Cognitive dissonance and medical practice conformity and different visions

Anyone who has practiced medicine for more than a week, or observed its practice as a medical student may recognize the truth of the following paragraph.

Medical science alone is inadequate to solve the contingencies of the day. Improvising is required.
The rules are riddled with exceptions and the world of caring for patients is a world of exceptions and the rules we devise are to generally point in the right directions at least some of the time.

Norton Hadler wrote of this issue:

"..for the most difficult critical and trying decisions involved in clinical care, the body of scientific information is inadequate,or incomplete or idealized....clinical truth is a contract between a physician and a patient based on trust."

The ambiguity and the inadequacy of medical science to solve every problem is so self evident that it is puzzling the degree to which guidelines and rules are not only promulgated but increasingly used to judge physician's practices and the quality of care given.

Dr. Atul Gawande in his 2004 commencement address at Yale Medical School said:

"...Information is inadequate.The science is ambiguous.One's knowledge and abilities are never perfect.The risks of the unforeseen consequences and terrible mistakes always loom."

Everyone seems to be quoiting Hippocrates one way or another.  Life is short,the art long, experience fallacious and judgment difficult.

On an individual level and as applied to the patient it is widely recognized that rules designed to standardize a world that is dominated by exceptions will have limited application at best and at worse frequently send us down the wrong road and generate perverse incentives to treat the chart at the expense of patient care and yet there are increasing efforts and acceptance of the use of rules and guidelines to judge the quality of a physician's practice and perhaps impose monetary consequences based on adherence to guidelines.

One of my medical friends suggested we might have an example of cognitive dissonance.

Maybe so for some physicians, but more to the point is that there are two different visions-the population treatment vision and the individual patient treatment vision.The individual treatment vision is played out by most practicing physicians while those who are proponents of the other vision are unfortunately often those in policy influencing roles, such as in medical schools and IOM and ACP and various of the "non-profits" more than a few of which are  funded largely by the Robert Wood Johnson Foundation.

Has medical care been reduced to Leave a message or call 911?

When I contact some medical practices by phone that is exactly what seems to be the situation.
Case in point- When recently  I developed a rapid heart rate that seemed to be atrial flutter I called the  medical practice where my EP cardiologist practices and the telephone prompts   gave me the choice of "in an emergency call 911" or when directed to the cardiologist's nurse," leave a message " which I did and then waited and then waited.

Finally we decided to drive to his office and insist to be seen. It was about 2 hours after the initial call , as I was sitting in his waiting room,his nurse returned my call which we had forwarded to my cellphone . Even then I had to insist  to be seen which I finally was, by which time I was back in sinus rhythm.

Medical care as is provided by physicians' offices seemed to have been simplified  and reduced to go to the emergency room  or leave a message. I wonder if this might be one of the factors leading to the increase in the number of urgent care centers as it offers a third way.

The heart will remodel itself whether you exercise a lot or not at all

Remodeling of the heart will occur whether you do anything about it or not. What you do about it may  determine what type of remodeling you get.

The prototypical  remodeling that occurs with a sedentary lifestyle seem very different from that of a long term exerciser.

Studies from the cardiology group at Southwestern Medical School and the Cooper Center Longitudinal Study  have described important aspects of  the structure and function of the heart in the sedentary and the persistent aerobic exerciser. Higher levels of exercise directly affect heart function and structure in a way different from sedentary aging.

In a study of over 3000 healthy participants at the Cooper Clinic in Dallas, Brinker et al characterized the remodeling patterns of individuals as correlated with their  "fitness" levels as determined by their levels of exercise achieved on a treadmill tests.

In a nutshell, the low fit individuals had smaller hearts,concentric remodeling/hypertrophy and poorer diastolic function while the fitter participants demonstrated a pattern of eccentric remodeling , larger hearts and normal diastolic function.

Definitions are in order.

Heart size  for this purpose, refers to left ventricular volume at the end of diastole( left ventricular end diastolic diameter) typically  determined by echocardiography. Concentric remodeling refers to increased wall thickness and normal ventricular mass while concentric hypertrophy means increased LV mass and increased wall thickness.Eccentric remodeling refers to increased LV diastolic volume  (hence LV mass)with no significant increase in wall thickness.

The relationship beween LV chamber size and wall thickness is expressed by the relative wall thickness (RWT) and defined as 2 X posterior LV wall thickness/ LV diameter at end of diastole.

Concentric remolding has a RWT of greater the 0.42 while eccentric remodeling  is less than 0.42. The range of normal is 0.32 -0.42

The distinction between concentric and eccentric remodeling of the heart dates back to the 1975 "Morganroth hypothesis" which described different  stereotypic  cardiac adaptations to endurance exercise and strength building or resistance exercise. The idea was that endurance training presents a volume overload while resistance exercise presents a pressure overload.  Remember though it is called an hypothesis.Several studies have reexamined the concept and reported that every endurance athlete does not get eccentric hypertrophy and many weight lifters do not have concentric changes.Futher ,activities such a bike racing and rowing involve a considerable amount of both volume and pressure overload and both group have among the largest hearts.



The diastolic dysfunction , in the Dallas study, was assessed by the ratio E/e' ( e over e prime) where e is the the early diastolic flow through the mitral valve  and e prime is movement of the mitral annulus.the ratio giving some measure of left ventricular compliance or stiffness.

The "Dallas hypothesis", my term as far as I know, is that the cardiac phenotype ( structure and function ) of the sedentary heart is a likely precursor of diastolic heart failure. aka heart failure with preserved ejection fraction ( HFpEF) . ( Note this designation is not the same as saying heart failure with preserved systolic function.EF is only one measure of systolic function. Some studies have shown decreased systolic function in HFpEF as measured by speckle echo exams measuring longitudinal strain.)

I have argued before that the lower level of the 2008 recommendation for exercise , while decreasing the overall risk of cardiovascular disease, is not sufficient to prevent heart failure. Exercise at at least twice  that level seems to be needed. The minimum recommendation was for 500 MET min per week which would translate to 2.5 hours of moderate exercise per week or 1.25 hours of vigorous exercise ( where vigorous is over 7 MET)

The argument is that the reduction is diastolic heart failure risk may be  brought about by endurance exercise induced structural changes in the heart and preservation of left ventricular compliance.  How much exercise, at what level and for how many years remain to be determined.

Can an individual's risk of a given disease ever be "determined"?

The risk assessment of an individual.that is determining a person's risk of a given disease has been described a peculiar,elusive,ambiguous process. The statistician,Richard Von Misses ( Ludwig's brother ) said that it is only possible to speak of probability in terms of a collective ( ie. a group or a set ) and that to say , for example that Mr. Jones has the probability of 0.3 in the next five years of , for example, having a heart attack is nonsense. Yet, physicians are encouraged ( and nowadays mandated in order to practice proper guideline driven medical practice) to do this in a variety of situations. The famous Framingham risk model is often used to assess the risk of a heart attack. For example,using an equation from the NCEP ( National Cholesterol Education Program) we find that a 67 year,non smoking man with a total cholesterol of 170 and an HDL of 75 would have a 10 years risk estimate of 9%. According to the Framingham data, there would be 9 deaths in a ten years period in a group of men with those characteristics ,but is it meaningful to say that a given member of that group has a 9% risk. Further, the risk number is not just something mentioned in the exam room but is often folded into guidelines from various organizations,for example the ACC .Someone with a risk of 10% ( or some committee derived cutpoint) might be advised to take a statin or aspirin.

What if we constitute another statistical collective since we can make up as many as our imagination and data allow.In a Framingham type study we could measure CRP,presence of absence of coronary calcification,results of a exercise stress test,blood sugar and whether or not the person takes daily vitamins. The person in the previous paragraph might now be determined to have a risk of 15%.So what is his " real " risk? Is there a real risk at all ? Is an elusive ,ambiguous risk number sufficient reason to recommend lifetime medications? I don't think so now; but that happens regularly in doctor's offices and I used to do it on almost a routine basis and thought I knew what I was doing. Frequently medical societies and committees will offer generic advice to generic patients by suggesting they complete a form or risk assessment tool but then consult with their physician /health care provider to discuss the issue and offer an "individualized" risk assessment. I wonder what sort of magical statistical tool the providers has at her disposal to achieve that result other than the same risk assessment tool the patient has already used.

The marked variability of subclinical atrial fibrillation makes risk assessment difficult

A post  hoc analysis (1) of the TRENDS study concluded "significant temporal variability of AF burden exists when measured continuously with an implantable CRMD ( cardiac rhythm management device)."

The authors examined data from 394 patients who had a mean CHAD2DS.Vasc score of 3.7 (average) and divided AF burden into three categories: 1) No AF, 2) Low AF (less than 5.5 hours per day on any given day) and 3) High AF (greater than or equal to 5.5 hours per day).

They then determined how often that classification changed over time. What category in which the patient was placed was dependent on the time period over which the sampling was analyzed. One day they might have " no AF" another day be placed in the high AF category of greater than 5.5 hours per day.


So to what extent do these data invalidate the conclusion of the TRENDS study? Certainly  one at least has to be much  more skeptical of the findings. If a significant number of patients were considered to have no AF and then developed into either category 2 or 3 the calculation of the relative risk for  stroke would likely be an underestimation of risk .So how good is the data regarding the question of  the degree to which  AF burden is an indicator of stroke risk at all?


The authors concluded: "The burden of AF is highly variable over time and cannot be accurately assessed by short-term monitoring. If burden of AF is shown to be an important variable to be considered when making decisions regarding long-term anticoagulation, perhaps continuous monitoring should be employed to follow changes in AF burden over time."






1 Kaplan RM et al Atrial Fibrillation variability on long term monitoring of implantable cardiac rhythm management devices. Clinical Cardiology 2017: 1-5 March June

Detailed cardiac study on a group of really extreme endurance athletes

Much has been written about the issues of what is the point beyond which exercise is no longer health promoting but rather damaging to the heart or is there a point.

Larry Creswell writing on his blog Athlete's Heart Blog reviews a recent article that studied 33 endurance athletes  with a history of prolonged intensive aerobic training. These guys trained so long and so hard that you might think that surely what they did would approach that limit and have evidence of cardiac damage. Yet that was not the case. (Dr. Creswell'sl blog continues to be a great source for issues involving what the blog title suggests.)

The data are interesting but finding 33 white swans does not rule out the existence of black ones.The fact that these athletes continued to be able to exercise at a prodigiously high level suggested that that did not develop some serious heart problem. Is there a survivor bias at play here?

addendum 0ct 21 2017.Typo in headline corrected.

Biggest change in medicine in 40 years-loss of autonomy and change in ethics

In regard to what has changed most in the last near half century some would answer medical advances, mainly in diagnostic techniques and therapeutics.For someone who has seen those happen they are incredible and marvelous but that is not what has changed the relationship between physician and patient. In the sixties, physicians used the tools of the day to diagnose and treat patient, so do they today even as the tools are much better and more varied. No relationship change there.

I submit that three factors acting alone and interacting with the other two have brought about a sea change. The factors are: 1) loss of physician autonomy, 2) a change in medical ethics (even the name has changed to professionalism) and 3) method of payment for physician services. I argue that the third has been a major factor in loss of autonomy and has triggered the ethical changes.

The basic narrative of medical collectivism as voiced by the ACP and ABIMF

The following two paragraphs are from a viewpoint commentary  entitled  "Resolving the Tension between Population Health and Individual Health Care " in the JAMA by Dr. Harold C. Sox, former president of the American College of Physicians and former editor of the Annals of Internal Medicine: See (JAMA November 13,2013,volume 310, number 18). Yes, I have written about this article before, obviously I find that commentary as disturbing as any I can remember reading.

"Throughout history, codes of professional conduct have called on clinicians to make each patient’s interests their highest priority. If resources become limited, clinicians will find themselves unable to adhere to this standard of practice for all patients. In 2002, a new code of conduct, the Charter for Professionalism, addressed this conflict by calling on physicians to consider the needs of all when treating the individual: “While meeting the needs of individual patients, physicians are required to provide health care that is based on the wise and cost-effective management of limited clinical resources. The provision of unnecessary services not only exposes patients to avoidable harm and expense but also diminishes the resources available for others.

This remarkable passage indicates that the physician has an ethical imperative to balance the needs of the individual patient with the needs of society. With this foundational principle of the population health approach, the Charter, in effect, calls on clinicians to allocate resources. However, it does not provide specific advice. Recent programs, such as the American Board of Internal Medicine Foundation’s Choosing Wisely campaign, are beginning to fill this knowledge gap, as do some practice guidelines."

 What  constitutes fairness-equal treatment for all? less treatment for all?only treatment if it meets  someone's definition of "high value" ,treatment based on considerations of "life years"? Who decides?

 Remarkable passage indeed. "consider the needs of all when treating the individual." How to bring about a fair and equitable allocation poses a problem for the practicing physician? Would ordering a MR on  Mrs. Jones somehow keep Mrs. Brown for having one?  The answer was so simple. Follow guidelines.They will be written by people who know that medical care is too important and too complex to be left to the individual physician and her patient, which is just the medical care application of the progressive medical credo .

 The alleged necessity of radically revising medical ethics was justified on the basis of  "If medical resources become limited". The nature or magnitude of this limitation is not further explained nor is how this would come to pass.The conditional nature of the sentence implies that the author thinks such limitation has yet to occur. When have resources not been limited?

Later in the same article Sox seemingly justifies a scenario in which funds are shifted from the treatment of a sick person to fund some preventive program and in doing so admits there will be some short run harm to some for the greater benefit of a large group. This is much more than simply  eliminating "unnecessary "provision of services. Sox never tells the readers who will make these decisions or how such an allocation of resources will be carried out. Amazingly in 2002 a relatively small group of internists affiliated with the American College of Physicians and the American Board of Internal Medicine ( and  a few like minded European internists) proclaimed a new code of medical ethics.A ethical physician must consider the needs of all when treating the individual. The Charter (1) did not specify exactly how that new ethical imperative could be accomplished but the ACP and ABIMF subsequently revealed the way in which the new ethics could be practiced.It is called the Choosing Wisely Campaign which will offer specifics  on things physicians should not do,certain tests and procedures that are deemed wasteful and/or harmful.Further certain practice guidelines which are based on cost effective considerations are or will soon be available.

 Can a group of internists simply change medical ethics,ethics that had persisted for many years ? Well so far they have made much progress along those lines at least if  ethical change proclamations by numerous professional organizations are an indication. I hope the typical practicing physician thinks otherwise .

1) ABIM Foundation, American Board of Internal Medicine; ACP-ASIM Foundation, American College of Physicians-American Society of Internal Medicine; European Federation of Internal Medicine.  Medical professionalism in the new millennium: a physician charter. Ann Intern Med. 2002;136(3):243-246.


addendum 12/30/2017. One minor wording change made to clarify meaning of one sentence.

Is a sedentary life style and not resistance exercise a cause of concentric cardiac hypertrophy?

Following the 1975 echocardiographic study by Joel Morganroth of endurance athletes and resistance exercise athletes and several cross sectional studies that seemed to validate his work the  "Morganroth's  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 more precisely  by the relative wall thickness (RWT) which is 2 x the posterior wall thickness dived by left ventricular diastolic diameter with the value greater than 0.42 indicating  concentric hypertrophy.

Skeptics have argued that echo studies have inherent  methodological errors  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 difference 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 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.

Spence et al (2) from Australia did a MRI study on   a small number  of subjects with one  group undergoing endurance training and the other resistance training.

 While Spence's study  suggests that six months of   resistance exercise does not lead to concentric hypertrophy,data from the group  Southwestern Medical School indicate that a sedentary lifestyle can bring about concentric hypertrophy at least some of the time.

 Brinker et al (3) studied cardiac function and structure in 2900 subjects from the Cooper Center Longitudinal Study. They found that the low fit subjects ( basically those with a sedentary lifestyle) had a higher prevalence of concentric remodeling as well as diastolic dysfunction that the fitter subjects. There was a 40% prevalence of concentric hypertrophy in the lowest fit group versus less than 20 % in the most fit group. So it is not an all of none thing.

 The notion of volume overload exercise and pressure overload exercise may well be a oversimplification. A recent meta-analysis provided data to support the notion that there is some pressure overload in endurance exercise and there is apparently some volume overload in such resistance exercise. Further a number athletic endeavors are mixed, such as rowing and cycling. The rowers and cyclists had the greatest remodeling changes with both increased left ventricular end diastolic volume and wall thickness. 

 But it may also be the case  to be the case there there is "inactivity remodeling", here referring to a sedentary lifestyle The ventricles remodel  whether  you exercise or have a sedentary lifestyle., you likely get a eccentric remodeling or hypertrophy with  aerobic exercise and  at least in some people without it you get concentric remodeling or hypertrophy.Further, they suggest as have others that the latter may well be a precursor to heart failure and the former may help prevent it.



 1. Morganroth, Jet  al. Comparative left ventricular dimensions in trained athletes.Ann Int Med. 1975,82(4), 521-524
 2. Spence,A et al A prospective randomized longitudinal study of left ventricular adaption to endurance and resistance training in humans. J Phys 2011 589, 543
 3.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.

Will 2-3 hours a week of aerobic exercise keep your heart from getting stiff?

Will a few hours of aerobic exercise per week practiced over along period of time (years) prevent the ventricle from becomes stiff and could the current epidemic of diastolic heart failure be diminished if many people follow that practice. Does sedentary aging resulting in stiff left ventricles play a major role in the increasing numbers of older folks with heart failure (HF). If it does could the sufficient amount of  exercise prevent it and what do we mean by "sufficient"?

Echocardiography and other imaging techniques have provided  detailed  information emphasizing the importance of diastole, the filling process of the ventricle priming the heart pump for systole or ventricular contraction.Indeed a key distinguishing feature of the endurance athlete's heart is its superior filling or diastolic function. The better diastolic function or ventricular filling the better is one's fitness or exercise level.

Knowledge of diastole has lead to a new concept of heart failure, one if which systolic function is said to be normal- at least at rest.Actually less than that is claimed as the systolic function is represented by one test of that function namely the ejection fraction done at rest. This has lead to the notion of  "HFpEF" or heart failure with preserved ejection fraction and HFrEF, or heart failure with reduced ejection fraction.  HFpEF is said to represent at least half of HF cases and other than    exercise training there seems  to be little evidence of an effective therapeutic approach. There are several echocardiographic tests used to assess diastolic function: EA ratio. E/E prime ratio,left atrial volume, etc .


Woody Allen's basic axiom of physiology  can be paraphrased : as we get older everything that should be soft gets stiff  and everything should be stiff gets soft. Aging certainly makes the left ventricle get stiff  and the aorta as well.

The group from Dallas having the wealth of patient data available from the Cooper Longevity institute has published several articles claiming that long time endurance athletes are able to maintain a much more compliant left ventricle than matched persons with little on no regular aerobic exercise.  Further their data suggest that a group with exercise levels lower than that of the competitive runner group  ( about 2-3 hours  per week of aerobic exercise) fare almost as well in regard to  left ventricular compliance.This suggest that training or exercise far short of running marathon every year or doing the full Iron man type triathlon will suffice. 

Ventricular compliance is one factor to consider in regard to diastolic function- another is the relaxation capability and in that regard long term endurance exercise does not mitigate the age related loss of optimal relaxation  function. One way to measure relaxation is with the isovolumic relaxation time  or.IVRT. This is the time interval after aortic valve closure and mitral valve opening. It is prolonged as humans age and the IVRT was no shorter in the fit group or the super fit group  versus the sedentary group in the Dallas articles. .

The heart remodels itself. The remodeling pattern is different  in the fit person from that in the  sedentary person, the latter  described by the Dallas group as a small heart, with concentric remodeling or  hypertrophy and impaired filling or impaired  diastolic function.

Heart size in this context  refers to the volume of ventricle at the end of diastole (end diastolic ventricular volume). Concentric remodeling means no chamber enlargement with ventricular wall thickening. The terms concentric and eccentric dates back at least to the Morganroth hypothesis in 1975 from his cardiac echo study of endurance athletes and resistance training athletes.

As more data was generated it appeared that there is more to it that what Dr. Morganroth suggested. Some data from the Dallas group suggested that in the first year of aerobic training at least some folks develop concentric type changes and only later  ( or perhaps with more intense  training-long runs and/or high intensity interval training) does the classical runners heart pattern appear. Another study failed to show any concentric hypertrophy after a six month period of weight training.Studies involving rowers and cyclists show a mixed pattern.

Basically,the athlete's heart (at least the endurance athlete's heart) is big (but not in a bad way) muscular and very compliant and can relax quickly so that it can pump large volume of blood rapidly for prolonged periods of time. How much of that picture is genetic and how much is due to long time training is not known Whether levels of exercise  equal to or slightly greater  than the 2008 party line recommendations will mitigate the  current  "epidemic" of diastolic heart failure is an attractive hypothesis and one that I would like to believe.

"A man hears what he wants to hears and disregards the rest" - Paul Simon,song "The Boxer",1969


addendum 11/7/17- Several typos corrected along with minor editorial tweaks.

Review of deaths occuring during triathlons

Most deaths that occur in a triathlon happen in the swimming phase.

A detailed report on triathlon deaths can be found in a recent issue of the Annals of Internal Medicine.
See here.

There were 135 sudden deaths,resuscitated cardiac arrests and trauma related deaths recorded in the period 1985 to 2016.

90 occurred in the swimming phase,7 in the bike phase,15 in the running phase and 8 in the post race period.

85% of  the events occurred in males and the average age of death was 46.7 plus.minus 12.4 and the risk of death was greatest in participants over age 60.Almost 40% of the events occurred in first time participants.

One of the co-authors, Dr Larry Creswall,who writes the blog " Athlete's Heart Blog" discusses the results and offers suggestions for way to improve safety and response to incidents. See here

What is the signficance of "myocardial fibrosis" in endurance athletes?

The quote around myocardial fibrosis is to make the point that the discussion is not about large areas of fibrosis or athletes with extensive fibrosis resulting in heart failure. The fibrosis refers here to small areas of uncertain significance detected by Cardiac MR studies with gadolinium. These areas are referred to as  areas of delayed gadolinium enhancement (DGE) and are presumed ( probably correctly ) to be focal areas of fibrosis and are typically found at the insertion points of the right ventricle to the left ventricle. There is no question that DGE may indicate myocardial fibrosis-what has been questioned is whether DGE necessarily indicates fibrosis in endurance athletes and whether there is any clinical significance to those DGEs which do not fit a pattern consistent with a coronary artery distribution.

A recent article by Eijsvogel (1) et al described extensive cardiac function studies including MR and 2D speckle tracking imaging in 4 long term endurance athletes in whom DGE was demonstrated  and compared the results to 5 other long term athletes without DGE . Both group had normal echo studies and normal and normal global function (longitudinal strain and strain rate) . However the DGE group had larger cardiac volumes and some ( remember there were only 4) showed some attenuation of strain in the regions of DGE or fibrosis. Both group has a long history of endurance training  ( around 42-42 years) and both group were in their late fifties.

So as sophisticated as this extensive  physiologic testing was in this project is my take is all we have learned is that some endurance athletes have more exercise induced remodeling and have bigger hearts and some-but not all- of those who had DGE have subtle regional decrease in strain but normal global function.

Another conjecture regarding the significance of DGE was offered by Trivax (3) who postulated that a demonstrated DGE in a runner was the cause of an episode of ventricular fibrillation. To his credit Dr. Trivax emphasized this was only an hypothesis , one I think that  has not been further substantiated   by subsequent case reports.

Levine (2) has offered commentary challenging the claim there is an increase in fibrosis in endurance athletes and also has suggested that the DGE-at least in some cases- might actually represent edema from acute prolonged strain in the  right ventricular  insertion points.





1)Eijsvogel TM et al Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis.  Eur J. of sport Science 2017,

2)Levine BD Can Intensive exercise Harm the heart? Circulation 2014:130, 987-991

3)Trivax JE,  Phidippides cardiomyopathy: a review and case illustration. Clin Cardiol.2012 #%  69-73

Annother observatonal epidemiolgic study wiill not settle the issue of the exercise cardiovascular mortality relationship.

There is no debate about the general  nature of the relationship between  regular exercise and cardiovascular risk  and even over-all mortality. As exercise levels ( duration,or frequency or intensity ) increases  the CVD risk decreases i.e there is an inverse relationship.

Controversy exists,however, about  1) whether there is a point beyond which  CVD risk is no longer reduced ( does the curve slope up?) and 2) is there a point beyond which there is actual harm

 The general point that exercise is inversely related to  decreased CVD risk is more than generally accepted even though all the data as regards primary prevention is observational There have been and never will be any randomized clinical trials ( However, there is RCT evidence that a cardiac rehab exercise program will decrease CVD mortality).


In recent years concern has been expressed concerning cardiac problems in  endurance athletes including increased risk of atrial fibrillation, and  the development of areas of cardiac fibrosis ( detected on gadolinium scans)  which have been reputed to   predispose to rhythm disturbance and abnormalities of the right ventricle resembling an genetic condition known as ARVD (arrhythmogenic right ventricular dysplasia).  These and possibly other heart conditions might provide a possible mechanism(s)  responsible for a purported U shaped curve describing cardiovascular mortality and exercise level.It should be noted that there is conflicting evidence as to the shape of this curve, i.e. inverse or u shaped and it is easy to reference a number of studies that support either proposition.The strongest evidence- in regard to the claim that "too much" exercise is harmful- is for the relationship between endurance exercise and atrial fibrillation but even  in  this regard  data also conflict.



Dr. James Okeefe along with Dr. Carl Lavie and others have written extensively  and  often spoken about the hazards of too much exercise and have recommend that relatively low levels of aerobic exercise are adequate to decrease cardiovascular risk.Low levels of exercise have been associated with significance reduction in CVD In fact, simply standing for greater than 2 hours per day is said to be associated with a 10% decrease in all cause mortality - a claim that strains credulity.

Dr. BD Levine from Southwestern Medical school has provided evidence that higher levels of exercise than the currently recommended levels not only protect against coronary  artery disease but can also provide some protection  of the age associated loss of ventricular compliance which arguably predisposes to  heart failure with preserved ejection fraction. (HFpEF) also known as diastolic heart failure. Other workers at the same  institution have recently provided some epidemiological proof of that concept.  Levin has argued that levels of exercise higher than the current recommendation but significantly lower that that practiced, for example by iron man triathletes,will importantly help maintain good left ventricular function and perhaps  ultimately favorably impact  the current "epidemic" of HFpEF.

Eijsvogel et al have provided evidence that the current recommendation regarding exercise to prevent cardiovascular risk may be too low as far as prevention of heart failure (HF) The current (2008) recommendation are for 2 1/2 hours of moderate or one hour and 15 minutes of vigorous exercise per week. (I am reminded of John Von Neumann 's quote " There's no sense in being precise when you don't even know what you're talking about")

Eijsvogel's article defines moderate as 3- 5.9 METS of energy expenditure and vigorous as greater than 6 METS.

For point of reference, running a fifteen minute mile requires about 7 METS ( 24.4 02 uptake) which is equivalent to the 02 requirement for completing Stage 2 of the Bruce protocol. About 5 METs are  needed to finish stage 1 ( 1.7 mph at 10% grade) . Running at  5 MPH or a 12 minute mile requires 8.6 METS. Running 4 MPH require a 02 uptake of about 25 ( 7 METS)

A sometimes used  prediction equation that approximates a person's maximal 02 uptake is 3.8 times how long in minutes the person could preserver  on the Bruce treadmill protocol.

Eijsvogel and co-workers used the data from the work of Wen and Tsai and of Arem  to construct a cardiovascular disease mortality -physical activity curve .  and found the "sweet spot" of  41 MET hours per week or 2460 METS hours per week The sweet spot  ( not their term) means the level of exercise at which the maximal benefit in terms of reduction of CVD risk is reached.

This corresponds to 9 hours of walking or 4.8 hours of running at a 12 minute mile.

This is 3 to 4 times higher than the widely quoted 2008 recommendations of 2.5 hours of moderate or 75 minutes of vigorous exercise per week.

Another study  by Lee et al also derived a activity CD risk relationship curve and found a lower sweet spot.

So the sweet spot from Lee's data is run for 3.5 hours  per week versus 4.8 in Eijsvogel's article. O'Keefe seems to rely on Lee's data when he recommends for one to "limit one's vigorous exercise to 30-50 minutes a day. Not every one would consider running 3 1/2 hours per week at a 12 minute per mile pace a small amount of exercise and this would represent about 2- 3 times the 2008 recommendations and accepting Levine's thesis would be sufficient (if done for many years) be enough to decrease not only te risk of CVD is general but also the risk of developing heart failure with preserved ejection fraction (HFpEF).

But what will happen in terms of cardiovascular harm if you exceed the fifty minutes per day recommended by Okeefe and Lavie.From reading  Eijsvogel's analysis- my sense of is , not much. His group was unable to show an increased CV risk at any level though using some parameters of exercise intensity or duration the curve sloped up slightly at the far right but was not statistically significant.

Another study demonstrating more coronary calcifications and myocardial fibrosis in Older endurance athletes

The article by Merghani et al (1) at least at first glance seems to be more bad news for long time endurance athletes in regard to the development of coronary artery disease.

The study subjects were 152 men who had logged an average of 31 years of endurance exercise type activities. All had echocardiograms,24 hour Holter, stress ECG,CT coronary angiograms (CAC) and cardiac MRs with gadolinium as did 92 age matched controls with similar Framingham Risk scores.

15  athletes and none of the controls had delayed gadolinium enhancement (DGE) on the MRs, 7 of which had a coronary artery pattern.(The DGE issue  will need to be written about at a later date-for now  the focus is on the  calcification.)

60% of the athletes and 63% of controls had a normal CAC score but only athletes (11.3%) has a CAC score of 300 or greater. So the incidence of any calcification was about the same in athletes and controls but the athletes had more calcium and more demonstrable luminal stenosis ( greater than 50%) in 7.5% of the athletes and in none of the controls.

So does this mean that long time endurance exercise increased the risk of coronary artery disease?
Maybe an answer to that is related to another question-does the increase in calcium scores noted in patients taking statins mean that statins increase the risk of coronary artery disease which is , of course, a conclusion contrary to realms of clinical trial results demonstrating the value of statins, at least in secondary prevention.

In regard to the second question there is a great deal of data regarding what could be called the statin plaque paradox-statins increase coronary artery calcium even as they shrike the plaques. A  calcium score could increase even as the plaques regress because of the increased density of calcification bought about by the statins.However not only did Merghani's runners have higher Calcium scores a few did have luminal stenosis related to the calcification.

A review of serial coronary intravascular ultrasound (IVUS) data gathered up from 8 large clinical studies  may shed some on light on that issue.

The bottom line is that statins may increase the calcium scores (Agatson score) by increasing the calcification of plaques while decreasing the volume of the plaques, the effect being greater with the more potent ( as measured by magnitude of cholesterol lowering) statins having a greater plaque shrinkage  effect.My sense of the literature is that other than the more fringy group of "statin deniers" there is no abundance of data suggesting that statins increase the risk of coronary heart disease.

More possible good news for long term exercisers who have already made up their minds that what they do is good,  can be found in  a 2016 article  (2)Shuaib Abdullah and Benjamin Levine reviewing their data of healthy exercisers stratified by exercise levels  and previous articles that made the association between myocardial fibrosis ( as indicated by late  gadolinium enhancement (LGE) on cardiac MRs) concluded "that increasing levels of lifelong physical activity were not associated with focal myocardial fibrosis ".Although some athletes may demonstrated LGE the authors suggest that they may not represent fibrosis but rather possibly "exaggeration of the normal local myocardial architecture or edema caused by exercise-induced right ventricular overload and paradoxical septal motion".The more commonly expressed view is that LGE is more common in endurance athletes and  does represent fibrosis typically at the insertion points of the right ventricle to the left but their significance is not known. 

No one since a pathologist decades ago (Tom Bassler) ( footnote 1)  would now claim  that endurance exercise is completely effective immunization against coronary artery disease but there will be a major paradigm shift if and when it is more conclusively shown that long term endurance exercise increases the risk of coronary artery disease.

Quoting from Levine ( ref 3):


"Although it would be foolish to argue that extraordinary endurance exercise can never be harmful, it is equally inappropriate  to frighten individuals who wish to undertake competitive endurance training, including marathons,triathlons, or even ultra endurance events, based on fear of accelerating coronary artery disease or initiating a cardiomyopathic process." [ Levine does not however, deny the epidemiologic evidence that there is a increase risk of atrial fibrillation though there are conflicting data and the magnitude of the putative risk is a open question]

Sorting out cause and effect is no easy matter and may not be possible   in cross sectional, observational  studies in conditions in which there is a high "causal density".The relationship between exercise levels, intensity of statin therapy and the list of  recognized coronary artery disease risk factors is by no means unraveled.



1)Merghani, A et al Prevalence of subclinical coronary artery disease in Master Endurance Athletes. Circ. 2017, May 2, 2017 Vol 135, issue no 12

2) Abdullah, SM et al Lifelong physical activity regardless of dose is not associated with myocardial fibrosis. Circulation Cardiovascular Imaging, 2016;9  e

3) Levine BD Can Intensive exercise harm the heart? Circulation 2014: 130, 97-99L

Footnote 1 Dr.Thomas J Bassler actually was slightly more circumspect saying that if one could finish a marathon in under 4 hours he would not  die of a heart attack in the next 6 years. He wrote and spoke often in the 1970s about the value of long distance running. He died Dec 2011 at the age of 79 . Maybe his best quote is (paraphrased):

 If you decide to lead a sedentary life style better see your doctor first.


Footnote 2  and disclosure

Paul Simon's lines  ( a man believes what he wants to believe and disregards the rest )
is a modern musical echo of  Hume's comment that reason is the servant of passion .

My history of marathon running over 40 plus years may well reveal
my biases.

11/13/17 Footnote 2 added as well as adding a new final paragraph.

Addendum: 1/31/18. Further thought.More statin and  maybe more running may increase the calcium score ( it seems to) but both may make a coronary event less likely.At least I like to think so.