Another battery related recall for Medtronic implantable electronic devices

 

Has Medtronic had more battery related problems than other pacemaker manufacturers or does it just seem that way because of the number of recalls and battery life estimation issues reported in the last 2 -3 years and the fact that Medtronic makes more units than any other company? Medtronic is not alone. both Guidant and St. Jude have had major recalls .

Premature battery failure lead to St Jude's recall of ICDs and CRT-D units involving over 300 thousand world wide with 250000 in the US.Reports indicate that St. Jude knew of the problem for years before the recall. One death was reported in 2014 and a second death in 2016 before the October 2016 recall was issued.St Jude was purchased by Abbott.

A similar narrative can be told about Guidant who became aware of a shorting issue in their Prize II IC which did not allow the unit to deliver a shock while also destroying the  shocking system . Guidant informed the FDA and fixed the problem but did not warn physicians nor patients and continued to sell some units that had not been modified.The Prize was introduced into the market in 2000,  the flaw discovered in 2003 but it was not until  2005 that the company disclosed the problem. Finally in  October 2013 Boston Scientific who had purchased  Guidant pleaded guilty to a false claims act litigation and agreed to pay 296 million dollar fine. 

There were problems with  Medtronic CIED programmers in units made between October 2018 and January 2019 that resulted in erroneous estimate of battery life.These were ultimately corrected and in the end seemed to be really more of an anxiety producing nuisance than a threat. 

Also in 2019 there were three reports of pacemaker batteries being completely drained resulting in one death.This problems involved five different Medtronic models and 131000 units and involved a potential capacitor damage. This situation was troublesome to both EP cardiologists and the patients as there was no way to determine which specific units were likely to fail and pacemaker replacement is not a risk free minor procedure. Having a complicated device under your chest wall skin is anxiety producing enough without the added worry that the type unit you have had been known to suddenly fail. It seems to be a recurrent situation with CIED recalls that there is no way to determine if a particular unit within a class of units subject to the recall is in fact one that is doomed to fail.

On 2/3/2021 Medtronic send an "Urgent Medical Device Correction" letter to all affected physicians.  On 4/12/2021 The FDA announced a recall of about 240,00 Medtronic CIEDS.These are seven models of  CRT-ICDs and pacemaker ICDs. see here for link  This is a class I recall which means a potential risk for serious  injury or  death.

When a Medtronic pacemaker reaches a certain predetermined battery life remaining signal  the device is said to go to a RRT  setting or condition (Recommended replacement time) which sets a 3 month clock ticking before it goes to the next condition which is called ERT (elective replacement time).This condition, which I understand is unique to Medtronic PMs involves a Mode switch  to a VVI mode at a heart rate of 65.

Some devices involved in this latest recall may move from the RRT warning to full battery depletion in as little as 24 hours.There have been over 400 complaints with these devices and 18 "injuries" also reported. Generally PMS do not have a system feature that notifies patient or physician when RRT is reached. I will not know if my PM has reached RRT until a remote  ( or office ) interrogation designates that.(I have a five year old Medtronic model "Consulta"

 Questions come to mind-

Has Medtronic contacted the approximate quarter million patients who have these units or does the letter send to the physicians put the onus on the docs to spread the word?

Does the typical PM clinic have computerized records of which PM each of their patients have? 

A 2017 report from office of the inspector general estimated that 1.5 billion dollars had been paid by Medicare for replacement of 7 different models of CIED in 73,000 patients during the time period 2005-2013.According to the report manufacturers do not typically pay for replacement costs, 

Medtronic has also had recalls recently for its HVAD units (see here) and its blood pump (see here)

Complications from Left Bundle Branch area pacing

 Chen et al (1) report their experience in 612 LBBA implantations from 2018 to  2020 .Mean time of followup was 12.5 months.

Complication rate was low. and consisted of:

2 post operative septal perforations,2 post operative lead displacements ,4 intra operative septal injuries and 2 intra operative lead fractures,none of which had serious consequences.

1) Chen, X. Procedures-related complications of Left Bundle pacing: A single center experience. 

frontiers of Cardiovascular Medicine,24 March 2021. Full text is available on line. 

What is the mechanism of left axis deviation in some cases of Left bundle branch block?

 Dr. Saer Abu-Alrub et al (1) offer one explanation for  the occurrence of left axis deviation (LAD) in some cases of left bundle branch block (LBBB).

Twenty nine patients with non-ischemic cardiomyopathy were studied with non invasive cardiac mapping, CT and MR imaging .Sixteen had a normal QRS axis while 13 had LAD .The LAD group demonstrated delayed activation of the basal anterolateral region.The LAD group demonstrated an apex to base activation pattern versus a circumferential pattern observed in the normal axis group.

 Imaging studies demonstrated no differences in cardiac structure between the two groups so the investigators concluded that LBBB with LAD was a "purely electrical phenomenon".

Some LBBB patients with LAD  treated with CRT ( either by BIV or conduction system pacing)have normalization of the QRS duration and of the electrical axis while others have only the QRS normalized with the left axis unchanged. I have been unable to find any explanation of that. 

1) Abu-Alrub,S et al Left axis deviation in patients with non ischemic heart failure and left bundle branch block is a purely electrical phenomenon. Heart Rhythm, 2021 April  33831543

Do some patients with idiopathic left bundle branch block have an underlying cardiomyopathy?

Janek Salatzki and co workers (1) present evidence that there may more at work in idiopathic LBBB (ILBBB) than simply dysynchrony. It is generally accepted than LBBB alone can cause heart failure (HF) and myocardial remodeling. Salazki present data using an innovative technique,determination of septal flash volume, which they believe suggests that a contractile impairment is a necessary condition for remodeling while dysynchrony alone may induce heart failure.

The authors state that another explanation for their data is that the LBBB group with remodeling were simply patients who had the LBBB longer. The retrospective nature of their data does not enable them to exclude that alternative.

The first description of ILBBB causing heart failure was in 2005 and one of the speculations at that time was that there was an underlying cardiomyopathy , i.e. it just was not simply the dysynchrony operative in causing HF to develop but a disease process affecting both muscle and conduction fibers.The various case series demonstrating a favorable and often super respond in lone LBBB patients treated with either  BiV or conduction system pacing  suggests that desynchrony is the dominant problem.  

1)Salatski,J et al Presence of contractile impairment appears crucial for structural remodeling in idiopathic left bundle branch block Journal of cardiovascular resonance.2021 april 23 

2). Blanc J et al. Evaluation of left bundle branch block as a reversible cause of non-ischemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace 2005;7,604

Left bundle branch area pacing as alternative for bi-ventricular pacing for refractory heart failure

 Should cardiac conduction system pacing replace bi-ventricular pacing for patients with refractory heart failure (HF)? The two forms of conduction system pacing are His bundle pacing and left bundle branch area pacing.

Vijayaraman et al(1)have  published the results of a retrospective multi center study to asses the feasibility and outcomes of left bundle branch area pacing (LBBAP) in patients as an alternative to bi-ventricular  pacing (Bi-V). See herehttps://www.jacc.org/doi/pdf/10.1016/j.jacep.2020.08.015

LBBAP pacing was attempted in 325 patients and was successful in 277 or 85%.LBBAP resulted in significant shortening of the QRS,clinical and echocardiographic improvement, and was achieved with low thresholds and adequately high R waves. In short, LBBAP seemed feasible and safe. No mention was made in the abstract regarding septal wall perforation an event that had been reported in some earlier case series. 

Among clinical indications for pacemaker implantation none equal the randomized clinic trial data supporting CRT using BIV.

There are observational data supporting the value of both His Bundle pacing and now LBBAP as an alternative to Bi V pacing. I think  a large RCT would be necessary to demonstrate superiority or more likely non-inferiority  of cardiac conduction pacing versus BiV.Where would funding for that be found?

1)Vijayaraman,p et al Left bundle branch area pacing for cardiac resynchronization therapy:Results from  the International LBBAP collaborative study. JACC Clin EP archives, vol 7 no. 2 135-137. 

  

Implantation of both His Lead and LBBA lead in atrial fibrillation patients

 In the early days of His bundle pacing (HBP) there was a issue of whether or not a backup lead should also be implanted.This controversy has apparently not been completely resolved and may have regained some steam as reports have appeared indicating  that some not insignificant number of His  leads develop high thresholds over time  even though the initial threshold was appropriate.

Yand Ye et al (1) describe an interesting variation of using a backup in conjunction with a His Lead.They studied 16  AF patients who were pacemaker dependent in whom they attempted to place both a His lead and a left bundle branch area lead.(LBBA).The His lead was the primary pacing lead and the LBBA lead was considered the backup lead. Thirteen of the sixteen were successfully implanted. Although the results section of the paper is somewhat unclear apparently at least one patient had a increase in the capture threshold leading to switching to the LBBA lead. During the six month follow-up there were no lead dislodgments or ventricular perforations.There have been a few reports of late perforations of the  LBBA pacing lead.

The authors conclude that the technique is doable and safe and may offer an approach at least for PM dependent patients with AF.In this group of patients the rivalry between HBP and LBBA pacing could be avoided.Maybe not a either or but a both.

1) Yand Ye, Feasibility and safety of both His Bundle Pacing and left bundle branch area pacing in atrial fibrillation patients: intermediate term follow-up.Journal of interventional cardiac electrophysiology. 2021 March 15 33723691

Does location of His lead (above or below the tricuspid valve) matter?

 A study of fifty patients by Y. Hu et al (1)  indicates that it does matter. Two problems with His pacing are higher capture threshold voltage are needed and lower R waves . Hu's data indicate that in the 25 patients who were implanted below the TV there were lower ventricular capture thresholds and higher R waves.Echo studies showed no tricuspid regurgitation.

 Somewhat different results were reported by Tang et al (2) in that they found capture voltage to be no different in the atrial leads  compared to the ventricular lead placement in a study of 13 atrial placed His leads and 16 ventricular placed leads. However, they also found that the R wave sensing values were higher in the ventricular lead group with values at implant being 1.87 V for the atrial lead and 4.53 V for the ventricular group. 

Also it is generally thought  in cases of AV block that a sub valvular implantation may be preferred  and that non-selective His pacing may to preferable to selective because it can be its own back up. 

 1)Hu,Y Electrical characteristics of pacing different portion of the His bundle in bradycardia patients 

Europace,2020 December 26, supplement ii 27

2)Tang, C Effect of implantation site of the His bundle pacing leads on pacing parameters a single center experience BMC Cardiovascular disorders. 2021 Feb 24 2021 (1) 112, 

His Bundle pacing can normalize ventricular activation but can it also actually reconstitute native intrinsic conduction ?

His Bundle pacing  (HBP) has been known for years to be capable of normalizing bundle branch blocks. By normalizing I mean that the QRS while the patient is being paced becomes normal with Selective HBP and nearly so with non selective HBP. By reconstitution I mean that the QRS remains normal after HBP is turned off.  Reconstitution  is what authors of 2 case reports document in a article in Heart Rhythm Case Reports.

Dr FM Ezzeddine at al  (1) report two case in which patients with long standing conduction defects were implanted with His leads and after several months of treatment with His bundle CRT  were noted on routine testing  to have resolution of their conduction defects.One patient who had an av block and LBBB had resolution of the AV block while the LBBB continued and the second patient had restoration of normal ventricular conduction no longer having an LBBB pattern. Both patients experienced a significant resolution of their heart failure symptoms when His bundle paced CRT was begun.

Quoting the authors with my underlining.

"His Bundle pacing can restore native intrinsic conduction in some cases after years of chronic conduction block". ..    this demonstrates new theoretical benefits of HBP , the ability to promote conduction down the native pathways that were previously non-conducting." 

 What I  believe  the authors are proposing is that  His bundle pacing had somehow brought about  electrical remodeling  leading to a condition in which pacing was no longer needed to bypass or override whatever specific type of conduction defect the patient had experienced. They consider mechanisms such as Wedensky facilitation which refers to an impulse arriving at a blocked zone and increasing the excitability of tissue beyond the block. Other electrophysiologic speculations are offered.

There have reports of exercise induced LBBB and intermittent rate related LBBB but the authors believe these are the first reports of long standing conduction defects that recovered native conduction following continuous His bundle pacing.

On page 412 of Serge Barold's illustrated guide to pacemakers and resynchronizatio (2)n  the authors suggest there is value to periodically "expose " the underlying spontaneous EKG. This was said in the context of followup on bi-ventricular pacing but perhaps Ezzeddine's paper offers a reason to do that for patients with LBBB who are being His bundle paced.   

 

1) Ezzeddine, FM et al Reconstitution of native intrinsic conduction in patients with chronic conduction block with His bundle pacing. Heart Rhythm Case Reports.2021 1-5,  https;//doi/org/10.1016/j.hrcr,2021.03.006

note: The same cases were presented as a poster, at the JACC meting march 20,2018 by Dr. Ezzeddine

2) Cardiac Pacemakers and Resynchronization , step by step  An Illustrated guide. Second Edition,

Bakrold,SS, Stroobandt, RX adn Sinnaeve, AF 

Some Pacemaker program features do not work well with His Bundle Pacing

 Some pacemaker programming features do not work well with His Bundle pacing and may cause some  problems raising the question of why have pacemaker manufacturers  not developed programs and algorithms specific to His Pacing . 

In particular the automatic  capture threshold determination(ACM for automatic capture management) program may give falsely high thresholds leading to  setting the capture voltage safety factor too high leading to premature battery depletion as illustrated in a case report referenced later in this article.

If the His lead is placed in the ventricular port (pulse generators used with CRT have three ports) the ACM  which is based on the evoked potential will indicate the RV capture threshold , i.e. not the His threshold. If the RV threshold is higher than the His threshold then the ACM determination will be falsely high. If ,by chance the right ventricular evoked potential is approximately the same as the His potential then ACM works just fine , except you don't know if it working right or not. 

If the His lead is in the LV port, since it is based on the LVP-RVS conduction times the threshold will be that with lowest value either RV myocardial or His. 

The ventricular capture program is activated nightly at 1:am and if unsuccessful another attempt is made every half hour.

Articles by Vijayaraman and Burri has explicated the problems with automatic capture algorithms and HBP and the basic recommendation is that those features be turned off or at most turned to monitor. 

Quoting Vijayaraman, 2018 JACC ;" Utility of automatic threshold testing feature is limited in HBP. In patients with selective HBP  due to lack of evoked potential,this feature may fail to detect the true  His capture threshold. On the contrary in patients with nonselective HBP this feature will detect myocardial capture threshold rather than His bundle capture. " 

Quoting Starr and Burri (Heart Rhythm 2019)

"The RV capture management algorithm of Medtronic devices considers an RVS event that occurs in the 110 ms window following pacing to be V capture ( i.e. it does not specifically detect the evoked  potential)." The authors  then explain that in cases of RBBB selective His Pacing  may have the erroneous diagnosis of non capture  could if the pace capture interval falls outside of the 110 ms window.

Quoting Burri,(2019) ;

"RV capture management algorithms are based on detection of the evoked potential which is absent in case of selective his bundle capture.Even in the case of non-selective capture, the algorithm seldom yields accurate results and the feature should either be inactivated to switched to  "monitor"

The following case report illustrates one undesirable clinical outcome when the ACM is set to "program" but fortunately the problem was quickly corrected.

Wu et al ( 1) report a case in Clinical Case reports in 2020 in which the Medtronic capture management algorithm caused a large and inappropriate increase in the voltage setting.The patient was a 72 year old man with a second degree heart block who was implanted with a His Lead resulting in selective His pacing with an initial Voltage of < 1.5 volts at 0.4 ms.However the next day the EKG now showed nonselective His pacing pattern and the Voltage was set at 5.00V at 1 ms.

 The authors believe that the automatic capture management system which was set on  the factory default setting of adaptive repeatedly noted "pacing capture loss" and reputedly increased the RV voltage. The treating physicians recognized the problem and changed the ACM setting to monitor before significant battery depletion had occurred.

It is not possible from the case report to know  when this event occurred .There were two articles published in 2019 that called attention to problems with the adaptive setting for automatic capture management systems such that the adaptive setting should not be considered the default position. 

As of this writing there seems to be no IPG (PM) specifically designed for His pacing nor is there an automatic capture threshold program designed for HBP. I wonder how often various pacing settings are just left to the factory settings when a PM is implanted with His pacing  even though there is information available in the literature indicating  that  a device features that worked well for right apical ventricular pacing  will not work in His-bundle pacing. 

1) Wu, Jung-Pin et al Automatic capture management may cause   unnecessary battery depletion in selective His Bundle Pacing Clinical Case Reports 2020. DOI 10.1002/ccr3.3168

Take home messages for "lone " Left bundle branch block

Introductory and personal note

Five  plus years ago I experienced a sudden decrease in my exercise ability.As a long time marathon runner I was well aware of running times and perceived exertional sensation for various speeds. My running times decreased by about 15% (comparing times for a one mile run at a comfortable pace).

My EKG at my  internist's office show an LBBB pattern. Neither he nor I were aware of the significant exercise impairment that can be caused by LBBB. A number of web sites even now offer misinformation about LBBB.  Over the past five years there has been much learned about LBBB,His Bundle Pacing,and the potentially harmful effects of pacing the heart from the right apex, and the entity of LBBB induced cardiomyopathy. 

 I also had developed an exercise induced high grade second degree heart block for which I received a pacemaker ( PM) importantly with a Bundle of His lead  (HB)  After recovery from the implantation  procedure I was able to return to running with an apparent recovery to my pre LBBB level. A number of blog readers have contacted me about exercise problems similar to mine and their frustration with the medical advice from their cardiologists. I was evaluated for coronary artery disease and none was found.(see endnote 1)

The following is a recap of what I have learned about LBBB and related  matters which may be of interest at least to folks with that condition. It is not offered as specific medical advice and is just my take on a subject of obvious great personal  importance from a non-cardiologist who over the last five years has enjoyed a non-sanctioned,personal,perhaps quiky ,self directed mini fellowship in electrophysiology. 
____
All LBBBs are not created equal. Even the subset of lone LBBB is not homogenous.

About half of patients whose EKGs meet standard  criteria for LBBB are shown to have a particular pattern on echocardiography.This seems to be the case whether the standard criteria are used or the more stringent Strauss criteria.(see end note 2)

This echo  pattern describes an abnormal,out- of -sync contraction pattern of the left ventricule (LV)
It begins with a electrical activation of the interventricular septum from right to left  (opposite to the normal direction of septal activation) and then a swift leftward movement of the septum and a bulging out of the left lateral ventricular wall,followed by a delayed LV wall contraction and rightward bulging of the septum.The septal movement occurs before the aortic valve opens (in the isovolemic contraction phase when mitral and aortic valves are closed as pressure builds up to snap open the aortic valve).Some ,but not all, patients with an EKG pattern of LBBB demonstrate this pattern on echocardiography or Cardiac MRI studies

This same pattern has been observed in  at least some cases of RV apical pacing.


Cramer and De Boeck (1)et al describe this mechanism by which abnormal electrical activation leads to abnormal contraction-a dyscoordination of contraction in at least many cases of LBBB.

 " This discoordination encompasses regional differences in timing,duration and amplitudes of contraction.When the differences are large enough,part of the contractile energy of the early contracting segments will be dissipated into abnormal stretching of remote areas during early systole and vice versa at end systole...The decreased global pump function will activate neurohormonal response mechanisms in an attempt to maintain normal cardiac output,favouring ventricular dilatation and remodeling. "




In some patients, LBBB is not associated with this pattern and in these it may be that electrical signals are merely delayed but occur in the normal left to right pattern .Several patterns of septal motion have been described.

The resting echo typically demonstrates no problem other than an ejection fraction (EF) that might be at the lower limits of normal and in the absence of a earlier higher value carries little diagnostic value.However some work indicates that the ejection fraction is not  accurately measured in LBBB using the Simpson method and that the "true" EF is lower than measured.

It should be noted that it may be possible to recognize the early left ward motion of the septal on echo and has been named "septal flash".Patients with this septal flash pattern generally respond well and sometimes exceptionally well with CRT-either with traditional bi-ventricular CRT or with His Bundle pacing.

With exercise, stroke volume fails to increase ,diastolic pressures rise and the patient may become short of breath. Human and animal work have demonstrated that   increased afterload (as with increased blood pressure) and increased heart rate cardiac function decreases significantly including decrease in EF.

A patient presenting to a cardiology clinic with LBBB,no symptoms and a negative evaluation for coronary artery disease would likely be reassured and followed.

A symptomatic patient poses a more difficult problem.If he had a normal echo some docs  would just follow the patient , a management plan not likely to be well received by an endurance athlete.If the patient had reached  a phase of cardiomyopathy with evidence of heart failure, the usual medications would likely be prescribed .However reports indicate that the usual goal directed therapy GRT) is not effective in LBBB induced cardiomyopathy.Some authors have suggested that earlier  (that is less than the standard three month  trial of GDT) pacemaker therapy should be used.

Five years ago His Bundle pacing was not a routine  procedure for PM implantation- now it has become the default procedure in a number of centers for AV block and for sinus node disease and for pacing after A-V node ablation and in some centers the preferred approach for CRT instead of Left ventricular pacing through a lead in the coronary sinus.

Although by 2000 there was great interest and enthusiasm for HBP  and had become a II A AHA/ACC/HRS guideline recommendation, more recent analysis of data from HBP follow up has revealed perhaps as many as a quarter of  successful His bundle  implantation with adequately capture voltages  over time increase voltage requirements to levels which likely will lead to premature battery replacements.This in part has lead to increasing acceptance of another,newer form of conduction system pacing namely pacing the left bundle  directly by advancing a lead further into the RV apex and screwing in a lead deep into the septum. As of this writing bundle branch area pacing has become popular in China, it s country of origin, and also apparently used a a primary means of pacing  in place of HBP at Virginia Commonwealth Medical School according to a recent article by Padala and Ellenbogen (2). As best I can tell as an outsider, some form of conduction system pacing has largely replaced the traditional pacing from the right ventricular apex. 



1 Cramer,MMJ and De Boeck, BW Three dimensional echocardiography and left bundle branch block:Prime time in cardiology. Neth Heart J 2007 Mar 15(3) 87

2) Padala, S and Ellenbogen KA  Left bundle branch pacing is the best approach to physiological pacing. Heart rhythm ,2020 


end note 1

As was the party line recommendation at the time,coronary disease was evaluated by a stress echo in a patient with LBBB.Abnormal movement of the interventricular septum,decreased septal blood flow not caused by obstructive disease and abnormal changes on the ekg generally make various testing methods less than optimally reliable, eg.regular treadmill exercise  and some isotope tests. The SPECT myocardial perfusion imaging is a problem because of septal perfusion defects occurring in patients who do not have obstructive lesions in the Left anterior descending artery. The stress echo test is popular in some centers but a recent review from the Cleveland Clinic discredits the stress echo considering it unreliable and favors CT angiography if patients  less than 65 and the pharmacologic nuclear imaging or dobutamine stress echocardiography if over 65 years of age.Older patients are more likely to have coronary calcification making the CT  angio less useful. (.https://consultqd.clevelandclinic.org/in-patients-with-left-bundle-branch-block-whats-the-best-test-for-cad/)

end note 2

Strauss criteria for EKG diagnosis of LBBB- QRS greater than 140 msec in males,and greater than 130 msec in women and mid QRS notching in 2 contiguous leads.(Strauss,D Defining Left bundle branch block in the era of Cardiac Resynchronization Therapy. Am J Cardiology 107 (6)2011

So maybe Bundle of His pacing (HBP) is not the holy grail of pacing after all.

 To understand why EP cardiologists might have considered  His Bundle Pacing (HBP) the holy grail it might help to have a brief survey of some of the history of pacing the heart and then look at why HBP , thought  to be the most physiological may not now be considered to be the best-at least by some EP cardiologists.

By the early 2000s EP cardiologists had not yet determined the best way to pace the heart even though the dual chamber pacemaker had been employed widely since the mid 1980s .

For example, in a patient with sinus node disease and bradycardia should the patient be implanted with a single lead in the  right ventricle or be given dual chamber pacing with a lead in the right atrium as well. At that time right ventricular pacing meant pacing in the apex of the right ventricle as opposed to pacing in the right ventricular septal wall or the right ventricular outflow path or actually accessing the His Purkinje system also now referred to a conduction system pacing. 

While it was known that pacing the ventricle alone could at times lead to something called pacemaker syndrome and it seems that synergy of the atria and ventricles made much more physiologic sense,there had been no clinical trial demonstrating the best approach.Looking back from the vantage of an outsider it seems that as recently as 20 years ago the EP cardiology community was not in agreement about how many leads did a patient with sick sinus syndrome need/

The MOST trial  was designed to settle that issue and results were published in 2002.That trial and the DAVID trial provided less than slam dunk evidence favoring the dual chamber (DDD) mode  ( 20% fewer instances of atrial fibrillation) but subsequent analysis of the data gave another important answer related to the harmful effect of pacing the heart from the right ventricle. That and subsequent analysis indicated that there was a significant risk of heart failure if the right ventricle were pacing more than 20-40% of the time. Consider that-the treatment that could be live saving for irreversible bradycardia could over time cause the patient to develop heart failure. Some EP cardiologists must have thought that there must be a better way. 

It gets worse -patients with pacing induced heart failure respond poorly to the usual heart failure battery of medications and the only fix was another pacemaker, which while  potentially very  helpful, implanting a pacemaker should be considered a big deal . Infection and other complications may occur more frequently when PM are revised or replaced.

The patient would  have to undergo another PM implantation procedure with the attendant risks of infection,pocket hematoma,pericardial  effusion,pneumothorax,etc. This time a lead would be placed from the right atrium through the coronary sinus into  a vein on the epicardial surface of the left ventricle. Then the PM would be programmed to attempt to optimize the timing of the right ventricle (still paced at the apex) with the left ventricle which is now depolarized from epicardium to endocardium  which is the  opposite of the usual route.Two wavefronts would be generated, one from the endocardium of the right ventricle and the other from the epicardium of the LV and the two would  hopefully fuse so as to improve  cardiac output and  even bring about often beneficial remodeling of the heart.

This Rube Goldberg arrangement worked quite well for these cases of pacemaker induced cardiomyopathy as it does for about 70% of patients with medication refractory heart failure   It seemed that those cases whose EKG showed a left bundle branch pattern were most likely to have a good and often impressive improvement, sometimes referred to as "super responders".

By 2013 the value of CRT was firmly established. CRT means cardiac resynchronization therapy and  at that time  was synonymous with biventricular pacing (Bi-V) and randomized clinical trials had proven its value in symptomatic relief,reduction in hospitalizations and  increased survival.As best I can tell, as a non cardiologist looking in, the randomized controlled trial evidence supporting pace maker implantation for CRT is more robust and convincing that for any other pacemaker indication.

A look at the time line regarding recognition and acceptance of  the role of loss of interventricular and intraventricular synchrony as exemplified by left bundle branch block (LBBB) is of interest juxtaposed to the evolution of thought concerning right ventricular apical pacing .

Blanc et al 2005 and Vaillant et al 2013 described cases of heart failure caused by left bundle branch block and treated successfully with CRT. Blanc's cases seem to be the first recognition that lone LBBB could cause heart failure and that this desynchrony  could be fixed by CRT often with dramatic resolution of the heart failure.

The abnormal depolarization and sequence of ventricular contraction in RV apical pacing and that induced by LBBB are very similar as are the EKGs and it should not be a surprise that CRT worked well for both, at least in many cases

The first clinical series of His Bundle pacing was done  in 2000 by Desmuhk  in patients with rate control recalcitrant atrial fibrillation patients who needed an av node ablation but its use did not become widespread due to the complexity of the implantation and lack of tools designed for the task.   

For the next decade there was little clinical application of His Bundle pacing in the US although  work was progressing in Spain and Italy.

Two important papers in 2015 contributed to a growing interest and application of HBP. A case series by Dandimundi and Vijayaramen from the Geisinger Clinic  demonstrated that HBP was not overly difficult after all and that results seemed good. Daniel Lustgarten from Vermont published a proof of concept cross over study  study that compared HBP with BiV pacing .

By 2017 at the Heart Rhythm Society meeting there was considerable enthusiasm regarding HBP and one prominent EP cardiologist referred to HBP as the Holy Grail of pacing and it seemed that   finally physiologic pacing was practical. The alternative, namely right ventricular apical pacing and Bi V pacing could hardly be considered physiologic.By 2020 the same EP cardiologist wondered in left bundle branch area pacing would be the new holy grail. 

In 2019 Dr. Kenneth Ellenbogen gave a presentation that was very optimistic regarding the future of His pacing in part based on a small ( n=20) group with five year followup.

However, by 2020 the bloom was less well fixed on the  His Bundle pacing rose. Though physiologically beautiful HBP had some negatives such as: High initial capture threshold, adequately initial low capture thresholds that subsequently rose to unacceptable levels in some cases,low R waves which may lead to sensing problems and  the technical difficulty of the procedure. Earlier  than anticipated pulse generator replacements were occurring because of the high thresholds. Padala and Ellenbogen claim that 25% of HBP patients will have an increase in capture threshold to 2.V at 1 ms. over time. In Zanon's report of 844 HBP patients the median battery replacement time was 5.8 years .

So When Dr. W Huang  published results of left bundle branch area pacing (LBBAP) which was technically easier,resulted in lower thresholds and higher r waves hence less programming problems  LBBAP seemed to be  very quickly accepted in China and in some US centers.

LBBP may not be quite as physiologic as HBP after all it in effect may cause a right bundle branch block ( it does not always though it should theoretically ). The LBBAP technique is now considered by at least one prominent EP cardiologist as the best even though at this point long term followup is lacking. 

In a YouTube presentation  given on  Feb 2010, by Dr. Santosh Padala from VCU  who  discussed his results with LBBAP and indicated they they now proceed with that modality without trying  His capture first. The reason for this seemed to be that they had seen some cases where the initial His capture threshold was acceptable but within a few months the threshold increased to unacceptable levels. He mentioned they had two out of 59 LBBAP cases with a LV penetration complication but the lead was withdrawn and apparently no significant consequences resulted.

I believe a good  argument can be made for saying that such a move is premature, We now  have fairly robust data on followup on HBP patients.In 2019 Zanon published a multicenter  experience of 844 patients with HBP who were implanted from 2004 to 2014 with a median followup of 3 years. (91.6 % were free of complications. Mean pacing threshold at implant was  1.6  V. and  2.0 at followup. In the second group of 476 in whom the fixed curve sheath was used the complication rate was 4.2 % versus 11.9 in the earlier group of 368 patients in whom a deflectable sheath was used. 

However, LBBAP is relatively new and the medium and long term results have yet to play out.How well a pacing lead inserted 1.5 cm  into the septal will perform  over time remains to be determined. There has been at least one case of a delayed migration of the lead through the septum penetrating into the left ventricle.

Venkatesh, and Sharma from Rush reported their experience with LBBAP regarding 59 patients done from June 2018 to April 2020 most of which were attempted because of unsatisfactory His implantation or unacceptably high His capture voltage.

There were 7 "lead related "complications during the short follow up period of about 6 months with 3 requiring lead revisions.In one patient an interventricular septal perforation occurred two weeks after the initial implantation.Penetratiion during the procedure apparently can be quickly recognized and at least so far  it seems  that no significant harm was done.Late penetration is a different matter. but it seems rare. Capture voltages were low(average 0.62 Volts at 0.4ms)and stable over the short followup period which should predict a longer battery life than is seen with HBP. Improvement was noted in left ventricular performance  in HF patients during the follow up as has typically been the case with HBP.

1) Venkatesh,R et al Pros and Cons of Left Bundle Branch pacing.A single center experience.Cikrculation,arrhythmias and electrophysiology 2020 13 12 

Battery problems with Medtronic Pacemakers, actual battery drainage and battery life estimation error

 The leads in a pacemaker (PM) is said to be the Achilles heel of those systems.A close runner up in the Achilles heel competition is the PM battery.

In 2019 Medtronic reported problems involving batteries.

In one case the problem did not  pose an imminent threat to patients as the issue was that some of their units (manufactured between October 2018 and January 2019 ) were displaying erroneous estimates  of battery life. The problem was said to be in the "programmers" and not in the units themselves and battery life was not altered. The term programmer here refers to the computers that are used to communicate with the PM in the doctor's office and to make programming changes and to make updates to firmware.

A much more serious battery issue also was reported in 2019.There were three reports of pacemaker batteries being completely drained resulting  in one death.The devices involved with this problem were the following models: Astra,Azure,Percepta,Serena,and Solara.Damage to a capacitor in the units was said to be the cause of the battery drainage. Unfortunately there was no way to determined if a given Pacemaker was likely to have a battery failure. The FDA was not recommending  replacing all of the units.Some 131,000 units were potentially affected.

PMs can be "interrogated" by bedside monitors providing various parameters of PM function including a value for battery life estimation.

In theory battery life determination seems  simple.It is the battery drain rate divided into the battery capacity which is measured in ampere hours. The devil is in the denominator of the equation. How accurate are these estimations.

My own PM was  implanted in October 2015.I am writing this in January 2021 .

An interrogation done on October 2016 gave an estimate of 2-2.5 years which corresponds to October 2018 to June 2019. An interrogation done October 2017 gave a estimation of 1.5 to 2.5 years which corresponds to June 2018 to June 2019.IN January 2021 the estimate was 4 to 10 months. By May the estimate was still 4 to 10 months.

So at least as regards my PM the estimations of battery life do not instill confidence. 

Addendum 5/17/2021 undated battery estimates were added to the next to last paragraph. 

    

Longevity in athletes -good genes,exercise levels or both

 There are several reports suggesting that endurance athletes enjoy good longevity .These studies have involved professional cyclsits,Ski racers,French oarsmen and Harvard rowers. 

Do the  genetic endowments that world class endurance athletes possess that facilitate their athletic ability also either alone or with other genetic contributions enable to live longer? Alternatively is it the long hours and perhaps years of exercise that lead to a long life? Maybe both.

A key, perhaps the key,to be a world class endurance athlete is a high maximum oxygen uptake (02Max).Although intense aerobic training can increase one's 02 max a moderate amount  (maybe 10-15%),world class endurance athletes inherit high 02 max values. A typical 25 year old man may have a value of 40-45 ml/kilo/minute while a budding world class marathon runner typically has a value of 80 or higher with few exceptions.Values as high as 90 have been recorded in some world champion cross country skiers. 

The prodigious exercise capacity of elite endurance athletes is characterized by a slightly larger than normal ventricular size with great capacity to fill quickly.

The maximal oxygen capacity of humans inexorably decreases over time.Whether continuing moderate or even high levels of aerobic exercise will mitigate that rate of loss is the topic of an ongoing debate.

 What is clear,however, is that if you have for example a 02Max of 60 or 70 when you are thirty years old you are more likely to have a 02 max in the high 20s or low 30's when you are 75 or eighty.

A  80 year old with a 02 max of 28 is more likely to come out the other side of a serious illness or accident than an 80 years with an 02 max of 18 or 20. 

 Practice,practice practice arguably may get you to Carnegie Hall but someone with a 02 max of 45 will not win the Olympic marathon regardless of how much training he endures and you will not have a 02 max of 50 when you are 80 years ( Ed Whitlock had an 02 Max of 52 at age 82))  unless you  had a very high  02 max in your youth.

For more on Ed Whitlock and how he slowed down marathon time wise during his 70's while his O2 Max seemingly was unchanged, see here.

Late gadolinium enhancement at Right Ventricular insertion points in highly trained endurance athletes

 A study from Spain (1)demonstrated late gadolinium enhancement in 37 % of highly trained young endurance athletes, all of which occurred at the insertion points of the right ventricle into the inter ventricular septum.See here for full text of article.

All of the athletes trained at least 7 hours per week for the previous five years.Compared to controls the study group had a 10 fold increase in late gadolinium enhancement (LGE) .

LGE is seen in patients with coronary artery disease with  a post myocardial infarction scar and in cardiomyopathy patients in whom the LGE may be considered a negative prognostic sign.

Early reports of LGE in older , long time endurance athletes were confusing and in one study confounded by a significant number of cigarettes smokers. Some of the cases demonstrated a coronary artery pattern ( i.e. LGE along the distribution pattern of the coronary arteries ) and some did not and some were noted in the insertion point of the right ventricle.

The authors described the LGE as a possible "matrix remodeling" and along with bi-atrial and bi-ventricular chamber size increase and superior diastolic function characterizes  the pattern of  the so-called athlete's heart.

1)Domenech-Ximenos,  Prevalence and pattern of cardiac magnetic resonance in highly trained endurance athletes Journal of cardiovascular Magnetic Resonance 2020 Sept 3, 22,(1) 62 

Normal pacemaker function near battery depletion can pose clinical problems

 Can normal pacemaker behavior near battery depletion cause alarming symptoms and clinical diagnostic difficultly?

To put the topic in context we need to describe normal PM functioning as the battery nears depletion.

My PM is a Consulta CRT-P model and according to the Medtronic manual, here is the sequence, which we can use as an example of PM behavior at near battery depletion. 

When the battery reading reaches a value equal to or less than 2.77 volts a replacement indicator named RRT or Recommended Replacement time is displayed on the interrogation.  More precisely, there has to be a reading of 2.77 V or less for three consecutive daily readings A "clock" is  then set to run for  3 months and when it is timed out ,another replacement indicator named ERI or Elective Replacement Indicator is displayed. 

At this point the PM is switched to a VVI Mode at 65bpm. If a magnet is paced on the PM ,the rate will read 65 indicating that the unit is in the RRI mode.If battery life is adequate this power saving mode will continue for three months and then the unit reaches EOS or end of service.

VVI mode works in the following way.The right  ventricles is  paced unless a spontaneous ventricular activation occurs first and then the lower limit for ventricular activation is reset.If a spontaneous ventricular activation does not occur first then the ventricle is paced.Atrial activity and ventricular activity are independent.

According to reference 1 and 2 (see below ) only Medtronic PMs exhibit this near end of service behavior.

A PM in the VVI  mode is in an asynchronous mode meaning that there is loss of synchrony between the atrium and ventricle possibly resulting in a clinical scenario called pacemaker syndrome .Symptoms can include chest pain,shortness of breath, fatigue.palpitations  and neck pulsation among others.The heart was not designed to have the atria contract against closed AV valves nor to have the ventricles contract with the AV valves open.

A 2020  case report (which seems to be very similar to a case referenced in 2010 (ref 2)) of a 70 year old man with a Medtronic  Adapta PM presented to ER with palpitations and dyspnea. Physicians were unable to do a PM interrogation ( another feature of the ERI mode in some . ( but not all) Medtronic models is  that the interrogation feature is disabled ) . The clinical problem was solved and a replacement PM was implanted with resolution all symptoms .

It should be noted the the device was not malfunctioning. At manufacture it was programmed to shift into an asynchronous mode when it reached ERI status. To the manufactures of the PM this was a feature not a bug. However, as a pacemaker patient, I consider this a bug-one in which "normal" behavior of the unit can cause serious symptoms and to add insult to injury have the interrogation function disabled making the diagnosis of the problems difficult even to cardiologists. 

The authors of both referenced  articles were critical of ERI management  in Medtronic PMs. Dr. John Mandrola (ref 2) stated in 2010  he has personally seen 4 cases in which this type of syndrome occurred in a patient with a PM whose unit shifted into a VVI mode with resultant pacemaker syndrome, a situation  in which the diagnosis may not be apparent potentially  leading to further  further diagnostic tests with missed diagnosis even by cardiologists.Mandrola mentions two patients who were subjected  to unnecessary  coronary angiograms before the diagnosis was finally made.Here failure to warn by the patient's EP doc and/or by the PM manufacturer lead to possible harm.Coronary angio is not a zero risk procedure. Siroky made his criticism obvious in the title to the case report ,"bad device behavior or malfunction".

 An obvious comment is -should not EP cardiologists and PM manufacturers inform patients of the untoward events that may  occur  as their battery approaches depletion. In my limited experience patient education before and after the PM implantation has much room for improvement .

 

1)Siroky,GP et al Shortness of breath and palpitation in an elderly man:Bad device behavior or malfunction .Journal of Arrhythmia,2010:36,1109 -1111

2) Madrola, J. https://www.drjohn.org/2010/09/answer-to-this-weeks-clinical-vignette/

Dealing with the covid pandemic is not science all the way down

Ross Douthat,writing in the WSJ on 12/19/2020 entitled his opinion piece "Why you can't just trust the science." I think he was not saying to distrust science but rather he was saying all decisions regarding how the human enterprise copes with the pandemic is not science all the way down. Logistical questions,ethical and moral decisions have to be  made and sometimes those decisions get camouflaged as a scientific decision . 

A key paragraph:

"Last month their Advisory Committee on Immunization Practices produced a working document that’s a masterpiece of para-scientific effort, in which questions that are legitimately medical and scientific (who will the vaccine help the most), questions that are more logistical and sociological (which pattern of distribution will be easier to put in place) and moral questions about who deserves a vaccine are all jumbled up, assessed with a form of pseudo-rigor that resembles someone bluffing the way through a McKinsey job interview and then used to justify the conclusion that we should vaccinate essential workers before seniors … because seniors are more likely to be privileged and white."

Software glitches and Pacemaker problems

 To discuss software problems and their effect on pacemakers  an overview of their "ecosystem" might be helpful.

The ecosystem of  Cardiovascular implantable electronic devices(CIEDs) consists of the device ,  which is a pacemaker (PM) or Implantable cardioverter  defibrillator,ICD),a programmer in the doctor's office,a home monitor,a cloud server and central achieving  unit ,and proprietary software in the physician's office and often with a third party vendor who interprets interrogation reports for the physician. 

More details: The CIED communicates with the monitor with an inductive coil telemetry (ICT) method or a radiofreqency  (RF) at 402 -405 band, which is known as the MICS ( Medical implant communication service).The data received by the monitor is then transmitted by VPN to the PM company server where it can be accessed by the physician's office or a third party service vendor which include among others :Rhythm 360,Ambucor and  Cardiac RMS solutions,

An important aspect of the ecosystem is that the CIED cannot be reprogrammed remotely. The patient has to have an in office doctor visit and have programming change or firmware update done by the programmer. This may be considered more of a feature than a bug as it provides an important level of security.In the doctor's office the programmers uses ICT to retrieve a token key which is then used to generate a session key. Importantly only the programmer can terminate the session so a careless tech could leave the channel open leading to CIED battery drainage or a pathway for hacking.

In the last few years software problems have affected hundreds of thousands of CIEDs manufactured by Abbott ( formerly St. Jude) and Medtronic.

On August 29,2017 the FDA issued a safety communication for 6 models of Abbott pacemakers (Accent,Anthem,Accent MRI, Accent ST,Assurity,Allure). Dr. Subrat Das and co authors in their 2020 article (see reference (1),full text on line) graphically  (see their figure 3)  illustrate the time lag between the FDA communication  of a cyberattack vulnerability and the actions by the pacemaker manufacturers.

A firmware update was required to fix a cybersecurity vulnerability that could allow an hacker to access the devices potentially harming the patients by causing rapid battery depletion or pacing problems.Patients would need to go to their physician/s office for the update as CIEDs cannot be programmed remotely.

At that time and as far as I determine by internet search no harm has occurred to a CIED patient by hacking into the units. However 3 instances of software malfunction was reported by one group of physicians  from Mayo Clinic (2) in one week in their effort to upload the firmware (version 23.1.1.) fix.So the fix itself possibly was a threat to patients in the course of the updating  particularly those who were PM dependent .In one case there was a 4 second pause in pacing and and increase in the battery current .In another the pacemaker mode was changed from the DDDR setting to DOO and assistance from the company engineering team was needed to restore the original mode setting. In patients who were pacemaker dependent it was a choice between eliminating a very remote risk (a cyberattack harming  the patient) and the risk of a problem encountered during the process of updating the  firmware.

Later,(April 2018) Abbott issued wider application of the security patch, this time involving 350,000 ICDs and CRT units. 

In 2018 a cybersecurity vulnerability was discovered in Medtronic's method for their Carelink programmers  receiving updates over the internet.The vulnerabilities was linked to use of a outdated operating system (Windows XP) and lack of digital code signing during the updates. Medtronic solution at that time was not to fix their internet communication system but rather the more hands on  and  arguably more hacking resistant method of insertion of a jump drive into the USB port on the programmers to supply the update.

In 2019 Medtronic notified physicians that some of their PM and ICD models  (manufactured between October 2018 and April 2019) were reporting erroneously short battery life estimates. This involved approximately 53,000 units .Apparently there no serious event because of this and a software patch was said to be available sometime  in 2020. The error resided in the programmers and the computational programs on Medtronic's Carelink system and not in the CIED and there was no actual effect on battery life.

Also in January 2019 150,00 of Medtronic models Adapta,Versa and Sensia ( manufactured between March 2017 and Jan 2019) were recalled because of a software error to an integrated circuit.See here for Medtronic Urgent recall notice)

This problem was said by Medtronic to be due to "a design change in an integrated circuit , i.e. another programming error. This glitch under certain pacing setting could lead to pausing in pacing in when in a dual pacing mode. Medtronic said they estimated a software fix could be sent to FDA  for approval by the second half of 2019.So help was on the way but not quickly and in some circumstances (patient with no ventricular escape rhythm and  who did not tolerate an asynchronous mode) PM replacement was the only option. In this case a programming error would lead to PM replacement, an example of extreme downstream effect of a programing error.

The  Medtronic  battery life estimation error  mentioned above should not be confused with a actual premature  serious battery drainage problem experienced by Medtronic  pacemakers also in 2019 leading to at least one death. A report in 2019 indicated there had been three medical reports in which the pacemaker was completely drained as a result of damage to the  unit's capacitor.  The devices potentially affected were 131,000 units of the following models; Astra,Azure,Percepta,Serena Solara.

This poses a vexing problem to patients with those units and their EP cardiologists. There was/is no way to know which devices have damaged capacitors only that certain models were vulnerable to that problem. Pacemaker replacement is far from a risk free procedure and the FDA was not recommending prophylactic replacement. Medtronic began using a different capacitor and a better method to detect capacitor failure.The psychological impact on a patient knowing that they have a pacemaker model that might suddenly loose battery power should not be underestimated.

Medtronic pacemakers have a feature not shared by other PM manufacturers.When the PM reaches ERT , a mode shift occurs and the PM is shifted into  VVI mode at a fixed rate of 65.This is an asynchronous mode and may result in a syndrome called pacemaker syndrome.See here for details about this situation in which a programmed feature may cause serious symptoms while the PM is functioning as it was designed to do. What some would consider a bug is actually a feature in the eys of the pace maker manufacturer.

1)Das S et al Cybersecurity:The need for data and patient safety with cardiac implantable electronic devices, Heart Rhythm 2020 1-9 , (full text on line) 

2)Lee,JZ et al Pacemaker firmware  update and interrogation malfunction.Heart Rhythm case reports, vol5,#4, 213-216,April2019 

addendum 12/24/20. Additional paragraph added with link.

EP cardiologists farm out monitoring of pacemaker remote interrogations to third party companies

 There are  an estimated 200,000 pacemaker implantations per year in the U.S and only about 2,000 board certified EP cardiologists. I believe many PM implantation must be done by cardiac cath cardiologists with the on-site technical assistance of a PM company rep.There are an estimated 1.5 million patients in the U.S. with pacemakers as well as many patient with ICDs  (defibrillators)

In 2015, the Heart Rhythm Society consensus statement stated that remote interrogations (RI) are the standard of care with one annual in office examination. Typically remote interrogations are done every three months. At least in the US and Germany  government health care programs will pay for RIs.

Medicare ( a high percent of PM patients are Medicare eligible) will pay for a RI every 91 days and the CPT code of a professional interpretation is  typically less than 50 dollars ( as of data from 2019)

So if you look at the math and the economics with several million RIs per year it is not surprising that a number of companies are now offering management services for RI for pacemaker  and ICD patients which  include a screening interpretation as well as follow-up for patients who miss their scheduled RI and reminders for scheduled RIs and perhaps other services as well.

For personal experience I can relate that the first year after my pacemaker was implanted the device clinic at the hospital where my EP practices provided good patient service, answering the phone and giving me a report on the results of my remote interrogation typically within a day or two. Over the next year or so service deteriorated significantly , never answering the  phone and only  getting a call back no soon than 4-5  business days.  

One interrogation report indicated that my PM had recorded 8 episodes of " AT/AF" which stands for atrial tachycardia/atrial fibrillation. The PM did not differentiate between the two. Actually what was being recorded was "far field R wave sensing, which should have been apparent to a trained technician viewing the recorded tracings in the printout but was not.It is not clear if the  EP doc reviewed the details of the report even after I sent a email asking about the "atrial fibrillation"

3 months later I had an in office interrogation and visit with the EP doc. The pacemaker company tech doing the interrogation said that the earlier report of AF was not correct but rather the tracings clearly demonstrated a PM pseudo arrhythmia  issue known as "far field R wave sensing. The atria channel senses R waves and double counts them. The  "fix" was simple.The tech lowered the sensitivity of the atrial channel and no such events occurred again. 

I learned that my PM has a program feature than is supposed to detect Far field sensing  ( aka far field R wave sensing) and not misdiagnose Far field sensing as AF. I contacted the Pace maker company and after several phone calls and emails exchanges I was told that the reason their algorithm missed the correct diagnosis was that my runs of far field  were  slightly too short  for the  algorithm  to detect them. I do not now if the company saw fit to alter their algorithm to be more accurate.

After my written complaints to my cardiologists I have been able to obtain my  RI reports  soon after they are transmitted. As a non cardiologist it took me no small amount of time  (and buying 2 books on PMs and electrophysiology) to learn how to read the reports at least on a basic level arguably with a degree of knowledge approximating the work  quality done by the original clinic. At least in regard to PMs , ICD interrogation reports are a different level of complexity and detail. 

After my complaints about the poor patient service delivered by the hospital device clinic the EP department of which my EP doc is the section head stopped using that device clinic and contracted with an outside proprietary firm to manage the interrogation reports. I am not claiming  my complaints played any role in the  change of procedure for interrogation report review but there is a temporal relationship.

A quick internet search yielded several companies that review PM and ICD interrogations including the following -Ambucor,Iron Rod Health and Cardiac RMS.

Are bradyarrhythmias more common in long time endurance athletes?

 The relationship between the volume of aerobic exercise and health benefits has been described alternatively as curvilinear or U shaped with the current consensus favoring the former .

The curvilinear relationship between aerobic exercise volume and cardiovascular and all cause mortality is firmly founded in multiple large epidemiologic studies. The suggestion that the curve turns upward at some range of exercise volume and becomes U shaped  has not been actually  demonstrated in large epidemiologic studies. and is conjectural. 

.A reported increase in atrial fibrillation, foci of myocardial fibrosis and increased coronary artery calcification may  provide mechanisms for this proposed  ascending portion of the proposed U shaped curve which is the graphic representation of the "Extreme exercise hypothesis".

Is it possible or likely that  there may be other deleterious effects of too much of a good thing in regard to aerobic exercise.?Sinus node disease and cardiac conduction defects might also represent long term deleterious effects of long time aerobic exercise.I say "might" because there is suggestive but not conclusive data to that effect. 

 My personal experience ( 35 years of marathon running  and  development  of  a left bundle branch block (LBBB) and an exercise induced,high grade second degree AV block requiring a pacemaker) and  personal knowledge of two other long time, local runners also needing  a pacemaker) peaked my interest.

 But so much for numerator based reasoning what is the evidence for long time aerobic exercise contributing to the development of  clinically relevant bradycardia induced by sinus node  disease and/or A-V blocks. Case series and some epidemiologic studies provide some insight.

Andersen et al (1) published a  widely quoted cohort study of 52.755 cross  country skiers who participated in the Vasaloppet,a 90 kilometer cross country ski race,said to be the oldest and largest cross country event in the world. 

Outcomes of interest were hospitalizations for atrial fibrillation (AF) or bradyarrhythmias( BA) as documented in Swedish national registries. When comparison were made between those who skied the race more times ( five or more)  with those who skied only once there was a statistically significant  increase in the hazard ratios for both AF and BA.For AF the HR was 1.29 (1.04 -1.61,for BA the HR was 2.10 (1.28-3.47).

A similar trend for AF and BA was noted when the faster skiers were compared with slower skiers but failed to reach statistical significance.

The bradyarrhythmias were mainly second degree heart blocks but the hospital codes did not distinguish between type 1 and 2 which is an important distinction as type1 (Wenckeback) is recognized in endurance athletes and is not usually considered an indication for pace maker implantation.

This was very coarse grain study and such important data such as history of elevated blood pressure,diabetes,obesity,alcohol abuse,habitual level of exercise, etc were not available ..

 Baldesberger at al (2)  studied 62 former professional cyclists who had long since retired from competition . and compared them to 62 age matched golfers for controls. Two had pacemakers.None had bundle branch blocks or second degree AV blocks while six were said to have sinus node disease based on heart rates less than 40 per minute. A question that the authors wanted to answer was -does the slow heart rate , first degree heart block and type 1 second degree block said to be  common in competitive racers persist in later years after their period  of  heavy training has ended. Their persistence would suggest that vagal tone which is usually  the proposed mechanism for those cardiac finding is not correct and that electrical remodeling of the SA node and AV node might be responsible.  Though a small study these data suggesting increased risk of sinus node disease  seem to be the best evidence so far since a comparison was made with age matched controls 

The remaining data are simply case reports.

 Dr R Northcote (3)  published a study of the bradycardias seen in 20 long time, older endurance athletes in Scotland.Nine of the twenty had heart rates less than 35,six had a prolonged P-R interval and four had Mobitz type 2 heart block which disappeared with exercise..One of the 20 had a pacemaker implanted. A follow-up publication in 1999 (4) indicated that 2 more of the original group has been implanted with a pacemaker. 

Doutreleau et al (3) published a report of 2 active  endurance athletes with type 2 second degree heart block that occurred during exercise. The authors claimed erroneously that their publication was the first to report a high degree AV block either at rest or with  exercise, somehow  having missed Northcote 's2 reports. Exercise induced heart block is uncommon.

The athlete's bradycardia has traditionally been attributed to high vagal tone but an alternative proposed mechanism is electrical remodeling, specifically downregulation of the so called funny channel AKA HCN4. In older endurance athletes "fibrosis" of the SA noted is often proposed as the culprit but remodeling is an alternative explanation. The sparse data so far available suggest that SA node disease may be more common in endurance athletes while there is less compelling data implicating AV blocks. 

In a comprehensive review of the "extreme exercise hypothesis" by Eijsvogels in 2018 (6) there is no discussion of the issue of bradyarrhythmias but perhaps  clinically significant BA should at least be considered candidates for still another consequence of too much of a good thing. 

In 1964 writing in the same journal Dr. Lev and Dr. Lenegre  separately  described age related fibrosis of the conduction system as a cause of heart block in the elderly. In 1999 ,JJ Schott (7) identified two families with progressive cardiac conduction defects related to a mutation in the gene encoding for the sodium channel SCN5A.

How could one know given  for example an older endurance athlete  with a heart block if Lev/Lenegre disease  were responsible or if the block was somehow induced by excessive aerobic activity? 

1) Andersen K et al  Risk of arrhythmias in 52,755 long-distance cross-country skiers: a cohort study.Eur Heart J. 2013 3624 31, Dec 34 (47)

2)Baldesberger,S et al Sinus node disease and arrhythmias in the long term follow-up of former professional cyclists.Euro Heart Journal 2008, 29, 71-78

3)Northcote, R et al Electrocardiographic findings in male veteran endurance athletes. British Heart J. 1989,61,155-160

4)Hood,A and Northcote, R of Cardiac assessment of veteran endurance athletes, a 12 year follow up study. British J Sports Med. 1999, 33, 239-243

5)D'Souza, A,Cross talk opposing view: Bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. J Physiol 2015 Apr 15 593 (pt 8)1749-1741

(6) Eijsvogels T. et al The "extreme exercise  hypothesis":Recent findings and cardiovascular health implications Current Threat Options Cardio Med (2018)20:84

(7) Schott, JJ et al Cardiac conduction defects associated with mutations in  SCN5A .Nature Genetics 23:20-21 1999

Addendum : 12/12/20 In the original posting the section of Lev/Lenegre and SCN5A was inadvertently  omitted, 

Left Bundle Branch mediated cardiomyopathy- impressive results from His Bundle Pacing

 At least as early as 1989 CL Grines described significant functional abnormalities in patients with left bundle branch block (LBBB).

Blanc et al in 2005 and again Vaillant et al  in 2013  described patients with LBBB induced heart failure (HR) that was impressively improved  by cardiac resynchronization therapy (CRT) in the form of bi ventricular pacing.Blanc commented that this was a new concept of left ventricular dyssynchrony - induced cardiomyopathy.

In spite of the fact that it has been known for 30 years  that  left ventricular functional changes are caused by LBBB and it has been fifteen years since a LBBB induced cardiomyopathy was described we continue to find current journal articles that depict BBB without other cardiac disease as not a clinical problem.

R Singh et al (1) recently reported the results of His Bundle Pacing on 9 patients with LBBB-mediated cardiomyopathy. The left ventricular ejection fraction increased on average from 25% to 50% while the left ventricular end-diastolic volume decreased from 55 to 48mm., while the QRS duration decreased from 152 to 115 milliseconds. This represents another article indicating that His pacing gives results as  good or perhaps better than Bi ventricular pacing for CRT. 

1) Singh, R et al His-Bundle pacing: A novel treatment for left bundle branch-mediated cardiomyopathy.

J of Cardiovascular electrophysiology 2020 vol 31 no 10.

Habitual aerobic exercise and arterial stiffness

It has been known for at least 20 years or more than endurance exercise done over a  period of  time can mitigate the age related increase in central artery stiffness.Work published by Tanaka in 2000 and  data from the BLSA in 2003 established that relationship. refs 2 and 3 The duration and intensity of exercise are important determinates of that mitigation .

Sedentary aging is associated with changes in the left ventricle (LV) , including :
increase in wall thickness,increased mass and decreased diastolic function.The LV is stiffer and relaxes less well It has been suggested that the heart burdened by these accountments of aging are sitting ducks for a second hit  (High blood pressure,obesity,diabetes) which could lead to heart failure with preserved ejection fraction (HFpEF), a type of heart failure constituting about  one half of all HF cases and for which there is no good treatment.

Gates and colleges (1)from University of Colorado studied the question of whether  attenuation of age related increased in arterial stiffness by long term endurance exercise might help preserve LV structure and diastolic function. This was a reasonable hypothesis as it had ben the general party line  for years that the increased afterload imposed on the left ventricle from stiffening of the aorta with loss of its capacitance function would produce deleterious changes in the left ventricle and secondarily left atrium .

 In a cross sectional study  of 138 young,middle aged and older men who were sedentary, recreationally active or endurance trained ,Gates  found that regular endurance exercise did not"consistently modulate the changes in LV structure and function that occur with physiological aging in men" . Several publications from Ben Levine and the group from the Institute for Exercise and  Environmental Medicine in Dallas  have provided data that I believe provides refutation of that conclusion,their data demonstrating favorable remodeling of the Left Ventricle with maintenance of a more youthful left ventricular  compliance.


1)Gates,P E Left ventricular structure and diastolic function with human ageing. European Journal of Cardiology. 2003,24,2213-2220

2)Tanaka,H Aging habitual exercise and dynamic arterial compliance. Circ. 200 102, 1270

3)Havlik,R Association of physical activity and less vascular stiffness in 70-79 year old.The health ABC Study. J of Aging and Physical Activity. 2003, vol 11 , issue 2 156-166

Covid19, the Pareto Principle, super spreaders and value of testing backwards

 The Pareto Principle or the 80/20 rule states that a small number of events are  often responsible for a large numbers of consequences or outcomes.

Influenza spreads in a deterministic way, person to person .There is epidemiological evidence that points towards covid19 spreading in a more random fashion or stochastic mechanism in which randomness plays a major role in the form of super spreader events. It is believed that many, perhaps most persons infected by the Sars Cov 2 virus do not spread the disease to a  large number of people but rather to one or two at the most . Others , however, if the personal and situational  circumstances are right can spread the disease to hundreds of others .

The circumstances were right when "Patient 31" in Daegu South Korea was shown to be the index case in the covid19 infection of  5,000 cases in a megachurch super spreader incident;  Covid19 spreader events such as the Biogen Conference in Boston and the  choir spreader event in Washington are well known. Of course,person to person spread can then occurs in households or through close contacts in work settings  after the big event seeding.

The role of super spreader events opens the door to "backwards" testing in which a positive case 's previous attendance at event ripe for spread could be investigated .

See the excellent article by Zeynap Tufekci  in the Atlantic that discusses these concepts. 

(See https://www.theatlantic.com/health/archive/2020/09/k-overlooked-variable-driving-pandemic/616548/)

Exercise may prevent age related motor unit loss

Regular exercise may prevent-or at least  significantly slow down- motor unit loss  in the muscle groups exercised.  GA Powers et al demonstrated that there was significantly less loss of motor units in the tibialis anterior  muscles of long time runner as compared with older sedentary otherwise healthy subjects.   

The estimated number of motor units in the group of masters runner (average 65 years)was the same as those in young active runners (age average 25)

 

Interestingly the arm muscle of the runners did not show less motor unit loss, although one would think the arm movement during running would be helpful in that regard.

Muscle loss can be due motor unit loss ( remember the motor unit includes the anterior horn cell) or muscle atrophy or both. You have to think that once anterior horn cells die no amount of exercise will rejuvenate the muscle.

1) Power, GA et al  Motor unit number estimates in masters runners: use it or losse it?

Med Sci Sports Exerc 2010 Sept 42 (9) 1644-50

Population Medicine, The Baptists and Bootleggers and risk factor epidemiology.

 Goeffrey Rose in his 1985 book "Sick Individuals and Sick Populations" likely never intended to provide  intellectual grist for the mill of the major pharmaceutical industry but I argue he did just that...

His thesis is  that a large number of people at small risk for a given disease may give rise to more cases than the small number of those at high risk. Rose's population strategy was that there would be a large benefit to the population by treating the low risk people .Large benefit to the community may offer little to the each participating person and in some instances harm and bringing more benefit to an individual may have small impact on the population's health. This was labelled the Prevention Paradox. 

Interesting, this conception assumes that it makes logical sense to speak of the health of an aggregate which I argue is a category error. Is there a health of the community distinct from the health of its individual members?

Rose's imperative was to decrease the total disease burden of a population.What is important in this formulation is that the aggregate is more important that any of the individuals who make up the aggregate.Individual bees,except  for perhaps the queen, mater little , it is the health of the hive that must be promoted.

Next the idea of risk factor comes into play. This notion was brought into prominence and became part of the the jargon of medicine by the  authors of the Framingham study who set out to find the cause of coronary heart disease and concluded there is not one single cause but rather there are a number of factors, designated as risk factors,the possession of which by a person can be considered to increase  his risk of developing coronary heart disease. The field was ripe for the "treatment" of risk factors and "preventive" medicine would find  many new things to prevent.

The slippery notion of the nature of risk was given little attention in medical journals.- as the risk factor revolution of medicine burst forth, first with coronary heart disease and then for as many diseases whose risk factors the epidemiologists   ( and young general medicine department faculty members with recently minted MPH degrees) could generate with increasingly broad based and coarse grained data dredging .To name a few - osteoporosis,hypertension, diabetes,cancers, all have accumulated their own array of risk factors as have  alcoholic abuse, depression and internet addiction.With greatly increased access to computer statistics programs and processing and p value hacking it seemed that almost everything is a risk factor for something and making big deals over small differences ( relative risks less than 2) increased the risk that reading the daily news would makes the average reader think he was at a risk for something.

With Rose's population thesis and the epidemiologists' increasing supply of risk factors the opportunities for the drug companies burst forth.The idea that just about any disease can be described as a public health issue opening the door for "public health solutions" which typically involves governmental involvement if not governable coercion, at least in the form  nudges consisting of grants and public education campaigns. 

People were increasing treated for pre-diseases; pre-coronary heart disease, pre- hypertension,pre-diabetes, and even pre-bipolar treatment for moody,irritable ,grumpy kids .Cardiologist Tom Giles sarcastically talked about everyone  possessing the risk factors for  being "pre-dead".

Pre-patients ,after being informed of some risk factor for something,were advised to see their physician health care provider to "determine" their personal risk.This is of course an impossibility because all the provider can do is to parrot what the pre-patient has already read, namely that he is a member of a group   which has allegedly an increased risk, there being no technique learned in medical school  health care provider school that enables the provider to magically provide a personal risk, that concept making no logical sense. 

Note: This is a lightly edited version of a blog entry from five  year ago. It hits on several of the themes I have obsessed and ranted about for some time and thought it would be a good posting for my 1200 th blog entry since February 2005. 

In regard to the topic of population medicine I highly recommend the book 'Moving Mountains" by Dr. Michel Accad. In the book Accad discusses the emergence of population medicine as the results  of developments in economics,science and the ethics of healthcare much to the detriment of the physician patient relationship.

In regard to The Baptist and Bootleggers.I am referring to the concept popularized by Bruce Yandle . See "Bootleggers and Baptists. How Economic and moral Persuasion interact to shape regulatory Policy." Baptists and bootleggers both supported laws forbidding alcohol sales on Sundays , but for different reasons. 

Thoughts about the epidemiology of exercise volume and health effects

Considerable data exist that  allow reasonable estimates of the volume of exercise required to : 1) decrease cardiovascular disease (CVD) risk 2) decrease the risk of heart failure.

There are considerable coarse grain epidemiologic data that support the notion that regular aerobic exercise will decrease heart attack risk, reduce heart failure risk and reduce all-cause mortality.

The 2018 Physical activity guidelines for Americans recommended at a minimum of  approximately 8 metabolic-equivalent hours per week ( 8 met-hours or 500 met minutes per week.)

The recommendations translate to 150 minutes of moderate exercise (less than 7 Mets) or 75 minutes of vigorous  exercise per week.

 Arem et al ( 1) pooled data from 6 studies (661,137 men and women) and  demonstrated a 20% reduction in mortality among those who exercised at the recommended level with an HR of 0.8 (CI 0.78-0.82) and a 37% lower risk for those who exercised at 2-3 times the minimum level and the maximal benefit at 3-5 times the minimum (  0.61, CI 0.59-0,62)

Further no excess risk was evident even at exercise levels of 10 times the minimum.Here more did seem to be better and no definitive upper limit was apparent.

Wen et al (2) published all cause mortality  data similar  to Arem and  also found that the maximum  CVD mortality risk reduction (45%) ( HR 0.55 CI 0.46-0.66)  at an exercise level of 523 minutes per week, a level roughly 3.5  times the minimum recommendation.


These 2 articles are part of the evidence  regarding the safety of exercise levels higher than the 2018 recommendation. Drs Carl Lavie and James O'keefe have spoken ( TED) and warned  in print about the purported hazards of long bouts of  or too many years of aerobic exercise. In 2015,  perhaps in part reaction to the Arem article and commentary by Dr. Ben Levine,  Lavie and O'Keefe toned down their emphasis on the risk of long distant running.See here for a Runner's World article concerning that issue.

The conclusion to the Arem publication is refreshingly non-ambiguous and prescriptive ,quoting
Arem:

"In regard to mortality health care professionals should encourage inactive adults to perform leisure time physical time activity and do not need to discourage adults who already participate in high-activity levels."


Coarse grain epidemiological evidence strongly support the generally accepted notion that people who exercise none or very little have the highest risk and those who exercise the most have the lowest risk.

In a nutshell-the large coarse grain epidemiologic studies demonstrated that relativity low levels of exercise are better than none and further these studies were not able to demonstrate a upper level of exercise that is more risky than no exercise  though some data indicted that risk reduction at the highest level studied may have reached a plateau.

It is possible that there could  be some harmful or potentially harmful cardiac effects in a small number of long time and/or high volume endurance athletes that would not be detected by large data analysis such as that of Arem and Wen.

 That appears to be the case.

There are  three  conditions that  appear to be more common in high level exercisers. These are 1) atrial fibrillation 2) myocardial fibrosis and 3)coronary calcification.

While the current consensus view is that the relationship between exercise level and all-cause and cardiovascular mortality is curvilinear and not U shaped, the same cannot be said in regard to atrial fibrillation (AF) .

In a  2018 review (4) of the "extreme exercise hypothesis", which states that there is some level of exercise   that results in a harmful effects. Three conditions have been considered in that regard: 1) atrial fibrillation (AF), 2) myocardial fibrosis (detected by MR gadolenium scaning) and 3) acceleration of coronary artery calcification (CAC).


Eijsvogels,Thompson and Franklin (4) concluded in regard to AF :

 "that the relationship between physical activity and incident AF is best summarized by a reverse J shaped curve.Light to moderate  amounts of exercise decrease but large volumes of exercise potentially increasing the risk of AF."

Two of the studies mentioned are their review are  the Henry Ford study and Anderson's cross country ski study .

Even though a study from the Henry Ford Exercise testing project (5) demonstrated that higher cardiorespiratory fitness was associated with a graded reduction in AF (the higher the fitness level the lower the risk of AF),a large cohort study of cross-country skiers showed that those who finished more races and those who raced faster had higher risk of AF than those who did only one race and those who raced at a slower pace. In that study by Anderson  (6) of  52,755 long distance skiers those who finished five or more races versus those who finished only one race had a Hazard ratio for AF  of 1.29 95% CI 1.04-1.61.

The Henry Ford study looked at the relationship between fitness and incident AF and the Anderson study looked at volume of exercise and intensity of exercise and while  fitness and exercise level are correlated they are not the same. After the entry into the study when fitness level was determined there are no data on  the exercise history of the participants at Henry Ford.The Anderson study used number of races and speed of racing to give some broad measure of amount exercise which relates to the questions of exercise volume versus AF risk which is not directly addressed by the Henry Ford study.


The large mega data studies,such as those by Arem and by Wen , lack the statistical power to detect any mortality effect that might occur from AF,CAC and myocardial fibrosis in endurance athletes whose exercise volumes fall at the  extreme right end of the volume axis since there are relatively few subjects exercising at mega volumes.

Even though the relationship between exercise volume and/or intensity and CVD and all cause mortality is not U shaped, the relationship between exercise volume and AF is. 

The issue of the relationship between exercise volume and coronary calcification is less straight foward. Defina's(7) study presents data that high levels of exercise  (3,000 Met min  per week which is about 6 times the minimal 2018 recommendation) are associated with prevalent coronary artery calcification but not  increase in cardiovascular mortality. This apparent paradox might be resolved if it turns out that the increased in runner's calcium scores represent density and not extent of calcium and that the increased density is related to heavy calcified plaques which are made less vulnerable to rupture. 

1)  Arem H   et al. Leisure time activity and mortality: a detailed pooled analysis of the dose-response relationship. JAMA Int Med 2015 Jun 175 (6) 959  (full text is on line)

2)Wen,CP Minimum amount of physical activity for reduced mortality and extended life expectancy .A prospective cohort study. Lancet 2011,378 , 144.

3)Franklin, BA Exercise related acute cardiovascular events and potentially deleterious adaptations
following long term exercise training. Placing the risks into perspective-An update A scientific statement from the American Heart Association. Circ 2020 Feb 26 PMID 32100573

4) Eijsvogels, TMH et al The "extreme exercise hypothesis":Recent findings and cardiovascular health implications." Curr Treat Options cardio med 2018 20  84 

5)Querishi,WT Cardiorespiratory fitness and risk of incident atrial fibrillation:results from the Henry Ford Exercise (FIT) project Circ 2015: 131 ;1827

6) Anderson K et al Risk of arrhythmias in 52,. 755 long distance cross country skiers: a cohort study
 Eur Heart J 2013 Dec 34 (47)36

7) Defina,LF Association of all-cause mortality and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification . JAMA Cardiolog 2019, 42 (2) p 174

addendum 7/27/2020 Several changes made in the et to clarify meaning .8/14/20 and again minor changes to clarify meaning. also on 11/19/2020.3/21/21 Minor editing and typo corrections. 5/26/21 still more typos corrected.9/27/21 Comments regarding Defina's data added .

If high levels of exercise increase risk of coronary calcification does it also increase CV mortality

Do long time endurance athletes have an increased risk of coronary calcification? If so, does that correspond to an increase risk of cardiovascular events?


In this study (1)  the life long exercisers in the highest activity level (5-6 hours of vigorous activity per week) did show an 11% increase coronary artery calcification (CAC) of a score of 100 or higher but that group had an all cause and cardiovascular mortality risk lower than that in groups with a lower level of exercise.

The author conclusions:

"This study suggests there is evidence that high levels of physical activity (3,000 MET-min/week)are n iassociated with prevalent  CAC but are not associated with increased all-cause 0r CVD mortality after a decade of follow-up, even in the  presence of clinically significant CAC levels."

To the extent these results reflect reality,there may be some reassurance to folks who may have spent arguably too many hours running or cycling.

1) Defina, LF et al. Association of all-cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiology, 2019 42 (2) P174 (full free text available)


" a man hears what he want to hear and disregards the rest" The Boxer,, Simon and Garfunkel

Gain in life expectancy related to exercise not a U shaped curve phenomenon

Moore et al published an analysis of the effect of leisure time activity and the effect on life expectancy with data from over 650,000 individuals with a 10 year followup in persons aged 40 and over.

At the lowest exercise level which was 3.74 met-hr/week ( a MET level of 3 is described by the authors as a brisk walk and this level being equivalent to 75 minutes of brisk walking per week) there was a gain of 1.8 years.

150-300 minutes of a brisk walk per week yielded 3.4 years gained.

300- 449 minutes of brisk walking was associated with 4.2 year increase in life expectancy.

The lowest level at which they demonstrated a life expectancy gain was less than the minimal recommendation of WHO and of the US panel. Benefit seemed to plateau at around 300 mintues of brisk walking per week. Moore's data display was not U shaped.



1) Moore, SC Leisure time physical activity of moderate to vigorous intensity and mortality. Plos Med 2012 e1001 335

2) Aengevaeren,VL Exercise and coronary atherosclerosis. Circulation vol 141 no 16, 21 april 2020 p 1338 1350

Nicholas Taleb schools public health specialists,libertarians and pseudo-libertarians

Nicholas Taleb addresses pubic health "thought leaders", non-devout libertarians and pseudo-libertarians in this commentary regarding the issue of recommending masks for the public.

Some of the points he made include:

1)A significant and vocal and authoritative portion of the public health coterie (PHC) mistook or ignored the important distinction between "absence of evidence of efficacy" and "proof of lack of efficacy".The PHC did not have anything in the second category in their argument tool box. They mistook or ignored the distinction between  absence of evidence and  evidence of absence,something emphasized in epidemiology 101.

2) The PHC failed to recognize how effective the widespread use of mask would be.If A and B both wear masks, both protect the other This Taleb labelled the compounding effect. Witness the hair care business in which 2 stylists were infected and none of the 140 patrons exposed developed covid19. The secret was both the stylists and all of the customers used masks.

3)Libertarians and pseudo-libertarians are admonished by Taleb to remember the primary principle of libertarianism which is the non-aggression axiom. Exposing fellow humans to a serious illness  with whom a person comes in contract just might be considered an act of aggression.

On 6/15/2020 Dr. Fauci admitted that masks were not recommended earlier because there was a serious shortage of masks. Interestingly once masks or face coverings were recommended by the PHC masks of all sorts were available all over the internet. What if the public had been told earlier  that cloth face coverings could help, would there have not been the release of entrepreneurial energy (and charitable efforts) to get masks to people that we see now. Wonder how many deaths could have been prevented.