Pioneering Interventional Cardiologist Defends Unorthodox Practices

–Bernhard Meier explains why he seals plaques and thinks PFO closure is ‘the best procedure in interventional cardiology’

(Updated)

Recently I wrote about an article by Bernhard Meier, a top interventional cardiologist, in which he rejected the idea that evidence based on randomized controlled trials should be the basis for the practice of interventional cardiology. In response to that article I received a message from another prominent cardiologist. He told me that at a public meeting some time ago Meier had made two provocative statements:

  1. After PFO closure Meier never uses intracardiac echo and doesn’t believe it is necessary.

2.After stenting severe lesions in the left coronary circulation Meier, if he saw a mild (<50% lesion) in the proximal LAD,  would inflate the balloon and pull it across the mild lesion to denude the lesion and stimulate atherosclerosis at the site in the hope of converting the potentially soft mild plaque that might be at risk of rupturing and occluding the artery into a mildly atherosclerotic plaque, which would be less dangerous for the patient.

I invited Meier to respond to my piece and to explain these unorthodox practices. Here is his response:

“I have been involved with PCI since the world’s first case in 1977 when I was Andreas Grüntzig’s assistant after having found the first patient for him. I still take care of this patient who is in good shape and looking forward to celebrating the 40th anniversary of his intervention next year.

“Watching the outcome of coronary (plain old) balloon angioplasty (POBA) patients over the first decade, before stents became a commodity, I was impressed by the fact that there were virtually no occlusions of sites treated by POBA except for the ones occurring early, i.e., during the procedure or before hospital discharge (after discontinuing heparin which was often continued overnight at the time). This led to the theory that treating a mild lesion with POBA kind of sealed the plaque (my term ‘plaque sealing by coronary angioplasty’ has since been discussed in the literature by a few others). Rupturing the plaque with the balloon led to a new endothelial coat during the healing process that, at worst, caused a restenosis but was free of the risk of spontaneous plaque rupture and thrombotic coronary artery occlusion germane to non-treated plaques. People warned about turning the initially nonsignificant lesion into a significant restenosis but I had observed that moderate lesions subjected to POBA had a restenosis risk that was only single digit (about 5%) and therefore not a real reason not to perform ‘plaque sealing’. Likewise, abrupt closure virtually never happened when dilating (with POBA) mild short lesions in large proximal vessels. This was important because there were no stents to prevent or fix that at the time.

“I had considered a randomized trial to test the concept of ‘plaque sealing’ following my tutor’s (Andreas Grüntzig) saying ‘if in doubt, randomize’ but I rejected the idea. First it would have taken a large number of patients followed for at least 5 years to make up for the initial disadvantage of POBA versus medical treatment. Assuming a risk of about 1% per year of a mild proximal stenosis to cause an event in the natural course, the 2%-4% risk of the procedure remained a disadvantage for at least 2-4 years. Second, the situation appeared crystal-clear to me (I was not in doubt), having observed thousands of patients with POBA over more than 10 years.

“Then came stents and they ruined my concept of ‘plaque sealing’ with PCI. The initial stents (BMSs or DESs) carried a risk for stent thrombosis of about 5% in the first 2 years and initial DESs had a continued respective yearly risk of about 1% for several more years. This forfeited an advantage of ‘plaque sealing’ with them over medical treatment at least for the first 5-10 years. Now, with the really low risk of stent thrombosis of modern DESs, the ‘plaque sealing’ concept becomes attractive again. Their excellent long-term outcome is also the reason why I converted to a default stent user after having cautioned against stent overuse for about 2 decades. I never argued against stents as such, just against default stenting while stents were not good enough for that, yet. Now they are. By the way, the ABSORB stent (bioabsorbable vascular scaffold or BVS) is not and is therefore not a good choice for any patient.

“I was never an uncritical advocate of interventional techniques. My review of new devices in the eighties was critical against the then hailed PCI devices you mention in your article as failures, while the majority of interventional colleagues were enthused over them. It took several years at the time, by the way, to find a journal (American Journal of Medicine) willing to publish the critical piece.

“As for renal ablation to treat hypertension, I agree with your assessment that the concept is valid but the initial approach was not. Renal denervation with the method used in the Simplicity HTN-3 trial was voodoo from the start as just a few focal points were heat-treated while the valid principle behind the idea asks for a circumferential approach. For that reason, our center had refused the offer to participate in that trial.

“As for PFO closure, I am indeed impressed by its potential to do good (prevent strokes, myocardial infarctions, and other paradoxical embolisms, and improve migraine, some sorts of dyspnea, and sleep apnea) at a price of virtually no side effects and very little discomfort for the patient or stress for the operator. The procedure takes normally 15 minutes, the patient needs only local anesthesia in the groin, holds the groin personally for 15 minutes after the procedure, and then gets out to a normal life including sports, just like after donating blood or mending a tooth. Echocardiographic guidance is not necessary, even not recommendable, as it consumes time and increases cost and discomfort of a procedure that is virtually always successful without echocardiography. In over 3000 PFO closures I have performed without echocardiographic guidance, there were only 2 short-term or long-term complications of clinical importance (1 groin problem and 1 late erosion, both not preventable by echocardiography) and there was no mortality. However, before PFO closure and once at follow-up, I do recommend a transesophageal echocardiogram but they are not indispensable. Working in a salaried environment of a public hospital, the financial incentive alluded to by one of your commentators is but a minor motive for this proactive attitude. Per net benefit, I find PFO closure the best procedure in interventional cardiology.

“I hope to have shed a little light on some of my ideas that startled you and others.

“Best regards

“Bernie”

Update:

In response to a comment Dr. Meier provided some additional information about his plaque sealing technique. Here is the exchange:

Dear Dr Meier

I read your paper “Interventional cardiology, where real life and science do not necessarily meet.” and later your comments to in cardio brief “Pioneering Interventional Cardiologist Defends Unorthodox Practices”. Your approach is very bold and against my usual practice (FFR, ischemia guiding, spot stenting etc) but your are from a pioneering team and I would like to understand your technique. Do you do plaque sealing by only PTCA to soft plaque or you for example in a 3 mmLAD with 40-50% soft plaque inflate a 3 mm balloon distal to lesion and pull it back and trim the soft lesion ? Do you have results or any written material about this technique. Thank you for being courageous to defend your point. Best regards

Ayhan Olcay MD
Bayrampasa Kolan Hospital
Department of cardiology, İstanbul, Turkey

Dr. Meier’s response:

Plaque sealing is performed exactly like normal PCI. The term simply refers to the fact that the primary goal is not improvement of flow (which may still be normal in mild lesions) but prevention of later plaque rupture and thrombotic occlusion. Plaque sealing made sense before stents were used because lesions treated by the balloon alone virtually never occluded late, i.e., they appeared sealed. Now plaque sealing starts to make sense again when modern DES (excluding ABSORB) are used, because their risk of late thrombosis is very low albeit not nil.

Meier B, Ramamurthy S. Plaque sealing by coronary angioplasty. Catheter Cardiovasc Diagn 36: 295-297, 1995
Meier B. Plaque sealing by coronary angioplasty. Heart 90: 1395-1397, 2004

Bernhard Meier
University Hospital of Bern
Switzerland

Comments

  1. James Stein says:

    He is a very confident man.

  2. Ayhan Olcay says:

    Dear Dr Meier

    I read your paper “Interventional cardiology, where real life and science do not necessarily meet.” and later your comments to in cardio brief “Pioneering Interventional Cardiologist Defends Unorthodox Practices”. Your approach is very bold and against my usual practice (FFR, ischemia guiding, spot stenting etc) but your are from a pioneering team and I would like to understand your technique. Do you do plaque sealing by only PTCA to soft plaque or you for example in a 3 mmLAD with 40-50% soft plaque inflate a 3 mm ballon distal to lesion and pull it back and trim the soft lesion ? Do you have resılts or any written material about this technique. Thank you for being courageous to defend your point. Best regards

    Ayhan Olcay MD
    Bayrampasa Kolan Hospital
    Department of cardiology, İstanbul, Turkey

  3. Bernhard Meier says:

    Plaque sealing is performed exactly like normal PCI. The term simply refers to the fact that the primary goal is not improvement of flow (which may still be normal in mild lesions) but prevention of later plaque rupture and thrombotic occlusion. Plaque sealing made sense before stents were used because lesions treated by the balloon alone virtually never occluded late, i.e., they appeared sealed. Now plaque sealing starts to make sense again when modern DES (excluding ABSORB) are used, because their risk of late thrombosis is very low albeit not nil.

    Meier B, Ramamurthy S. Plaque sealing by coronary angioplasty. Catheter Cardiovasc Diagn 36: 295-297, 1995
    Meier B. Plaque sealing by coronary angioplasty. Heart 90: 1395-1397, 2004

    Bernhard Meier
    University Hospital of Bern
    Switzerland

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