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. 

Exercise and the aging heart versus aging in the sedentary heart

What are the arc (s?) of the normal aging heart ( the sedentary ageing heart and the exercising ageing heart).Are they different?

 Humans seem good at finding patterns-sometimes even from patternless noise.One of the stories told  by physiologists and cardiologists regarding the age related downhill course of cardiac function seems to go  something like this.

One way to simplify  cardiac function is to consider two parts of the cardiac cycle,1) contraction and ejection of blood and 2) relaxation and the refilling of the ventricle.

There are data indicating that the first signs of an impending problem are seen in the filling phase ie. diastole.From extensive echocardiographic and invasive physiologic measurements in humans the following sequence can be sketched out and penciled in.

First, there is impaired relaxation following by decreased elastic recoil and later diminished  compliance ( which is to say increased stiffness) and then -at least according to work from the IEEM group- remodeling of hearts with thicker walls and smaller ventricular volumes).Simply put- a sedentary ageing  lifestyle leads to a small stiff heart and long time endurance exercise leads to a larger more easily filled heart.The contractile function of the heart is well preserved with ageing , at least as indicated by measurement  of the resting ejection fraction.( increasing stroke volume with exercise is another matter as is left ventricular stress measured by speckle echo.)

This is largely consistent with the mainstream echocardiographic model which proposes a predictable,progressive process beginning with impaired relaxation,followed by decreased compliance and ultimately- as a compensation- elevated left side filling pressures.This model describes three phases of diastolic dysfunction indentifiable by combination of echo findings believed to reflect  how well or poorly blood flows into the ventricles from the atrium. This model recognizes that the various indices ( e.g E/A ratio, IVRT,maximal E wave velocity and the time constant of isovolumic pressure decay (Tau) change with age so that what would be abnormal in a 20 year old is normal in a 75 year old.It is thought that that filling pressure can be estimated by use of this model. NOTE-see end note 1 for reference to data that challenges the mainstream model by in part  providing data that cardiac cath measurements of left sided pressures do not regularly correspond with the three echo defined stages of diastolic dysfunction)

Next, I consider  what I have labelled as the "Dallas or IEEM theory" of cardiac ageing.

I do not know if Dr. Ben Levine would approve of my label or not. Maybe we could call it the Levine Theory.  see end note 2

A series of articles from the University of Texas Southwestern Medical School and the IEEM have provided extensive invasive and noninvasive data regarding cardiac function at various ages and the effect of longtime endurance exercise versus sedentary ageing on  cardiac structure and function.

Levine et al first demonstrated that lifelong endurance athletes ( 25 years or more of running a lot) had left ventricular compliance virtually identical to those of sedentary 20-30 years olds. Then they compared ventricular compliance in four groups of 25 each of people who exercised at various levels over a 25 years period. These were all subjects over the age of 64 and were screened to excluded pre-existing heart disease.Group 1 was sedentary people who exercised no more than one session per week. Group 2 were labelled "causal exercisers" and exercised 2-3 times per week. Group 3 (Labelled as committed exercisers}worked out 4-5 times per week and the "competitive" group trained 6-7 times per week and regularly raced.The racers had the most elastic  or compliant ventricles while group 3 was "very close" in terms of ventricular compliance while groups 1 and 2 has significantly stiffer hearts.Note: while exercise seemed to help maintain compliance , long time endurance exercise did not mitigate the age related loss of ventricular relaxation-as measured by the isovolumic relaxation time  (ivrt) which is the time from aortic valve closure to mitral value opening.

Next, Levine studied a group of 70 year old subjects  and an vigorous  exercise program was unsuccessful in improving the reduced compliance observed in that group. Next another study demonstrated that middle age subjects with a year long exercise program ( that involved in part high intensity interval training) were able to increase their ventricular compliance.This implies that past some point in time you cannot improve LV compliance with endurance training  with some interval training but middle age may not be too late.This does definitely not mean that exercise for those 70 years of age and older gain no benefit from aerobic exercise,,just that it looks like they will not  improve left ventricular compliance (at least withinthe time frame of Levine's subjects)

In another article Levine said that exercise in the range of that performed by the "committed exerciser" might be adequate.

My main question in this regard is "how much exercise "is sufficient to maintain a healthy compliant left ventricle." Levine's amazingly compliant  (pun intended) subjects not only stuck with program for a full year but after the first 6 months participated in a hig intensity interval program using the demanding 4X4 workout program that involves 4 minutes of exercise at 95% of maximal heart rate followed by 4 minutes of rest done four times.

End note 1. Grant et al (Grant A, Grading diastolic function by echocardiography:hemodynamic validation of existing guidelines.Cardiovascular Ultrasound 2015 513 :28) compared echocardiography results with  left heart catherization data in 460 patients.The data demonstrated that there were no differences in regard to left ventricular pressures between patients with normal diastolic function and those with grade 1 or 2 diastolic dysfunction but there were differences between normal and grade 3 diastolic dysfunction in patients with reduced ejection fraction.In those patients with preserved EF, there is no statistical difference between normal and any grade of diastolic dysfunction. (see figure 5 of their article which graphically illustrates the lack of the "predictable, progressive process "which characterizes the  current paradigm.)If the detection of elevated LV pressures which generally correlates with exertional shortness of breath is in part the goal of echo studies of diastolic function it appears to not be reached based on Grant's data.

end note 2. Dr Ben Levine is the director of the Institute for Exercise and Enviromental Medicine (IEEM) housed at the Texas Health Presbyterian Hospital Dallas and professor at University of Medicine Southwestern. His group have done a series of comprehensive physiological studies on subjects recruited from the Dallas Heart Study, a population based sample of 6100 subjects in Dallas .

In a nut shell the concept is that everyone with aging develops some degree of diastolic dysfunction related to impaired relaxation and loss of diastolic suction,Later aging (particularly sedentary ageing) is associated with loss of ventricular compliance ( AKA increased stiffness). A long term endurance exercise program is capable of mitigating the changes in compliance but not the decrement in relaxation and diastolic suction. IEEM's studies  further indicate that a sedentary lifestyle may lead to a small stiff heart which may be the precursor to heart failure with preserved ejection fraction (HFpEF) ) and the Dallas group suggest that an appropriate amount of endurance type exercise begun no later than early middle age may play an important role in the prevention of HFpEF.

"Humans are pattern-seeking story -telling animals and we are quite adept at telling stories about patterns, whether they exist or not".Michael Shermer.

End note 3:In 2008, Shermer coined the term "patternicity" -the tendency to find meaningful patterns in meaningless noise. I am not suggesting that the extensive,very carefully done research referenced above is meaningless noise.I just really like the quote but I certainty hope the "Dallas hypothesis" is a reasonably accurate approximation of the ways things  really are at least sometimes- having spent a lot of time running a lot over the last 40 plus  years.

.

Has the issue of keep closed longer or open up quicker now a political non-debate?

The following is a quote from a commenter named Handle on Arnold Kling's blog from 4/25/2020 entitled Henderson-Wolfers Non-Debate.

"One of the most terrible things than can happen in our society is that some important and formerly neutral questions becomes politicized and the position one espouses become a strong signal of affiliation to a particular team....once there is a party line on the matter thinking ends all together."

Two  examples-Several members of the Republican party appear in Congress not wearing masks
presumably to make a point. ER Nurses stage a counter protest against a open things up protest,shouting matches break out.

Should Runners,walkers,cyclists beware the Coronavirus slipstream

The slipstream is the zone behind a person moving (walking, running,etc) which pulls the air along with the person.In the racing world it is known as drafting.

A recent news article about a study done by Belgian engineers has gone a bit viral itself.The wave of air flowing carrying respiratory droplets or drops  in the wake of a runners goes behind him   for distances greater than the magic 6 feet that we are admonished to respect as regards proximity to other humans in the world or preventive social distancing. At least the animations released by the researchers give that impression as do their data which at this writing has not yet been published in a peer reviewed journal.

See here for details.

If their  animations reflect the actual path  of exhaled particles,one might decide that even when you are out for a run to wear a mask at least some of the time.

See here for some questions and answers from one of the authors of the paper.

My personal take home is that when a runner passes me I should move to the side to avoid potential particles in his slipstream and ( with an abundance of caution) pull my mask up until the passer is 20 to 30 thirty feet  away. In the increasingly unlikely instance in which I actually overtake a runner and pass her I should move to the side and keep to the side to keep the passed person out of my slipstream.

Perhaps the equivalent of "My mask protects you,your mask protects me" for runners could be
"I'll keep you out of my slipscreen,you keep me out of yours"


According to the authors data a cyclist should stay 60 feet directly behind the bike in front or keep off to the side. Also they suggest that 16 feet behind a walker and 32 feet behind a runner to be approximations of the "aerodynamically equivalent social distance" which is six feet for stationary people.







.

Role of masks for COVID prevention outside of hosptial use

The following is my opnion and not a medical recommendation.

 Public face mask use appears to be common in Asian countries and also is now required in 

the Czeck Republic where people wear masks as a civil duty with the  shared realization that "I protect you by wearing a mask and you protect me by wearing a mask."

Corona virus is spread by droplets by infected persons even if they are asymptomatic and both simple surgical type face masks and the more expensive and protective N 95 masks can significantly reduce spread of coronavirus.

Both type of masks have been scarce in the US as Covid 19 cases exploded. Expectations and then realization of actual mask shortages in medical care facilities lead public health officials to discourage the public from using masks in the hope that more would be available for health care workers

Sometimes it has been argued that the masks were not effective when used by the public while at the same time saying that the masks should be reserved for medical personnel use in whose hands they would somehow offer important protection to them. Of course, protection is not a function of one's profession.

It is likely that it was believed that  officially recommending masks would lead to a large public demand  , making it even more difficult for health facilities to obtain masks.

As Covid  19 cases continue to increase and the mask shortage worsened, the CDC  said that masks can be reused and ,that homemade masks and scarfs could be used as a last resort by health care workers. This was a major change in CDC recommendations.Home made masks and scarfs can be used to protect the public as well, although that was not said by CDC.

Jeremy Howard,a Deep Learning specialist from Stanford, has posted an excellent review of the use and value of face masks by the general public to decrease COVID spread and describes widespread use by the public in many countries.See here

https://www.youtube.com/results?search_query=jeremy+howard

He gives links to sites with important information on how to clean masks and how to make masks at home from towels, t shirts etc. Some may worry about being accused of taking masks away from doctors and nurses if they wear a mask in public. Home made masks hopefully defuse  that issue.

Summary:
Covid 19  is spread by droplets by asymptomatic as well as symptomatic persons
Various kinds of masks decrease risk of spread
Masks can be made at home and worn in public  without shame .A great DIY project
Masks  protect others perhaps even more than they protect the wearer
It has been suggested that it would be unpatriotic for the public to wear masks.I suggest the opposite.
wearing masks is patriotic.An asymptomatic covid 19  infected person being in public exposing others to the disease is certainly not patriotic.
I am not recommending  to bid up prices of masks,No one wants to take masks away from HCWs.
 But if you already have masks on hand ,wear them .If not they really can be made at home and will offer some important protection . Yes, less than the properly fitted and correctly worn N 95 and less than surgical masks but significant protection nevertheless.
Bottom line wear masks in crowds (including grocery shoping)

Finally, imagine for a moment if only 25% of subway riders in New York (8 million riders per day) wore masks for the last 2 -3 weeks what the results might have been. Also imagine the potential benefit after we all come out emerge from sheltering in place how potentially important wide spread use of mask might be in decreasing the risk and/or impact of a second wave.

The following quote is from Scott Alexander writing on his blog slatestarcodex.com on 3/23/20 giving a detailed analysis on the research of various masks and the protection they provide;

". So should you wear a mask?

Please don’t buy up masks while there is a shortage and healthcare workers don’t have enough.

If the shortage ends, and wearing a mask is cost-free, I agree with the guidelines from China, Hong Kong, and Japan – consider wearing a mask in high-risk situations like subways or crowded buildings. Wearing masks will not make you invincible, and if you risk compensate even a little it might do more harm than good. Realistically you should be avoiding high-risk situations like subways and crowded buildings as much as you possibly can. But if you have to go in them, yes, most likely a mask will help.

In low-risk situations, like being at home or taking a walk, I mean sure, a mask might make you 0.0001% (or whatever) less likely to get infected. If that’s worth it to you, consider the possibility that you might be freaking out a little too much about this whole pandemic thing. If it’s still worth it, go for it.

You are unlikely to be able to figure out how to use an N95 respirator correctly. I’m not saying it’s impossible, if you try really hard, but assume you’re going to fail unless you have some reason to think otherwise. The most likely outcome is that you have an overpriced surgical mask that might make you incorrectly risk-compensate.

If you are a surgeon performing surgery, bad news. It turns out surgical masks are not very useful for you (1, 2)! You should avoid buying them, since doing so may deplete the number available for people who want to wear them on the subway."

Here is a quote from a blog post by Tomas Pueyo entitled "Coronovirus:The Hammer and the Dance"which has attracted considerable interest.Here is the link.https://medium.com/@tomaspueyo/coronavirus-the-hammer-and-the-dance-be9337092b56

Pueyo considers masks part of the solution." (my bolding)

"the massive impact of policies like those of Singapore or South Korea:

• If people are massively tested, they can be identified even before they have symptoms. Quarantined, they can’t spread anything.
• If people are trained to identify their symptoms earlier, they reduce the number of days in blue, and hence their overall contagiousness
• If people are isolated as soon as they have symptoms, the contagions from the orange phase disappear.
• If people are educated about personal distance, mask-wearing, washing hands or disinfecting spaces, they spread less virus throughout the entire period."

(note the blue and orange wording references refer to charts in his article)

Maybe it is this simple: If asymptomatic patients are not contagious, the masks only for the symptomatic rule works, but if the  asymptomatic are contagious that rule does not work.

addendum: 4/11/20 Several glaring typos finally corrected. Also now the CDC has blessed the wearing of face masks by the general public, preferably of the home made variety.Two days ago at the grocery about 50% of the shoppers wore masks, most not of the DIY type.

Addendum 5/8/20 Today at Krogers only 2 of the approximately 40-50 person did not have masks.All of the store workers did and now they have erected plexiglass barriers shielding the checkers.

Do ARBs and ACEis make COVID 19 infection worse?

A recent article in the BMJ raised concern that drugs that inhibit parts of the RAAS system might be harmful to patients infected with the new novel corona virus  known as SARS-COV2 while the disease it produces is named COVID 19.

 Coarse grain epidemiologic data from the Wuhan outbreak indicated that one of the risk factors for bad outcomes was hypertension.It was then hypothesized that the increased mortality might be due to the subset of hypertension patients who were taking ARBs or ACEi as those may increase levels of ACE2 which has been shown in animals and possibly humans and ACE2 is the receptor for both SARS-CoV and SARS-COv2. So with more ACE2 would the results be a higher viral load?

On the other hand in an animal model of SARS-COV ARMS seems to reduce lung injury.

All this and a detailed recitation of the RAAS system as it relates to Corona viral infection can be found in the link found at the end of this post as can the citation for the BMJ article..That link is an article by Dr. GM Kuster et al published March 20 2020 in the European Heart Journal which reaches this conclusion:

In conclusion, based on currently available data and in view of the overwhelming evidence of mortality reduction in cardiovascular disease, ACE-I and ARB therapy should be maintained or initiated in patients with heart failure, hypertension, or myocardial infarction according to current guidelines as tolerated, irrespective of SARS-CoV2. Withdrawal of RAAS inhibition or preemptive switch to alternate drugs at this point seems not advisable, since it might even increase cardiovascular mortality in critically ill COVID-19 patients.

This is in agreement with a recent statement made by ACC/AHA.See herehttps://www.acc.org/latest-in-cardiology/articles/2020/03/17/08/59/hfsa-acc-aha-statement-addresses-concerns-re-using-raas-antagonists-in-covid-19



https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehaa235/5810479?utm_medium=Email&utm_source=ESC&utm_campaign=ESC+-+Newstetter+-+week+13


addendum 4/620 clarification of the nomenclature for the virus and the disease caused by it