In some , is college football enough to cause CTE?

 I believe the answer is yes.

202 donated brains from former football players  were examined by the Boston University CTE center. Of those who played in the NFL 110/111 had criteria that the center believes to be diagnostic of CTE.

 Finding CTE in former NFL players is not breaking news. The data from men who did not participate past the college level is in a way  more striking and alarming. 48 out of 53 college players' brains demonstrated pathological finding of  CTE and 27 of the 53 were classified as severe. There were 14 brains from men who only played high school football and of those 3 had changes said to be typical  of  CTE.

 This  , of course, does not speak to the issue of what is the prevalence of CTE in any group of players. The data here is highly selective The brains were donated typically by family members often in part because of concern that their family member has some mental or behavioral issue.This is numerator based statistics.

Data was not presented but it seems a reasonable assumption that the college players had experienced at least 8 years of football, i.e. high school and college and likely many also took part in Pop Warner of some such youth league .It is an open issue as to whether repetitive  subconcussive or concussive head blows are more likely to cause to cause damage to the young brain.It was a reassuring false believe prevalent for many years that young kids just did not hit each other hard enough to cause concussions or brain damage. Data from accelerometer measurements in helmets of youth league players have been shown to reach  the range  of impact forces seen in high school players so parents should have been disabused of that notion. but I doubt that most are.

The bubble wrapped,helicopted parented  generation(s) of kids protected from tri-cycle falls with helmets are for the most part not discouraged from high school football and in many instances cheered on by their parents who seem not to realize why there is often an ambulance parked near the playing field.

Is subendocardial fibrosis a reason for the age associated decrease in diastolic function?

It seems to be all about diastole.Simply put- the aging heart has more functional loss in ventricular filling than in  ejection of blood ( as least as depicted by the usual measures of systole namely the ejection fraction (EF) at rest and stroke volume at rest).  Similarly the  largest  difference between the exercise capacity of the average jogger and the elite endurance athlete is found in diastole-the elite athlete has markedly superior diastolic function likely on a genetic basis.

Hollingworth and co-workers from Newcastle on Tyne (1) studied left ventricular torsion and diastolic function in presumably healthy adults in various age ranges using  cardiac magnetic imaging with tissue tagging.

First some background;

The architecture of the left ventricle  has left handed subepicardial fibers and right handed subendocardial fibers which leads to a rotational deformation during cardiac contraction referred to as torsion. The subendocardial fibers are activated first leading to a  brief clockwise rotation ( as viewed from the apex of the heart as if you were on the spleen looking up) and then a counterclockwise rotation  while the base rotates clockwise. This action has been compared  to the two handed movement of wringing out a washrag.

The twisting of the left ventricle during systole is followed by a recoiling  or untwisting releasing the energy stored during systole. The untwisting largely occurs mainly in the isovolumic relaxation time . (IVRT). The IVRT is the  time after the aortic valve closes and before  the mitral valve has not yet opened-a period when no blood is either entering or leaving the ventricle.

 The rotation action of the heart can be explained by the orientation of the muscle fibers. The subendocardial  fibers are oriented in a right handed direction while the subepicardial fibers run in in a left handed direction and a midlayer is oriented circumferentially .The contraction of all three sets of fibers account for all contractile actions  of the heart and the rotational movement.

What at first seem counter-intuitive is the observation that  subendocardial disease is associated with hyper-rotations. (2) This is possibly explained by subendocardial fibrosis decreasing the rotational counterbalance to the mechanical advantaged ( longer radius) epicardial rotational direction.

Hollinsworth's study showed the expected decreased early diastolic filling and a " torsion to shortening ratio" that was consistent with lessened subendocardial shortening possibly  due to subendocardial fibrosis. So possibly some of the age related diastolic dysfunction may be related to altered and unbalanced untwisting mechanics.



1) Hollingsworth, KG et al Left ventricular torsion energetic and diastolic function in normal human aging. Am j Physiol heart circ physiology 302, H 885-H892,2012  (full text is available on line)

2.Nakatani, S. Left Ventricular rotation and twist:Why should we learn? J. Cardiovas Ultrasound 2011;19 (1): 1-6. Full text is available on line)

After 40 plus years ABIM does audit to see if I have a medical license

What is that all about?

 I received a letter from the ABIM informing me that " during a recent audit, ABIM was unable to confirm that you have a valid license to practice medicine." I was requested to send a copy of my license within 30 days and " if ABIM is unable to confirm that you hold a valid license to practice medicine,ABIM will be obliged to suspend your Board Certification and report your certification status as "Not certified".

I replied the same day by Email and send a hard copy of my license by letter . A few days later I received a second letter identical to the first and again I replied by mail with a copy of my license.I have had no reply.

I wondered about their audit procedure. I was able to verify my license in less than 2 minutes by going the website of the state of the medical board in the state in which I have had an uninterrupted license  at the same address for over 35 years.If their audit process is as inadequate as it appears to be they will waste more than a little time and effort to confirm licenses and waste time and efforts of diplomats replying to the requests.

Why , after forty years, does ABIM consider it necessary to determine if I have a license?

Is this somehow related to their widely criticized  maintenance of certification (MOC) program and the efforts of some organizations to link MOC with state medical license requirements?

Have others received similar letters? Any thoughts about what this is all about?

addendum: It is now more than 2 months and ABIM has still not replied to my email which they had promised in "2-3 weeks" saying they were very busy. 8/19/17

More on subclinical atrial fibrillation (SCAF) and what to do when we find it

A 2014 study-Crystal AF- examined patients with cryptogenic stroke using a implantable cardiac monitor and reported that over a three year period 30% had episodes of atrial fibrillation(AF) lasting 30 seconds on longer. This study likely energized the effort to implant cardiac monitoring devices and to anticoagulate those patients found to have atrial fibrillation (AF).A more recent study might serve to cast some doubt on that practice.

The study,Reveal AF,studied 394 patients using an implantable cardiac monitor with no history of AF but who  were considered high risk for stroke  based on the CHADS2 score.At the end of 18 months 29.3 % of the patients had episodes of AF of six minutes or more and at 30 months 40% had AF. Further, 12% had AF durations of 6 hours or more.

 So we know that  AF is common in 1) patients with history of stroke and no obvious  cause  2) patients classified as high risk using the CHADS2 scoring system and 3) patients with pacemakers.

Should all patients with cryptogenic stroke shown to have AF by a implantable  device receive oral anticoagulation? That seems to be common clinical practice but I am aware of no clinical trials showing the efficacy and safety of that approach. Should all patients with a CHAD2 score similar to that used in the Reveal AF study receive anticoagulation? ( in the trial 56% of the patients were actually prescribed OAC by their private physicians). Should all patients with pacemakers (PMs )with SCAF ( above some level of AF burden) receive OAC?

There are at least 2 randomized clinical trials underway which are designed to determine the effects of OAC on patients  with subclinical AF (SCAF) as determined by data collected on patients with pace makers.

In addition a recent study ( see here) and analysis casts more than a little doubt on the validity of the various CHADS risk determination systems.

The prolific EP cardiologist author and blogger John Mandrola  puts it this way in his discussion of the Reveal AF  " ..if the average high risk older person has the same amount of short-duration AF as a person who just had a stroke how does this ( long term monitoring) help decide on therapy?"  Point well taken. Actually at the end of 30 months in Reveal AF trial 40% had SCAF versus 30% with SCAF and 36 months.Taken at face value could nt  one claim that AF is protective? I think not but still that just amplifies Mandrola's point.

Dr. H Kamel and associates have published an excellent commentary and review (3) of the mechanisms of stroke and atrial fibrillation which along with the Reveal AF trial results might slow down enthusiasm  for implanting devices in all patients with cryptogenic stroke and the increasing call for more screening for the detection of afib.

1)Sanna, T Cryptogenic stroke and Underlying atrial fibrillation NEJM 2014: 370, 2478


2) Reiffel, JA presented at Heart rhythm Society Meeting, May 10-13, 2017.

3)Kamel, H et al Atrial fibrillation and mechanisms of stroke.Time for a new model.Stroke 2016 47 895-900.


Additions made Aug 2,2017 .

An increasing cardiac calcium score may not mean increased CVD risk

The coronary calcium score (  for example as done with a EBCT heart scan) is well recognized as a tool to estimate  cardiac risk, a higher score meaning a higher risk.

Coronary calcification is by definition coronary artery disease. Calcification may be in the media of arteries or in the intima. Intimal calcification may be dense as is  found in fibrous, basically stable plagues which are not prone to rupture and cause an acute coronary event. Spotty calcification can be found in soft, vulnerable plaques that are at risk of rupture.

Serial calcium scans on patients taking statins have shown increase in coronary calcification and yet there is more than abundant  evidence that statins ( at least in secondary prevention) can reduce plaques and  decrease the risk of coronary events,a situation referred to by some as the "statin paradox" or the "plaque paradox".

A possible explanation  to this alleged paradox may be found in a study (1) from Cleveland Clinic in which the authors analyzed intravascular ultrasound images of patients from 8 clinical trials.

Patients with coronary artery disease treated with statins show an increase in coronary calcification.The so-called high intensity statins bring about more increase in calcification while also causing the greatest regression of plaques. The increase in calcification may be one mechanism by which statin therapy stabilizes plagues and makes them less likely to rupture. So serial calcium scans in a patient taking a statin demonstrating increased calcification may not be a warning of increased risk at all.

Quoting Cleveland Clinic's  Dr . Steve Nissen:

"This is an important observation that tells us statins work to stabilize plaques by converting softer,cholesterol -laden plaques that are prone to rupture into more stable calcified plaques that are relatively inert.It explains the paradox of why serial measurements of calcium doesn't necessarily work to track the progression of disease and it explains to some extent how statins work.

Internists who like to talk about mechanisms and how things work may find this a compelling story but as an accompanying editorial (3) said this is a hypothesis generating study,causality cannot be inferred and the techniques used have multiple limitations. Human are pattern seeking story telling creatures and this story might catch on-at least until something better comes along.


Shifting gears-there are at least 3 articles that have reported that long time endurance exercisers have higher calcium scores than age matched  sedentary controls controls,an observation offered by some authors as  more proof that too much exercise is not good. Juxtaposed to that is the epidemiologic evidence that longtime endurance exercise decreases the risk of a coronary event and that elite athletes life longer than sedentary colleagues and yet more calcium in the athletes.Another plaque paradox?

Merghani and co-authors studied 152 maters athletes ( ages 51-63) They found that "most" )( 60%)  of the lifelong exercisers  has a normal CT coronary angiogram as did a similar number of the controls. However they also reported that the male athletes were more likely to have a CAC score of 300 or more compared to the sedentary controls.The plaques in  the athletes were predominately calcific.

Similar results were reported by V.L. Aengevaeren et al (2) who studied 284 lifelong exercisers. In regard to their findings they said:

"The most active group did however had a more benign composition of plaques with fewer mixed plaques and more often only calcified plaques.These observation may explain the increased longevity of endurance athletes  despite the presence of more coronary atherosclerotic plaques in the most active participants ".

Eijsvogels and co-workers published an excellent, detailed and extensively referenced  review( 4) of the possible harmful effects of acute and chronic exercise .  They only briefly mention what was then the preliminary evidence that longtime runners have higher calcium scores as their review preceded Puri's work as well as that of Aengevaren and Merghani

1.Puri, R Impact of statins on serial coronary calcifications during atheroma progression  and regression. J Am Coll Cardio 2015;65, 1273-1282


2 Aengevaren VL et al The Relationship between lifelong exercise volume can coronary atherosclerosis in Athletes. Circulation 2017 april 27

3. Shaw LJ The Never Ending story on Coronary Calcium.Is it predictive,punitive or protective? Editorial Comment J of Amer Coll Cardio, 2015 ,65 no 15 1283-1285

4. Eijsvogels,TMN et al Are there deleterious cardiac effects of acute and chronic endurance exercise? Physiol Rev 96 99-125,2015

The annualized decrease in exercise capacity may be even worse than we thought

The longitudinal decline in aerobic capacity is typically said to be 5 -10% per decade from age 40 to about age 70  then a more rapid decline occurs. Data from the Baltimore Longitudinal study of Aging (BLSA) (1) suggests that the decline is not constant across age ranges  but rather" accelerates markedly   with each successive age decade".

 How so?

In cross sectional studies " each succeeding age decade  represents a more highly selected group than it predecessor, thus healthy 70 to 90 year-olds may have been physiologically superior to current 20-40 years olds when they were on a similar age. In other words there is inherent selection bias in cross sectional data.

I will not attempt to explain the statistical model used but here are their values for the reduction  in men in peak O2 uptake expressed in ml/kilo/min for various decades:

age
30- 39 minus 7
40-49  minus 10
50-59  minus 15
60-69 minus 20
over 70 minus 26
                  
 A similar pattern was found in women.

They found that the oxygen pulse (oxygen consumed per heart beat) rate of decline mirrored the rate of decline in peak 02 .Since oxygen pulse is a function of stroke volume and peripheral muscle uptake of oxygen it is not possible to determine if it is cardiac output or muscle uptake that is largely responsible for the decline.

Caveat-The published results are from a mixed-effect prediction model and the median followup was only 7.9 years and prediction is the operative word. Though the study is "longitudinal",numbers in their tables do not represent for example following the same people over a lifetime and noting the per decade change in oxygen uptake. Still their data suggest that the often quoted 5-10 % decrease per decade may be too optimistic and rates of changes likely accelerate with aging.The confidence intervals for each age range are quite large and you have to wonder what are the mechanisms responsible for such wide variation in loss of exercise capacity within an age range. If subendocardial  fibrosis is the ( or a) culprit what are the factors that accelerate or retard that process.



1) Fleg, JL Accelerated Longitudinal Decline or Aerobic Capacity in Healthy Older Adults"
Circulation 2005, 112: 674 -682.

"Para Hisian Pacing" as well as selective Bundle of His pacing may bring about a hyper response

I have written before about a sub group of Cardiac resynchronization patients (CRT)   who have a hyper response with marked improvement in indices of cardiac   function, e.g. ejection fraction and end diastolic volume.

Such responses have been reported with Biventricular pacing  (Bi-V) and  His Bundle Pacing ( HBP). There are two forms or types of HBP: 1) pure HBP also known as selective and 2) Para Hisian pacing also known as non  selective HBP.

The QRS is normalized with selective HBP while in nonselective although the widened QRS duration is significant reduced it may not be restored to the pre  bundle branch block  configuration. There is both activation of the His Bundle fibers and adjacent ventricular septal muscle giving a fused or fusion ventricular activation pattern and an EKG with a delta wave resembling pre-excitation pattern.

According to Lida et al writing in the December 2016 Journal of Arrhythmia (1) "there seems to be no significant clinical difference between selective HBP and non selective HBP because both do not alter physiological impulse conduction and possibly maintain rapid and synchronous LV ( left ventricular) activation "

A similar case report was published by Ajijola et al  from UCLA in 2015 (2)

His Bundle pacing seems to gaining momentum both as an alternative to right ventricular pacing and as a method of cardiac resynchronization.

1)Lida, Y et al Successful resynchronization by permanent His-bundle pacing in patient with pacing -induced cardiomyopathy' J Arrhythmia , 2016 Dec. 32(6), 499-501

2)Ajijola,O et al Hyper-response to cardiac resynchronization with permanent His bundle pacing:Is parahisian pacing sufficient? Heart Rhythm Society, open access article http://dx'doi.org/19.10.hrcr.2015.05.006

Addendum:  5/26/2017  Several papers presented at the May 2017 meeting of the Heart Rhythm Society indicated that His Bundle pacing is ready for prime time.  See Dr. John Mandrola's  article on Medscape entitled " His Bundle pacing hits the mainstream at HRS 2017".

 9/6/2019 On a personal note-It is now almost four years since I was implanted with a Pacemaker with Bundle of His pacing before the practice became more mainstream. I had developed a left bundle branch block and an exercise induced second degree heart block. The LBBB had  markedly decreased my exercise tolerance . My LBBB was "fixed" and after getting over a few complications of the procedure my exercise tolerance was back to my pre LBBB level with an EKG pattern that appears to be Parahisian.

2/3/21 The term  "Parahisian" is no longer used to refer to non-select HBP.In the current terminology  "parahisian" is taken to mean close to the His System but not capturing the His Bundle. His capture can either be elective on non selective.

If peak load is the determing parameter runners should have more osteoarthritis

Perhaps it seems counter intuitive that runners do not have a higher incidence of knee osteoarthritis or so the preponderance of epidemiologic data contents.After all the peak load of the articular cartilages in running is much higher than in walking or so the kinesiologists tell us and would not the cumulative higher peak load after many miles of running wear out and maybe chew up the articular cartilages.

Or maybe the explanation does not lie in the peak load.

 Ross H Miller from the Department of Kinesiology at the University of Maryland offers an alternative view (1) and an alternative analysis of the relevant forces conspiring to "wear out" the knees.

He suggested that peak load is not the relevant variable but rather it is the "average load per distance traveled"  which is said to be surprisingly low and purportedly similar to walking.

Ross also discussed the notion of cartilage conditioning .Knee cartilage glycosaminoglycan content( which affects lubrication and shock absorption ) has been  shown in one study to be greater in recreational runners and even greater in high volume runners.

"... a man hears what he wants to hear and disregards the rest" Paul Simon.The Boxer



1) Miller, RH "Joint loading in runners does not initiate knee osteoarthritis" Exerc Sports Sci  Rev 45(2), 87-95,4 2017

CRT-non-responders, responders and the rare super responder

About one third of patients with heart failure (HF) do not benefit appreciably or respond to cardiac resynchronization treatment (CRT). Some other have a clinical benefit with physiological confirmation in the form of echocardiographic demonstration of reduction in heart size and increase in the ejection fraction. A relatively small subset show a marked improvement both symptomatically and in terms of impressive  improvement in terms of ejection fraction and reduction in left ventricular size.

Neither EKG nor echocardiographic  patterns accurately predict who will respond and to what degree. However, patients with a LBBB EKG pattern -particularly using the new criteria suggested by Strauss (1 )- are much more likely to have a favorable response.  In fact CRT basically "treats" the electric and associated mechanical dyssynchrony imposed by the left bundle branch block.Some of the variables influencing response include how much myocardial damage may have already occurred in the patient  ( e.g. heart attacks) and the location of the left ventricular lead in relationship to left ventricular scar(s).

The most dramatic example of super responders was reported  by Vaillent et al in 2013. (2). They described 6 patients with a diagnosis of LBBB without evidence of coronary or other heart disease and an EJ of greater than 50% at the time of diagnosis. Over a period of five to 21 years all developed  heart failure severe enough to warrant referral for CRT. Following CRT, ejection fraction improved greatly , five of the six within 3 months .Mean EJ increased from 31 to 56.In one patient , from 26 to 60.Other cardiac functional indices improved as well

The authors suggest that these cases "strongly support the concept of LBBB-induced cardiomyopathy".This idea was apparently suggested earlier by Blanc et al in 2005 (4)

LBBB induced heart failure represents a vary small percentage of patient who are treated with CRT. Ghani et al (3) report on the predictors of long term outcome of "super-responders to CRT which they define as Left ventricular EF (LVEF) greater than 50% ( mean of 54.9%, +/-6) on follow-up echocardiogram.The group whose EF was between 30 and 50% were labelled as "responders"

They describe 56 patients from a group of 347 patients with primary CRT D indication. The predictors were female sex,nonischemic  etiology,higher EF at baseline and wider QRS duration.

Vaillant's patients , when compared to Ghani's patient, perhaps could be considered "super super" responders.


1. Strauss DG et al, Defining Left Bundle Branch block in the Era of Cardiac Resynchronization Therapy. American J Cardiology 2011,Vol 107 pg 927-934

2. Vaillant C et al. Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J. Amer College of Cardiology 2013,vol 61, p 1089

3. Ghani, S  et al  Predictors and long term outcome of super-responders to cardiac resynchronization therapy. Clin Cardiology 2017

4.Blanc J et al. Evaluation of left bundle branch lock 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

Do low levels of cardiovascular fitness predispose to cardiac hypertrophy?

 There is evidence  that suggests low levels of cardiac fitness predispose to maladaptive cardiac remodeling  typically manifest as concentric remodeling and concentric hypertrophy and increased ventricular stiffness and diastolic dysfunction.

Lovic and Kokkinos and co workers correctly point out that the cardiac hypertrophy consequent to  high blood pressure differs from the typical physiological cardiac hypertrophy of the endurance athlete realizing that  extreme examples of the latter can be difficult to distinguish from the former.

Lovic et al  makes the following  argument in a 2016 issue of the Journal of Hypertension.

Low fitness level individuals will reach a systolic blood  pressure of 150 at low levels of exercise, e.g. 4-5 METS , which are  levels commonly encountered in some activities  of everyday living.
150 systolic  blood pressure is necessary to trigger cardiac remodeling. Individuals, who are more fit, are able to do that level of work without that degree of BP rise. So individuals with low fitness may spend considerable  time each day with a BP of sufficient magnitude to trigger hypertrophic changes in  the left ventricle, even though their BP as measured in their doctor's office may be normal.

Their data (1) found an inverse relationship between exercise capacity, blood pressure response to exercise and  left ventricular mass.Further, they have published data that showed 16 weeks of aerobic training resulted in subjects having  a significantly lower blood pressure  level when they  exercised at the every day activity level of 3-5 METS. A reduction in previously elevated left ventricular mass was also shown.

Other data consistent  with this notion comes from a study by Brinker et al ( 2) from Southwestern Medical School in Dallas. They studied subjects aged 42 -67 years of age with stress testing and echocardiography. Those individuals in the lowest fitness category ( they divided the group into 3 fitness levels ) had 40 % concentric hypertrophy as well as a 9% prevalence of diastolic dysfunction ( as defined  by the e/a ratio on mitral valve echo flow studies)

Data from the Dallas group and others have outlined the concept of there being two distinct cardiac phenotypes related to the development of both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).They are:

1)Subclinical systolic dysfunction (EF may be normal but abnormalities detectable by measurement of global strain with speckle echocardiography)),with eccentric cardiac hypertrophy with increased LV diameter)-the proposed precursor to HFrEF

2)Subclinical diastolic dysfunction with concentric LV hypertrophy; with increased relative wall thickness (RWT) -the proposed precursor to diastolic heart failure (HFpEF)

Increasing data strongly suggest that low fitness levels predispose to the precursors of HFpEF.
Lovic's work suggesting that exercise induced elevated blood pressure in the unfit during the usual daily activities  may be one possible mechanism involved.



1)Lovic, D et al Left ventricular hypertrophy in athletes and hypertensive patients.J Clin Hypertension 2017,

2) Brinker SK et al. An association of Cardiorespiratory Fitness with left ventricular remodeling and diastolic dysfunction. JACC Heart Failure., Vol 2, no 3, 2014, p 238


5/1/17 An embarrassingly large number of typos and misspellings were corrected and again on 5/16/17.

Cardiac remodeling -some old and new theory and some data

Following the 1975 echocardiographic study by Morganroth (1) of endurance athletes and resistance exercise athletes and several cross sectional studies that seemed to validate his work the  "Morganroth  Hypothesis" became  the standard exercise physiology party line.

The story goes like this:

Endurance exercise brings about a volume overload or a preload stimulus to the ventricle that lead to eccentric hypertrophy which is an increase in ventricular cavity size and only slight increase in wall thickness. Resistance exercise brings about a pressure overload or an afterload stimulus which leads to concentric hypertrophy in which there is little change in cavity size but thickening of the ventricular wall.,The 2 types can be defined  by the relative wall thickness (RWT) which is 2 x the posterior wall thickness divided by left ventricular diastolic diameter with  a value greater than 0.42 indicating  concentric hypertrophy.

Skeptics have argued that echo studies have inherent  methodological error  ranges too great   to separate groups whose absolute values are not that far apart and MR is a much more precise method and that cross-sectional studies have limited ability  to sort out group differences that  are due to training  from other causes of individual differences. So, what did a longitudinal study with MR imaging show.

A 2011 MRI longitudinal study, Spence et al (2) provided interesting data from which one might conclude that endurance exercise does bring about eccentric hypertrophy but resistance exercise does not increase wall thickness-at least not in the small group of resistance exercisers who worked out three times a week for six months reported in this publication .Of course, it is possible that the resistance group had not been studied long enough.


It is certainly possible that the six months training program in Spence's study was  not enough to bring about concentric hypertrophy. A more recent  meta analysis supplies data and analysis that indicate that there is a typical pattern for endurance exercisers and a pattern for resistance exercise more or less consistent with Morganroth's hypothesis  and a in- between pattern for those who engage in activity in which there is both significant amount of volume and pressure overload such as rowing and cycling.

 Plium et al (3)analyzed echocardiographic data  on 1451 athletes gathered up from some 59 studies.All subjects were  under the age of forty, older athletes excluded so as to not muddy up the data with the effects of aging on heart function and structure.

 Basically the data conformed with Morganroth's hypothesis. Quoting the author's conclusions;

"Divergent cardiac adaptations do occur in the athletes performing dynamic and static sports..However,the classification as an endurance trained heart or a strength-trained heart is not an absolute and dichotomous concept but rather a relative concept."

So a stereotypical runner will have a different  pattern from a wrestler or body builder  but ventricular volume changes and wall thickening occur in both  to varying degrees with the runner tending to a eccentric hypertrophy-remodeling pattern and the wrestler to a concentric pattern while athletes such as cyclists and rowers demonstrate the most marked changes both  in ventricular volume and wall thickness. 

More surprisingly and maybe more importantly  is the observation that a sedentary life style may evoke a remodeling pattern  characterized  by concentric changes, i.e.  no increase in ventricular volumes and a tendency to develop diastolic dysfunction.

This is what was reported by Brinker et al (4) from Southwestern Medical School in Dallas in their study of  cardiac function and structure in 2900 subjects from the Cooper Center Longitudinal Study.The subjects age ranged from 42 to 67 years of age and all were either self referred or physician referred to the clinic  and had a normal stress test.Based on the exercise levels achieved on the stress test four fitness levels were designated.  They found that the lowest fit subjects ( presumably  those with a sedentary lifestyle) had a higher prevalence of concentric remodeling as well as diastolic dysfunction than the fitter subjects. There was a 40% prevalence of concentric hypertrophy and 9 % prevalence of diastolic dysfunction ( defined as an E/A ratio greater than 1) in the lowest fit group versus less than 20 % concentric change and 2% diastolic dysfunction in the most fit group. So it is not an all on none thing and fitness does not seem to immunize against concentric  hypertrophy and diastolic dysfunction but made both less likely.

 Both resistance and endurance training cause cardiac remodeling but there may also   be a "inactivity remodeling", as might occur in a sedentary lifestyle The ventricles remodel  whether  you exercise or have a sedentary lifestyle and Brinker's group suggest that the inactivity remodeling may be a precursor to diastolic heart failure (aka HFpEF) and further suggest that long term exercise might be preventive.

That is a thesis I would like to believe. I would be more convinced if it were not for the fact that while  66% of the low fit group were hypertensive so were  only 38% of the fittest group were hypertensive. You wonder if that might not play a role in the concentric hypertrophy. I discussed other work by the Dallas group (see here) which, IMO, provides better evidence for the idea that long term aerobic exercise can reduce the risk of diastolic heart failure.


1. Morganroth, J et  al. Comparative left ventricular dimensions in trained athletes.Annl Int Med. 1975,82(4), 521-524

2. Spence,A et al .A prospective randomized longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise J of Physiology 14 nov 2011

3.Pluim,B The Athlete's Heart. A Meta-analysis of cardiac structure and function. Circulation 1999:100: 336

4.Brinker, SK et al. Association of Cardiorespiratory Fitness with Left Ventricular Remodeling and diastolic dysfunction. JACC Heart Failure.Vol 2, no.3, 2014, p238

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

Parameters on Utopias-something politicians don't want

Peter Boetke in his new book, "Living Economics" throws out the following:

"Economics put parameters on Utopias".

The more famous quote of Friederich Hayek strikes a related chord:

"The curious task of economics is to demonstrate to men how little they really know about what
they imagine they can design."

So politicians need to be careful to have supportive economists on board for their various utopian plans. They will need some that will be very parsimonious with the parameter placements.Fortunately for the politicians they can  always find a least one PhD economist to argue for  whatever position.

Some parameters might have disabused apologists of belief in  the promised utopia of ACA (aka Obamacare) .The hucksters promoting the plan prior to its passage spoke of saving the country from bankruptcy and increasing access to care and improving quality. So how has that worked out for you?

Professor Gruber has been late in providing some parameters .

The major barrier to third party payers control of medical costs is being dismantled

A major barrier ( I argue the major barrier) to control health care costs by the third party payers has been and still is to a lesser degree medical ethics ; more specifically, the duty of the physician to act as a fiduciary for the patient. At one time not long ago when the physician and patient believed or had determined that test x or treatment y was in the best interests of the patient the physician would be the  advocate for the patient  not an agent or employee of the insurance company whose interest was to deny the tests or treatment.He was not tasked with working in some type of mythical society-physician alliance to conserve collective medical resources acting as the steward of those resources.

Not infrequently the physician's desire to be the advocate of the patient and the insurance company desire to limit costs were in opposition.The patient versus the company with the physician on the side of the patient was the common narrative.

What if the medical ethics were different? What if the physician felt an ethical obligation to conserve the " resources of the collective"? What if the impetus for that ethical transformer seemed to take place from within the medical profession?

Whereas once if the physician did not advocate for his patient he might be ashamed but now according to the new ethic a physician might feel guilty by failing to act  as would "stewards of finite resources".  Victor Fuchs in a commentary in the NEJM carried this  insult to logic to its limit in the following way.

In his closing paragraph, Fuchs tells us that when a physician works in a health care collective in which there is a fixed annual budget the physician resolves the dilemma ( between favoring the individual and the collective) by favoring the cost effective option. This according to Fuchs become "appropriate". So,the cost effective choice is the appropriate choice and also the ethical one. It is ethical in the moral calculus of Kant he claims "because if all physicians act the same way,all patients benefit" .It is hard to find statements any sillier in a major medical journal.

 A  major  barrier demolition  occurred in 2002 with the publication of "The Charter" ( Medical Professional in the New Millennium- A Physician Charter) authored by the ABIM  Foundation , the ACP foundation and a European Foundation of Internists.

A number of forays against the barrier had been made earlier including a multi part series in JAMA in which the author proposed a way to increase quality of care while decreasing cost by a egalitarian-utilitarian, cost effectiveness calculus in which the group benefited while a given individual patient might not.  Notable also was the publication  of "New Rules" by Troyen Brennan and Don Berwick in which they advocated elimination of the traditional doctor patient relationship and moving away from "decentralized individualized decision making".  

In The Charter, three major ethical principles were put forth; patient welfare,patient autonomy and social justice. Previously medical ethics was concerned with the relationship of the physician and the patient.Now the authors of the Charter presumed to define the relationship of the physician and society. Further, the relationship they claimed was one in which the physician was the steward of society's resources. This colossal, gratuitous assertion represented a sea change the implications of which might not have been immediately apparent. To many it was not apparent that implementation of the third principle was in conflict with the first while a number raised objections  the majority took little notice.The dogs barks and the caravan moves on.

 But all of the above really just relates to the intellectual smokescreen. The real elements that have fee for serve on life support and thereby strike a major victory for third party's payers cost saving and profit  enhancing initiatives are ACA,HITECH and now MACRA.

Is the athlete's slow heart rate really due to increased vagal tone as conventional wisdom suggests

An article from three British researchers makes a good case that vagal tone is not the reason for the athlete's bradycardia in a 2015 commentary in the Journal of Physiology.see footnotes

Traditionally, the slow heart rate of endurance athletes is attributed to increased vagal tone but the authors argue that this increased tone has never been demonstrated at least in part because it is not clear how that could even be measured as the vagus carries both afferent and efferent fibbers. Further experimental blockage of the autonomic nervous system has not lead to mitigation of the bradycardia.

They suggests that the slow heart rate is also not due to SA node fibrosis ( apparently a common explanation for SA node disease) as that also has never been demonstrated. They present evidence that the culprit is remodeling of the ion channels and related molecules in the sinus node-more specifically downregulation of the HCN4 channel  (also  strangely known as the "funny channel") . They reference a number of articles claiming there is remolding of  ion channels in aging and familial bradycardia and pulmonary hypertension.

Endurance exercise is known to cause heart remodeling leading to the features of the so called athletes heart ( so called eccentric hypertrophy). It is also know that cessation of exercise will lead to some degree of "re-remodeling" returning the athletes heart  to some degree of that of the sedentary person. Will a similar reversal happen in he electrical system in endurance athletes who quite exercise? or is this remodeling permanent? Baldesberger  et al published a long term followup  in retired professional cyclists who had stopped training for over thirty years and did report an unimpressive lower heart rate on Holter monitoring in 62 cyclists versus 62 golfers ( 66 +- 9 versus 70 +- 8 but 20% did have a HR less than 40 during the day. versus 6 % in the controls.So is the sinus nodes remodeling to some degree not reversible-these cyclists had not trained for 30 years. (There is more interesting data from this study which is a topic for another blog commentary,here the interest was in the bradycardia not other possible cardiac complications . and it did appear the cyclists had a bit more bradycardia.) 





footnotes

1) D'Souza, A et al . Cross talk opposing view:Bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. Journal of Physiology 593 no. 8 1749-1751,April 2015

2) Francesco, D. The Role of the Funny Current in Pacemaker Activity. Circ. Research 2010;106, 434-446

3) Baldesberger, S et al Sinus Node  disease and arrhythmias in the long term follow-up of former professional cyclists. Eur hear journal 2008 29, 71-78

The minimum exercise levels of the 2008 guidelines won't prevent heart failure.

IMPORTANT CORRECTION:Since this commentary was posted I  realized I misinterpreted the two articles I quoted leading to the title conclusion which is incorrect.That has been corrected on 9/6/18 by the posting entitled " Is the minimal level of recommended exercise sufficient to decrease the risk of heart failure?"


The 2008 U.S. and WHO  exercise guidelines recommend a minimum of 2.5 hours of moderate intensity exercise per week or 1.25 hours of vigorous exercise per  week. This can be expressed as 500 METS Min per week or 8.3 MET hours per week.

This minimum value is widely quoted but often unnoticed is that  the panel also suggested that further gains could be made by increasing those exercise levels to twice those values, i.e 5 hours of moderate or 2.5 hours of vigorous exercise.

 Moderate intensity was defined as between 3 and 5.9 METS and vigorous as over 6 METS.For example running at a 15 min per mile pace is about 7 METS which would be the lower end of what the panel meant by vigorous.(This does not address the problem of relating exercise levels to a person's exercise capacity. For example, to  a person with a 02 max of 60 a fifteen minute mile is  mild exercise while the same pace for someone with a 02 max of  25 the term vigorous is  appropriate. Since age strongly correlates with 02 max should  the guidelines somehow take age into consideration in the recommendations.How to do that is not clear.

Cardiovascular disease (CVD) risk reduction has been shown in a number of epidemiological studies for people exercising at those  minimum levels and arguably at even lower level. Lee et al (1) showed that running at little as 5 to 10 minutes per day would significantly  reduce CVD mortality.This would make a little running seem very effective  while others (Pandy et al see below) did not show that degree of risk reduction with that low  level of exercise but the minimal recommended  level will likely reduce CVD risk according to several epidemiologic studies.

Eijsvogels (2) reported that the maximal risk reduction was found at a volume of 41 MET-hrs/week, which is 3-4 times the minimal recommended level.However, only 3.5% of the subjects exercised at that level or above and therefor the confidence interval for  hazard ratio (HR) estimation was wide and not statistically significant. The authors emphasized that they found no evidence of harm or adverse cardiovascular outcomes at this level but the relatively small number  of people in that category raises the possibility of a type11 error.

While rather low levels of exercise seem to decease CVD risk, heart failure  risk  reduction may require higher levels of exercise. Pandy et al (3) and coworkers from Southwestern Medical School reported that heart failure (HF) risk reduction occurred only at levels  significantly higher than the minimum guideline recommended values. "We observed a linear dose response for HF risk with a marked reduction in risk at very high doses of PA (physical activity  ) ( 35% risk reduction in HF risk at 2000 MET-min per week)".. This would be 4 times the minimal recommended value or 10 hours of moderate or 5 hours of vigorous exercise per week.

Schnohr et al (4) reported that their analysis of a data set from the Copenhagen City Heart Study demonstrated a U shaped association between all cause mortality and dose of jogging. A number of other articles cited by Schnohr  in that publication actually report a inverse relationship  showing no U or J shape. Accepting the thesis of  the existence of a U shape curve, he goes to comment on results from several large studies and speculates where the curve might ascend.The studies found that running  about 35 miles per week was the upper limit of incremental health benefits and "these studies found that a weekly cumulative dose of approximately 30 miles of running per week or 46 miles of walking is approximately the "safe" ( my quotes) upper limit for optimizing long term CV health and life expectancy", So if the curve turns upward  it does not seem to do so at running volumes in the 30 miles per week range. This volume of running would seem  satisfy the running volume "requirement" sufficient to decrease HF risk. suggested by Pandy's work..

So the epidemiological data would tend to confirm that the 2008 minimum guidelines would decrease CVD and all cause mortality but not the risk of heart failure which seems to  require at least twice that level of exercise.

Several publications from a group in Dallas (5) provide useful insights regarding the mechanism by which a higher level of exercise might  lessen heart failure risk, that is diastolic heart failure ( i.e  heart failure with preserved resting ejection fraction frequently abbreviated as HFpEF).

 Dr Paul Bhella and his  associates  did extensive physiological studies on four groups of healthy volunteers over the age of 64. Four groups were designated   on the basis of their exercise history for the preceding 25 years. (not a typo) 1) sedentary-no more than one exercise session per week  2) casual exerciser-2-3 session per week 3) "committed" exercisers-4-5 session per week and 4)competitive master level athletes -6-7 session per week and competed regularly.  All had normal systolic function ( as defined by a normal resting ejection fraction) but groups one and two has decreased left ventricular compliance while the committed and competitive groups had left ventricular pressure volume curves and left ventricular masses similar to young healthy controls. ( see here for my  further comments and a few caveats regarding this paper including reference to Tanaka's work that challenges the notion that long term endurance exercise  does in fact preserve  ventricular compliance)

Quoting Bhella ". . at least 30 minutes of dynamic exercise per session for 4-5 days per week over a lifetime can  sufficiently prevent most of the decreases in LV compliance and distensibility observed with sedentary aging" So the idea is that sedentary aging leads to stiff left ventricle and life long running may mitigate that process.

 In other words 2.5 hours of vigorous exercise per week which was the higher level of exercise ( i.e. twice the minimum  recommenced by the 2008 panel) might beneficially reduce the age related increase in ventricular stiffness. It does not take that much exercise per week but you have to put in a lot of weeks- and it was vigorous. Remember  Bhella's groups activity levels were for the 25 years before the testing. The authors speak of Lifelong exercise. 


 This exercise level is far below the typical exercise histories that one typically  finds in the cases of athletes with atrial fibrillation or the athletes in whom an abnormal gadolinium uptake was reported and whose cases are  sometimes emphasized by various writers warning the public about the dangers of "excessive exercise". I suggest that  2 to 3 times the  2008 Panel's minimal recommendation should not be considered excessive.

1)Lee, D  Leisure-time Running Reduces All-cause and cardiovascular mortality risk. JACC 64. 472-481.2014

2) Eijsvogels, T, Exercise at the extremes-The amount of exercise to reduce cardiovascular event
JACC, 67, 316-329, 2016

3)Pandey,A Dose-Response Relationship between Physical Activit and Risk of Heart Failure.A meta-Analysis, Circulation 2015, 132 1786-1794

 4) Schnohr,P Dose of Jogging and Long term Mortality. JACC, 65, 311-410,2015

 5)Bhella, P Impact of Lifelong Exercise "dose" on left ventricular compliance and Distensibility.
JACC 64, 1257-1267 2014

John VonNeumann " There's no sense in being precise when you don't even know what your're talking about"

addendum: 5/22/17 Several editorial flourishes made  and spelling errors corrected and more were made on 9/3/18. 9/6/18 Notification posted on this commentary referencing the correction made on 9/6/18.
 

High school and college football deaths average about 3 per year

A recent report by KL Kucera et al give details on high school and college fatalities related to head and/or spinal injuries .

From 2004 through 2015 there were 28 deaths reported related to head or spinal injuries,24 in high school players and 4 in college. 1.1 million play high school football while there are 75,000 collegiate football players.

Four of the 22 high school players had suffered a concussion in the four weeks  preceding the fatal injury and in three cases the second impact syndrome was implicated .Running backs and linebackers were the two most common positions.The head down-head first position was frequently implicated.

 I wonder what  parents and grand parents of high school footballers think about the ambulances frequently parked off to the side of the playing field.

two studies reassuring endurance athletes re long term heart damage

Two, articles, one from Germany and one from Italy might provide some reassurance to long time endurance athletes worried about too much of a good thing damaging the heart.

Bohn et al from Germany reported  a group  of long term endurance athletes with many years of endurance exercise history whose extensive cardiac evaluation showed nothing to suggest that ARVC is a problem.

Pelliccia and co workers studied 1777 active competitive athletes and described echo findings and concluded their tendency to have somewhat larger left atria represented physiological adaptation which is largely without adverse clinical consequences and found a fib to be uncommon, less than 1% and similar   to that of the general  population. He also concluded that left and right ventricular exercise induced remodeling were basically balanced.This conflicts with some of the work of La Gerche  and Heidbuchel who postulate that the right ventricle is less well designed that is the left ventricle  for endurance exercise and and predisposes it to arrhythmias arising from right ventricular  remodeling . But finding a bunch of white swans does not preclude the existence of black ones.

The often quoted , case control studies  reporting hazard ratios of 4 and five in regard to atrial fibrillation in long time endurance athletes ( and the meta analysis that summed them up with some statistical trappings) just might be vulnerable to selection  bias while these two studies cited above just might be vulnerable to survivor bias.

Can "too much" exercise increase risk of atrial fibrillation in men but not women?

Can "excessive " exercise increase the risk of atrial fibrillation in men but somehow spare women hyper-endurance exercisers from that risk? That seems to be what the data show in a 2016 Meta analysis by Mohanty et al published in the June issue of the Journal of Cardiovascular Electrophysiology . See here.

The really fun thing about meta analyses is the frequency with which one can cite conflicting results from various studies. In  another meta analysis Kwok et al found no association with increasing exercise and risk of AF in either sex.  In spite of these conflicting data sets a quasi consensus seems to be that at some level "too much"  exercise predisposes to atrial fibrillation.- determining the level of too much is another matter.  As in  many biological and medical issues it is easier to get a pretty good idea of the direction of the vector than is  ascertaining the magnitude but  sometimes the direction is in dispute as well. 

Risk of stroke in patients with atrial fibrillation -with and without anticoagulation

Previously, I had commented on the risk of stroke in atrial fibrillation patients not treated with oral anticoagulants (OAC).In that commentary I quoted Dr. Overvad -"...current guidelines discrepancies also reflect the fact that the level of stroke risk among men with a score on 1 and women with a score of 2 is on the borderline of where the  impact of anticoagulation  treatment shifts from beneficial to harmful."  His comment seems reinforced by a recent publication in Circulation.

After that commentary I became aware of a very important -and perhaps dogma changing- article published in Circulation by GR Quinn. I added an addendum to that post but  the article is important enough to be highlighted in another commentary. I re-post that addendum here:

"Unfortunately I became aware of the 2016 Circulation article by GR Quinn et al after the above commentary was published.  That very important article  provides good reason to question the dogma that the CHA2DS2-VASc scores translate to fixed stoke rate. It is generally accepted that if a person's stroke rate is estimated to be 1-2% per year then treatment with an OAC offers a  net clinical benefit and that the risk score clearly relates to a quantitative stroke risk, e.g. a CHA2DS2-VASC score of 1 means the person has a risk of about 1 % per year and a score of 2 indicates a risk of 2%. 

However, analysis of 34 studies of patients not treated with anticoagulants demonstrated that the stroke rate varies widely in various cohorts. For example, with a risk score  of 2, 27% of the cohorts reported a stroke risk of less than 1% and 33% reported stroke risk greater than 2% per year. So the correlation between risk score and stroke risk varies with the cohort studied.The numbers from the Northern European studies formed the basis of the alleged relationship between the CHA2DS2-VASc score and annual stroke risk and the North American Cohort analyses indicate significantly lower ( about 1/3 of the European rate) stroke rates for untreated AF.

 Quoting from the authors conclusions: ' The majority of cohorts did not observe stroke rates that would indicate a clear expected net clinical benefit for anticoagulating AF patients with a CHA2DS2-VASc score of 1 or 2.' "


Prediction is difficult, especially the future. Neils Bohr 

The most that can be expected from any model is that it can supply a useful approximation
to reality .   George Box

The old and the new paroxysmal atrial fibrillation- new questions raised by new technology

Paroxysmal atrial fibrillation (PAF) has typically been diagnosed in a patient with cardiac symptoms seeking care for   episodic symptoms  which ultimately- by either  office EKG or some monitoring device shown to have atrial fibrillation ( AF).

The medical literature is conflicted in regard to the risk of PAF versus permanent or persistent AF. It is not surprising that expert opinion in that regard is conflicted as well, While opinions may differ current US guidelines recommend oral anticoagulation( OAC) for PAF patients based on their risk assessment score. Usually the CHA2DS2-VASc score is used and a value of 2  or more would lead to recommendation of OAC.In other words. the same recommendation for persistent or permanent AF applies to PAF.Note this refers to what I will call "clinical PAF"  subclinical PAF (SCAF) has become an  clinical management  issue as huge amounts of data has become available from the rate and rhythm recordings of pace maker patients.

A 2014 report by Vanassche which analyzed data from 6563 AF patients not treated with oral anticoagulants (OAC) determined that stroke risk in permanent AF was roughly twice that of PAF.
They reported that  AF pattern ( PAF versus non PAF )  was the second strongest predictor of stroke second only to previous history of stroke. If their data are  conclusive in this regard that does not necessarily mean that OAC  not be used . Even though the risk of stroke is lower, still the stroke risk may overwhelm the risk of  serious bleeding  from OAC leading  to a positive clinical benefit or trade-off and a reasonable recommendation for OAC.

A new and expanding data base has emerged from the experience of pacemaker (PM) patients. The ability of PMs to store and analyze large amounts of rate and rhythm data has lead to the realization that typically asymptomatic bursts or runs of subclinical atrial fibrillation  are very common in PM patients, values from several studies reporting  an incidence of 30-55%.

The questions arises-is the risk of  these SCAFs equivalent to that of the classically diagnosed PAF. Further, is there value to quantitative the SCAF perhaps in terms of duration or frequency . The literature has adopted the concept of atrial fibrillation burden ( AFB) and several studies have attempted to determine if there is a correlation between PAF ( as in minutes per day) and stroke risk). More importantly  is it possible to find an AFB threshold associated with a clinically important risk of stroke or how much SCAF is necessary to warrant OAC.

In general ,reports  of these attempts  indicate  there is a correlation between PM detected  AFB and stroke risk , however the reports differ in regards to  finding  burden levels that demonstrate an increase hazard ratio- usually in the range of 2 or under (and  sometimes statistically significant and sometimes not). The small number of events of interest-stroke and peripheral emboli- in various duration based subgroups lead to wide confidence intervals and HR values that fluctuate as burden levels increase-sometime being statistically significant at lower levels but  surprisingly not at higher which was the case, for example in the SOS-AF project.

Some of the of  AF burden levels at which a increased hazard ratio (HR) for stroke or other embolic events) have been reported from various studies are shown here: ( note with one exception runs of SCAF less than five or six minutes-depending of the particular study-are not analyzed.) So to date with one recent  exception there is essentially no data on the risk of SCAF events of less than 5 minutes

ASSERT six minutes
TRENDS -5.5 hours
SOS AF - one hour
CARELINK/VA 5.5 hours

These studies were reviewed by Chen-Scarabelli et al in 2015 and also by Camm et al in 2016 and they reached opposing conclusions. Camm's review concluded that data were insufficient to recommend OAC in SCAF while Chen-Scarabelli  and Kenneth  Ellenbogen said that OAC should be initiated on the basis of stroke  risk assessment using the CHA2DS2-VASc score regardless of the mechanism of detection of the atrial fibrillation.

 In the observational TRENDS project, data from 3035 PM patients were analyzed. Those characterized as a "low" AF burden (AFB) ( low is  defined as less than or equal to 5.5 hours on an single day) gave a risk estimate similar to having zero  AF.  An AF burden of greater than 5.5 hours doubled the thromboembolism risk.

Also a sub-study of the TRENDS project showed that 29 of the 40 patients who had a embolic event had no AF detected in the 30 day period  preceding the event suggesting that the relationship between AF and stroke may not be a simple as the former invariably causing the latter.  


As Glotzer and his co-authors in the TRENDS project emphasized, the available data-even combining data from several studies as  was done in the SOS AF project- do not necessarily make it possible define a "safe "AFB that confers no risk greater than observed with no AFB. The event rates ( i.e stroke and other embolism events) are low in all of these studies, lower than predicted based on a widely accepted 4% per year rate in atrial fibrillation patients) and this  limits statistical precision and produces wide confidence limits as well as limits the number of threshold ranges that can be analyzed with the expectation of statistical significance.

 Small numbers in each  duration subgroup lead to results that sometimes seem counter intuitive- for example : In the SOS AF a statistically increased HR was found for the five minutes cutoff and the one hour cutoff but not the six hours or 12 hour or 23 hour. A long duration would have been thought to impair a higher HR.

The RATE RHYTHM study was designed to determine if there is a definable burden of AFIB that will be predictive of thromboembolic events. At this writing I have only access to an abstract of the findings. I believe that the investigators found there were no risk for bursts of atrial fibrillation less than 20 seconds. . 


The data indicate  that the risk of PM detected SCAF is lower than the clinically detected classical PAF but there is a  correlation between SCAF and stroke risk and SCAF is an independent risk factor for or  predictor of stroke. ( An independent risk factor is not necessarily causal- see here) .  Of course  the question is with the variable  coarse- grain risk values derived from any of  these studies is anticoagulation for these SCAF warranted and in that regard there is not unanimity of expert opinion.

Guidelines ,with the exception of the Canadian Cardiovascular Society guidelines, do not recommend  specifically to give OAC for device-detected AF. The Canadians suggested that OAC could be given to patients 64 and older with a CHADS score one or more who have SCAF episodes lasting a day or more  or for those with a shorter interval if they have recently had a cryptogenic stroke. ( ref 1)

A number of researchers have argued that randomized trials are needed to determine the clinical  benefit for OAC in PM detected   PAF. Two such trials are now in progress The ARTESIA project aims to enroll 4000 patients and randomize patients with at least one episode equal to or greater than 6 minutes of AF  to either apixaban or aspirin. 2019 is the projected end date.  Note even after this trial is complete there will still not be any RCT level evidence about what to do with patients  with AF burdens of less than 6 minutes per day.  The NOAH project will compare edoxaban or aspirin/placebo in patients over 65 years of age with one additional CHA2DS2VASc risk factor.

RCTs do seem to be needed, I believe we have learned all we can from the type the observational trials mentioned above and expert opinion differs regarding the management of SCAAF detected by PM recordings. An optimistic view is that these 2 RCTS may allow recommendations regarding OAC and device detected to move past battling expert opinion and trying to tease clinical truth from conflicting observational data.


1.Verma A et al 2014 Focused update of the Canadian Cardiovascular  Society Guidelines for the Management of Atrial fibrillation. Can J Cardiol. 2014 30 114-1130

update 12/16/16 A paragraph inadvertently omitted was added. 
addendum 1/18/17 and 2/4/17  several minor changes made in syntax and typos corrected.