AF, Ablation, Stents and Five Nuances

Joan has left an excellent comment on my recent 2019 AF ablation update.

She brings up many important issues. Let’s dissect it.

Q: Joan asks if it is common to see patients who think they are cured after AF ablation but are still in AF? 

A: The scenario I described in my previous post is not common, but it is not rare. Since AF ablation entails much instrumentation and many burns, it can affect how the heart feels things. The heart has its own nervous system; yes, the heart feels. Also, the bigger the procedure, the bigger the placebo effect. 

Q: If ablation doesn’t work, then I sure know a lot of people walking around who had ablation and are convinced it changed their lives. 

A: First, I did not say AF ablation does not work. I wrote that we don’t know; it has not been adequately tested in a placebo-controlled blinded trial. 

But let’s consider how ablation might change people’s lives without eliminating AF. 

The sites of ablation in the left atrium are close to neural inputs to the heart. It may be that we change how the heart perceives AF simply by instrumenting the heart and ablating in the areas near where the nerves attach to the heart. This statement should induce little surprise because the majority of people who have AF do not know it. All cardiologists have observed a huge disconnect between an actual heart rhythm disorder and its symptoms.

A Canadian study called DISCERN AF found that the ratio of asymptomatic to symptomatic AF episodes increased more than threefold after ablation.^[1] In 2017, a study called CAPTAF found that AF ablation compared with drugs improved quality of life, but the improvement occurred without a statistically significant reduction in AF burden. Hmm?

Another problem with assessing “success” of AF ablation is uncertainty about the meaning of AF episodes. That sounds like a crazy sentence, as AF on an ECG defines the condition AF. The traditional way to determine ablation success is the absence of even 30 seconds of AF on any monitor. That makes little sense because if someone had persistent AF before the ablation and after the procedure has a couple of 30-second episodes a month, why isn’t that a success?

But it’s even more complicated than duration of AF episodes. We are beginning to understand that AF on an ECG may be an end-result of underlying atrial disease. In other words, the AF may be a symptom or sign of other stuff that is awry in the body and negatively affecting the atria. (Stress, high blood pressure, inflammation from fat around the heart, and many many other things.)

An apt analogy is infection and fever. When we get a bacterial infection, we also get fever. The treatment of a bacterial infection is to kill the bacteria with antibiotics not just relieve the fever with acetaminophen. Is AF ablation acting like acetaminophen—merely covering up something else?

This is a super disruptive notion because in the past we considered the electrical episodes of AF as a good surrogate marker for symptoms and a predictor of stroke. 

There are many studies showing a poor (temporal) relationship of AF episodes to stroke—meaning, when people with AF had stroke, they often had no AF episodes before the event. How could that be if AF caused stroke? What’s more, AF drugs reduce AF episodes but don’t reduce the rate of stroke? How could that be if AF caused stroke? Dr. Hooman Kamel has written one of the most important papers on AF. ^[2] He and his co-authors make the case that we need a new framework of understanding AF and stroke. I would say.

Q: You have done AF ablations for a long time, are your personal observations irrational or unscientific? 

As for my experience with doing more than a thousand AF ablations over 15 years, I believe the procedure helps people. I wouldn’t do it otherwise.

But I am not sure; and the procedure is expensive, invasive, risky and… it needs to be tested.

If medicine is to be scientific, we must ascribe to the Feynman principle: “the first principle is that you must not fool yourself and you are the easiest person to fool.”

Doctors have been fooled often. 

• Cardiologists used to use pacemakers to treat benign fainting. Until this was reversed in a placebo-controlled trial.
• Heart surgeons used to tie off the internal mammary artery to treat chest pain. Until it was reversed in a placebo-controlled trial. 
• When I came to Louisville in the 1990s, heart surgeons were doing transmyocardial laser revascularization–burning holes in the heart for the relief of angina. This was reversed in a placebo-controlled trial. 
• Neurosurgeons used to place embryonic fetal cells into the brain for Parkinson’s disease. This, too, was reversed in sham-controlled trial, which even involved drilling holes into the head of patients in the placebo arm. 
• Orthopedists used to think knee arthroscopy for arthritis reduced pain. Nope. This common practice was reversed in placebo-controlled trial. Here is review article^[3]describing five ortho surgeries, including the common procedure called vertebroplasty, which have been proven not to work by sham-controlled trials. 

Q: How can patients agree to be in a placebo-controlled procedure trial, and would insurance pay for it? 

The way ORBITA investigators arranged for a placebo arm of their trial was that all the patients were promised the stent procedure; the ones in the placebo arm simply had to wait a few weeks–after the treadmill test and questionnaires were done. For AF ablation, this period will be longer, probably six months to a year.

On the matter of insurance, in an American system of private insurance, providers can change each year. That means there is little incentive to keep people healthy in the long term. Thus, there is little incentive to pay for people to be in a placebo-controlled trial. But in most countries, the government pays for healthcare, and would have an extreme incentive to prove whether or not a costly procedure works.

Q: Stents are still being used. How could this be given the “weird” ORBITA study? 

The tricky thing about stents are that they work great for patients having a heart attack, but no study shows they work (on average) for patients with stable heart blockages. 

While the use of stents for stable blockages has decreased, the practice still continues in earnest. The way around this is use of different diagnoses. Instead of saying the stent is being used for stable coronary disease, doctors often label the symptoms as unstable angina. ^[4]

The core reason stents are being used despite numerous studies showing that they do not reduce heart attacks or death is that the clogged pipe theory of heart disease is deeply engrained–among doctors and patients alike. It will take decades to change this thinking. (Though there is one more trial testing stents; it’s called the ISCHEMIA trial and it’s had its share of controversy.^[5])

Nobel winner Max Planck famously said that science advances one funeral at a time. This is often true in Medicine. 

Resistance to de-adopt unproven therapies is one of the reasons I am a medical conservative, and why I advocate for evidence of benefit before therapies are accepted.

References:

1.         Verma A et al.Discerning the Incidence of Symptomatic and Asymptomatic Episodes of Atrial Fibrillation Before and After Catheter Ablation (DISCERN AF): A Prospective, Multicenter Study. JAMA Intern Med2013; 173(2): 149–156. doi:10.1001/jamainternmed.2013.1561.

2.         Kamel H et al.Atrial Fibrillation and Mechanisms of Stroke Time for a New Model. Stroke2016; 47(3): 895–900. doi:10.1161/STROKEAHA.115.012004.

3.         Louw A et al.Sham Surgery in Orthopedics: A Systematic Review of the Literature. Pain Med2017; 18(4): 736–750. doi:10.1093/pm/pnw164.

4.         Wadhera RK et al.Association of the Hospital Readmissions Reduction Program With Mortality Among Medicare Beneficiaries Hospitalized for Heart Failure, Acute Myocardial Infarction, and Pneumonia. JAMA2018; 320(24): 2542–2552. doi:10.1001/jama.2018.19232.

5.         Rajkumar CA et al.‘Faith Healing’ and ‘Subtraction Anxiety’ in Unblinded Trials of Procedures. Lessons from DEFER and FAME-2 for End Points in the ISCHEMIA Trial2018; 11(3). doi:10.1161/circoutcomes.118.004665.