce the future probability of a heart attack, stroke or death. Do not make the mistake of thinking statins are for cholesterol lowering. The drugs do lower cholesterol levels, but that’s a mere blood test. There are plenty of drugs that lower cholesterol but do not reduce the risk of heart attack or stroke.

The benefit of statins, therefore, is a probabilistic one. It’s like a lottery. You take the pill every day in hopes it will prevent a serious cardiac event in the future.

Numerous randomized controlled clinical trials (the highest level medical evidence) confirm that statins do reduce the probability of a cardiac event.

In absolute terms, the degree of statin benefit depends on whether a person has had a cardiac event.

For those without a previous heart attack, stent, bypass or stroke, statin benefits are small—no mortality benefit and about a 1% reduction of nonfatal cardiac events over the next 5 years. Doctors call this primary prevention.

For people with a history of a cardiac event or stroke due to a blockage of some sort, statin benefits are greater—about a 1.2% lower risk of dying and 2.5-3% lower risk of a non-fatal heart attack over the next 5 years. Doctors call this secondary prevention.

What are the harms of statins?

The best known harm of statins are muscle issues. I use the word issues rather than damage because true muscle damage is rare—about 5 in 10,000.

The actual frequency of muscle symptoms is hotly debated. Randomized controlled trials (in which patients don’t know whether they are taking the statin or placebo) report very small increases in muscle complaints—about a 1-2% increase. Observational studies, however, reveal higher rates of statin muscle complaints—in the range of 10-20%.

The second potential harm of statins is a small increase in diabetes. One of the smartest doctors on the Internet, Dr. Richard Lehman, says “the issue of [statin] induced type 2 diabetes is just an artifact of the way we define the threshold for T2DM. Statins often cause a small rise in blood sugar, which would only be of significance if it was associated with an increase in macrovascular or microvascular disease. On the contrary, statins reduce macrovascular disease end-points, and there is no evidence to suggest that they increase eye or kidney microvascular disease (which are very rare in the glucose range we are talking about).”

A third potential harm of statins is the burden of taking a pill every day. Scientists call this pill “disutility” and its measured in how much extension of life one would trade for taking a pill every day. People have different feelings about pill burden.

Another possible (emphasis here on possible) harm of statins is that the drugs may interact in a negative way with lifestyle. In a 2014 theheart.org | Medscape Cardiology column that went a bit viral (647 comments), I cited two observational studies, one that reported a higher calorie intake of statin users and the other less physical activity in male statin users.

Are there simpler safer options?

Opinion alert here: I strongly suspect that a healthy lifestyle delivers similar benefits.

Eating modest amounts of real food, not processed food in packages, doing regular exercise and managing stress would likely deliver lots of probabilistic benefits for reducing the odds of having heart disease.

This “intervention” however, has not been compared to statins in randomized controlled trials. Cardiologists Aseem Malhotra, Rita Redberg and Pascal Meier, writing in the British Journal of Sports Medicine, point to the obvious reason for this: “There is no business model or market to help spread this simple yet powerful intervention.”

What happens if I do nothing?

The most likely outcome of not taking statins is the same as if you take one—nothing. In the best case, that of secondary prevention, the risk reduction for nonfatal cardiac events is about 2.5-3%. That means one has to treat about 39 patients for five years to prevent one event. The odds are you would be in the 38 of 39 category, but you don’t know.

Doctors think this is a good trade. If these stats are applied to populations, many heart attacks can be prevented.

The ultimate decision is up to you. You are not a population.

JMM

You can do this exercise for any medical intervention or medication. Why we don’t do it more often is hard for me to understand.

Four Crucial Questions To Ask Your Doctor

By

I am seeing an increasing number of patients who did not know they had a choice about taking a medicine or having a procedure.

  • Why did you have that heart cath? A: My doctor said I should.
  • Why are you on that medicine? A: My doctor prescribed it.

It’s time we re-review the basic four questions you should ask your doctor.

I wrote about this in April of 2015 for WebMD. Here is 2017 update:

1. What are the odds this test/medicine will benefit me?

Medical decisions are like gambles. Benefit is not guaranteed. In my field, catheter ablation of supraventricular tachycardia (SVT) has a success rate approaching 99%, but the success rate for ablation of atrial fibrillation or ventricular tachycardia is much lower.

Another aspect of discussing benefit is defining what is meant by benefit.

Statin drugs, for instance, are quite good at lowering cholesterol levels, especially LDL, the bad cholesterol. But LDL is what we call a surrogate marker. Having a lower LDL is supposed to deliver future benefit–say a lower chance of a heart attack, stroke or death.

If you don’t have heart disease, just a high cholesterol level, your future benefit of taking a statin is small. Abramson and colleagues, writing in The BMJ, estimated the average future benefit of statins in low-risk patients to be in the range of a 7 in a 1000 risk reduction of a non-fatal event over the next five years. That means that about 140 patients have to take a daily statin to prevent a heart attack or stroke in one patient. Is that small but statistically significant benefit worth taking a statin? That’s up to you–not your doctor. (Note: the risk reduction with statins is higher if you have established heart disease.)

Another example in the news lately is the benefit of PSA screening for prostate cancer. The USPSTF, a major governmental guideline committee, recently changed the recommendation for PSA screening in younger men from a D to a C. In one sentence, the benefit of PSA screening is that it reduces your risk of dying from metastatic prostate cancer by about 1 in a 1000, but that small risk reduction does not translate into a survival advantage overall. (See oncologist Dr. Vinay Prasad’s review here.)

2. What are the downsides or harms of the test/medicine?

No intervention in the practice of medicine is free. Here I don’t mean costs, I mean harms. You can’t have an ablation without incurring the risk of procedural harm; no doctor is perfect. You can’t take a drug without exposing yourself to the potential toxicities of the drug. (Even antibiotics come with the risk of severe allergy or secondary infection with Clostridium difficile colitis.) This is where you need your doctor to help balance the probability of harm versus the probability of benefit.

An important warning though: Doctors under-estimate harms and over-estimate benefits. I recently wrote about a systematic review from two Australian researchers which showed clinicians rarely had accurate expectations of benefits or harms, with inaccuracies in both directions.(1) This group has also found patients, too, over-estimate benefit and under-estimate harms.(2)

3. Are the simpler safer alternative options?

When I explain options to patients, I always tell them there are alternatives. An alternative to catheter ablation is an attempt to control the rapid heart beat with a medication. In heart disease prevention or treatment, one of the most common alternative therapies is an improved lifestyle. For instance, the alternative to taking a statin drug for cholesterol or a blood pressure drug for hypertension, is a better diet, weight loss and more exercise.

4. What happens if I do nothing?

As mainstream medicine increasingly medicalizes much of the human condition, this last question grows in importance.

The famous French philosopher Voltaire said that the art of medicine consists in amusing the patient while nature cures the disease. Time is an underused tool in the treatment of illness. Despite our dominance as a species, patients and doctors underestimate the ability of the human body to heal itself. The main advantage of watchful waiting is that it allows patients to avoid harm from healthcare.

Another aspect of not taking a drug or not having a procedure is living with the condition. This comes up a lot in atrial fibrillation care. Sometimes, often even, the presence of atrial fibrillation episodes does not diminish the quality of life enough to warrant taking the risks of treatment–say drugs or procedures. It’s a very similar story in surgery: maybe the hernia or inflamed joint bother you, but not enough to have the surgery.

JMM

References:

  1. Hoffmann TC, Del Mar C. Clinicians’ expectations of the benefits and harms of treatments, screening, and tests: A systematic review. JAMA Internal Medicine. 2017.
  2. Hoffmann TC, Del Mar C. Patients’ expectations of the benefits and harms of treatments, screening, and tests: a systematic review. JAMA Intern Med. 2015;175:274-286

I am changing…

By

Seven years have passed since I started this blog.

In that time…

I have learned some basics about writing. (I almost wrote, “I have learned to write,” which would have been foolish, since, writing-wise, I have plenty to learn.)

I have learned to stay upright on the bicycle. Concussions made me understand that the joys of criterium and cross racing don’t outweigh their risks. I still ride nearly every day; I’m a pretty fast bike commuter now. And I’ve shifted my endurance-sport goals to running, which is a far safer sport for the brain. My goal is to run 10k in less than 40 minutes.

The main thing that has changed about me is my views as a doctor, especially when it comes to dealing with people who complain of nothing.

Medicine is most pure when we treat people with illness. The infirmed come to us with a problem and we use our intelligence, experience and procedural skills to help them. It’s immensely gratifying. The joy of helping people still negates the stifling burden of administrative nonsense. I’ll do your damn corporate safety modules one more year because helping sick people get well feels so good.

But when people complain of nothing, our first job is to do no harm. I know prevention of disease is better than treating it, but the process of prevention gets dicey. When we prescribe things (screening tests, statins, aspirin, diabetes drugs etc) to people who complain of nothing, we should have the highest evidence these therapies deliver benefit. Too often, we cite eminence rather than evidence.

I’ve come to believe the medical profession is too paternalistic, too arrogant. I fear the medicalization of the human condition. These days, I order fewer tests. Medical tests put people into the “system,” on the metaphorical train of healthcare. This train accelerates quickly, and it’s often hard to get off. Even a simple echo scares me. I could tell you stories.

More often than not, I tell patients to stop checking their “numbers.” If they insist on health numbers, I favor three–the scale, the belt size and a Timex to measure walking speed.

A 2002 article from Dr. David Sackett (a pioneer of evidence-based medicine) perfectly captures my views on preventive medicine.

It’s called The Arrogance of Preventive Medicine. It’s worth a look, now more than ever.

Shortly after I tweeted the Sackett article, Harvard economist and professor Amitabh Chandra chimed in with this:

JMM

P.S. For a longer and more polemic view of preventive medicine, see also, Piotr Skrabanek’s… The Death of Humane Medicine. Be warned; you can’t unsee this stuff.

Give Local Louisville — Have A Heart

By

Folks —

I’ve written more than 1000 essays on this blog over the past 6 years.

I have no ads. I don’t write to make money. (I have a good job.)

I don’t ask for anything on this site. You have been supportive in your comments and emails. Thank you.

Screen Shot 2016-09-14 at 6.31.47 AMThis week, in Louisville, is a campaign called Give Local Louisville. It’s a one-day (tomorrow — September 15) giving campaign.

My ask is that you consider donating to Have A Heart Foundation.

Have A Heart is a non-profit I’ve been volunteering at over the past year. We deliver free cardiac care to those in Louisville who cannot afford it.

My partner Dr. Mike Imburgia has led this effort. Many people from my group at Louisville Cardiology volunteer.

The thing about giving tomorrow is that Give Local Louisville also has matching funds.

It’s a one-day thing. Tomorrow! Thursday. If you decide to donate, even 10$ makes a difference, what you do is click on the Have A Heart link and a place to enter your credit card will be there. Maybe they will have PayPal (I don’t know.)

Here is the URL for those of you who get this by email:

https://givelocallouisville.org/npo/have-a-heart-foundation

Thank you in advance.

JMM

Are women with AF being under-treated with ablation?

By

This post is an introduction to commentary I made recently over at theHeart.org on Medscape. Gender features in the discussion, but there are lessons for men and women with AF.

***

A large study from a group of Stanford researchers made three big observations on AF ablation:

  • Women, compared with men, presented for first AF ablation at an older age and with more risk factors (higher CHADSVASC score.)
  • At 30 days after the ablation, women compared with men, suffered from more complications.
  • At one year after the ablation, women compared with men, had more re-hospitalizations but fewer cardioversions and repeat AF ablation.

The first two findings confirmed results of previous studies. For whatever reason, it’s not well-understood, women who come for first ablation often have more advanced atrial disease. It’s also well established in cardiology, not only EP, that women have higher rates of complications with procedures.

The third finding was provocative. It tempts one to think women are getting cheated out of repeat ablation and cardioversions.

Here are the Stanford authors (italics mine):

“Our findings, in context, may be indicative of potential barriers to optimal or sustained rhythm-control strategies in women. . . . These data call for greater examination of barriers and facilitators to sustain rhythm-control strategies in women.”

A reader could infer two benevolent biases in these words: women are getting stiffed out of more cardioversions and AF ablation, and that’s bad because rhythm-control strategies are good.

I would propose a contrarian view. Women who undergo first AF ablation present with more associated diseases, older age, and more advanced forms of AF. They also experience more procedural complications. It’s possible, therefore, that more rhythm control (with ablation) could worsen a gender gap in outcomes.

In other words, women might do even worse with more ablation.

The reason I propose this contrarian view gets back to the guts of the AF ablation procedure. Pulmonary vein isolation, the agreed upon foundation of AF ablation, was first described as a treatment of focal atrial tachycardia coming from within the pulmonary vein muscle bundles. (A rare form of AF.) A focal treatment for a focal disease.

Now, doctors have extended the use of PVI to people with diffuse atrial disease, metabolic risk factors (obesity, high blood pressure, diabetes), and inflammation. This can be a wrong target problem.

A 2010 study from Dr. Natale’s group showed that a higher burden of structural disease in the atria may be the reason women have more non-pulmonary vein triggers. Non-PV triggers are bad because it’s very hard to find and ablate them.

Here is the take-home:

The Stanford findings allows doctors to make opposite explanations: the easy and conventional one is that women are under treated with redo ablation; the other view is that maybe women should not get more ablation after failed ablation.

The reason we could have such opposite views is our lack of understanding of the disease AF.

Recent evidence on AF suggests that AF is often the heart’s way of manifesting “tension” or disequilibrium. The tension may be too much inflammation (pericardial fat or recent infection/surgery); or maybe the tension is too much stretch (obesity, sleep apnea, hypertension, excess endurance exercise); or maybe the tension is too much neural disruption (stress, lack of sleep, alcohol). Sometimes it’s multiple combinations of these.

The AF ablation procedure can do only one thing well: isolate the pulmonary veins. This electric fence around parts of the left atria does little to treat most of the above conditions that ail the atria.

The title and link of my referenced article is here:

Less AF Ablation in Women: Gender Bias or Appropriate Care?

JMM