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Is the new professionalism and ACP's new ethics really just about following guidelines?

The Charter ( Medical Professionalism in the New Millennium.A Physician's Charter) did not deal with just the important relationship of ...

Friday, November 17, 2017

The division of internist into hospitalist and "officist" and its demise.

It is the 20th  anniversary of the birth of the hospitalist.A recent article describes what was presented as a fairly widespread feeling among hospitalists  of "not getting no respect. ".

Some of the doctors interviewed  spoke of the hospitalist being a gopher for various attending physicians,a clerk and paper work finisher for numerous physicians and thought of more or less as a intern or junior resident and one who often seemed not worthy of a return phone call.The duties of the hospitalist when I was briefly  in the hospital last year with a pulmonary embolus seemed to fit that pattern. A very pleasant young physician mainly ushered the consulting cardiologist and pulmonary doc in and wrapped up the paper work as both of the consultants made the real decisions regarding testing and treatment. A colleague of mine who attended at that hospital said he made the decisions regarding patients he admitted while the hospitalist was useful in relieving him of paperwork. I realize that the above description does not apply to the situation of all hospitalists.

While the officist has become barely distinguishable from the FP or GP or even NP, the hospitalist , at least in some settings seems to have devolved into a junior  house officer while the real management of the critically ill fall to the cardiologist, the pulmonologist and the intensivist.


In the 1970s and 80s in our internal medicine  practice it was routine for GPs ( they were not FPs at the time) to  refer complicated,sick patients to our groups. ( It seemed to more often than not happen late on Friday afternoons. The physician to whom the referral was made would personally  care for the patient in the hospital  often aided by his  internist specialists partners.)

The sequence was that the patient or referring physician would call the physician in our group -if he was not on call one of the partners would  admit the patient to the hospital and attend to him calling on other partner subspecialists as the situation warranted. Now the patient calls ,for example after hours and the recorded message advises the patient to go to the ER. He is seen by the ER doctor who may admit the patient and the hospitalist would see the patient and consult as needed various specialists. The internist, assuming the patient had one, would often learn of the event when the patient was discharged back to the internist who had nothing to do with his treatment and may or may not have received a copy of the discharge summary.

In describing that archaic situation to young house staff  I would feel like describing the quaint rotary phone that I used when growing up in the 50s.

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Monday, November 13, 2017

James Gailbraith combines a belief in perpetual motion machine with believe in there IS a free lunch in his economic advice

Dr. James Galbraith is the son of John Kenneth Galbraith and here the apple falls very close to the tree. See here for his  thoughts published in the Nation. Here is discussion of those comments as formulated by Dr.Paul Hsieh and published on line at Pajamamedia.com blog.

Here are the major points as Dr. Hsieh summarizes them:
  1. The political push to reduce government deficits is economically misguided, based on an irrational “phobia” of deficits.
  2. If we want economic growth, we need more spending. Only banks and governments can stimulate spending because (in his words): “Governments and banks are the two entities with the power to create something from nothing.”
  3. We shouldn’t worry about the alleged impending bankruptcy of Social Security or Medicare — or of the U.S. government itself. Why? Because the government is the source of money and therefore can’t run out.
  4. Government debt is not really a “burden on future generations,” because it never has to be repaid. Each generation can just pass that debt onto the next generation, so there’s no problem.

Think about what he said. Governments and banks can create something from nothing. Yes, I know that the government can "print money" and that banks create money in the fractional reserve banking system but you can't fool all of the people all of the time. The government and banks in Greece seem to have not understood that universal principle as they have made nothing out of something as they made tried to make something out of nothing Apparently the government in Greece has not consulted with Dr. Galbraith as they seemingly have run out of money. His perpetual motion money making machine is that you just keep rolling over debt which was the something that governments made out of nothing and there is no problem. So why did the Germans and the EU have to bail out Greece? Why could not the government just continued to make something from nothing?Why did we see hyper-inflation in Germany? Why are Not all countries made prosperous by this simple technique print more money and spend it.


Wednesday, November 08, 2017

Before Obamacare it was the other people's money effect -Afterwards more so



 When something is being payed for with other people's money, more will purchased. This is also true if you merely think someone else is paying for it, as in the situation that exists with employer paid health care insurance.

Quoting myself from 2006:

Medical care came to be "managed " by the managed care sector because of the concept of "other people's money". To a large degree individuals pay for only a portion of their health care the remainder paid by either employers or the government. There was not much fuss made by these other people until the costs of health care rose to some threshold above which employers and other third party payers including CMS thought costs were getting out of hand. Then entered cost containment via the various cost savings actions of managed care.

The effect on the traditional fiduciary duties of physicians to patients by the duties of the for-profit corporation vis-a -vis its shareholders is the root cause of many ethical problems generated by managed care. Basically the HMO and third party payers generally strive to make money or save it and they introduce mechanisms to control physician behavior to that end even if that control involves abrogation of the fundamental duty of the doctor to place the patient well being and interests first. The efforts of the third parties in that regard weaken the physician-patient relationship and damage the trust element in the relationship.Ethical cover for this abrogation was provided by the introduction and unfortunate widespread acceptance by medical professionals organizations of the "New Professionalism" which alleged a physician's duty to society to be a good steward of society resources must somehow be balanced against the physician's duty to the patient.

With Obamacare, more people will be trying to spend other people's money.The biggest other people is CMS who along with HHS will have mandates to control costs. Mix in the decreasing number of primary care doctors to the number of patients seeking care with HHS/CMS moving to decrease health care providers reimbursements and you have a situation in which patient need more than ever an advocate. But patient advocacy will be not longer be the prime directive but merely a factor to be weighed against the imperative to be a steward of society's scare medical resource to the extent that physicians actually internalize the bogus arguments of the New Professionalism.

Monday, November 06, 2017

What is the evidence that prolonged endurance execise damages the conduction system of the heart.



In 1985, RJ Northcutt studied 20 males endurance athletes that were recruited from a Scottish Harrier's club. All were  older than 45 years and ran for 25 miles per week  or more. Stress testing and 48 hour Holter type monitoring were done.. He found that 9 had heart  rates less than 35 beats per minutes,6 had a prolonged PR interval, 4 had Mobitz type ii heart block and three with complete heart block one of whom had a pacemaker implanted. With exercise all of the various blocks disappeared.

Northcott with co-author Stuart Hood (1,2) studied 19 or the 20 twelve years later.Two of the group had pacemaker implantation in the interval, one for complete heart block with atrial fibrillation and the other for asystolic intervals up to 15 seconds. None of the others had any "bradycardic problems". 7 of the 20 in 1985 has systolic pauses greater than 2 seconds and 5 of those had none on follow-up. The other two had decreased the intensity of their running. ( not clear from the article if those 2 had pauses or not) Quoting the authors: "Our finding nonetheless suggest that clinically significant bradycardia symptoms are a real but rare potential complication of lifetime endurance exercise."

Baldesberger et al  (3) studied 62 former professional cyclists who had long since (over thirty years) retired from active competition.Two had pacemaker implantation. None had complete RBBB or LBBB and two had EKG pattern of left anterior hemiblock.None had second degree heart block. Six had "sinus node disease which the authors defined as heart rate less than 40 beats per minute.

Andersen's 2013 article (4) is often quoted in support of the argument that there is an increased risk of atrial fibrillation in endurance athletes but it also has data on the risk of  "bradyarrhythmias".The authors studied the records of over 52 thousand participants in a 90 km cross country race in Sweden  (the Vasaloppet). They then compared those who raced more (five or more races) with those who only did one race and compared the faster skiers with the slower. The  Hazard ratio (HR) for atrial fibrillation was 1.2 (0.93-155) while the HR for bradyarrhythmias was 1.85 (0.97--3.54). When comparing those who did more races with those who did one they reported a HR for AF of 1.29 (1.04-1.61 and a HR for bradyarrhythmias 2.10 (1.28-3.47).The bradyarrrythmis were mainly type ii heart block but the ICD s codes used did not enable the investigators to separate type 1 and 2 second degree block, an important distinction as Wenckeback is usually considered much less  serious that type 2 second degree block. No mention was made on any one requiring a pacemaker. The rhythm outcome endpoints were obtained from hospital records those race finishers hospitalized with rhythm disturbances.

Comment.This is a very "coarse grain" study.All that was known about the subjects was the race numbers and times ,ICD codes of those hospitalized with arrhythmias, and their age, education and occupational status. How much they exercised outside of this race and other pertinent health factors that could influence the outcome ( BP,diabetes,obesity,height,smoking history,alcohol use) were not known and the various hazard ratios were not all statistically significant. Incidentally,  the HR for atrial fibrillation were much lower than the five times increased risk often quoted for AF in several case control studies.



1.Northcote R. et al. Electrocardiographic findings in male veteran endurance athletes. Br Heart J. 1989, 61: 155-160

2.Hood S and Northcote,R Cardiac Assessment of veteran endurance athletes;a 12 year follow up study. Br J Sport Med, 1999, 33: 239-243

3.Baldesberger S,  et al Sinus Node disease and arrhythmias in the long term followup of former professional cyclists. Eur Hear J. 200829.71-78

4.Andersen K. Risk of arrhythmias in 52,755 long-distance cross country skiers: A cohort study.
Eur Heart J 2013 Dec 34(47) 3624-3631

Monday, October 30, 2017

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.

Thursday, October 26, 2017

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.



Wednesday, October 25, 2017

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 remolding , 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.



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 ME\T 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. 




Tuesday, October 24, 2017

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.

Monday, October 23, 2017

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

Saturday, October 21, 2017

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.

Thursday, October 19, 2017

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.

Tuesday, October 17, 2017

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 progressives' 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.

Sunday, October 08, 2017

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 a all of none thing.

In fact 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 athletics endeavors is 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.

Friday, October 06, 2017

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 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 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 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 athlees and resistance treaining 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 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 higher 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


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

Thursday, October 05, 2017

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

Tuesday, October 03, 2017

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 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

Monday, October 02, 2017

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,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 s 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)

An  prediction equation that approximates a person's maximal 02 uptake is 3.8 times how long in minutes the person could last 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.

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 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.

Friday, September 29, 2017

Will the real Phidippides Syndrome (if there is one ) please stand up

The legendary Greek courier who ran back and forth in the days surrounding the big battle between the Greek and the Persians in the fifth century BC was named Phidippides. The story goes that he first ran from Athens to Sparta carrying a request of the Athenians to the Spartans for aid and then ran back to Athens with the bad news that Sparta could not help, something about a religious holiday not allowing them to fight,running a total of 280 mile  round trip which took about 36 hours each way. That is about 3.8 mph or a 15.7 minute per mile pace- more of a brisk walk but the course was hilly. Then after the Athenians upset the Persians he ran from the site of the battle, the plains of marathon, to Athens to warn the city that the Persians  fled Marathon and were hoping to rush to Athens  by sea and attack again. This time Phidippdes was in a more of a  hurry and ran the 26 miles distance in about 3 hours or about a 7 minute per mile pace and died on arrival.

At least three different  clinical presentation have been deemed to be Phidippdes Syndrome (P syndrome)

James O' Keefe commented on the death of a legendary trail runner, Micah True AKA Caballo Blanco, who died on a run and at autopsy was said to have a dilated cardiomyopathy saying that this was an obvious case of P syndrome s if there were no other causes of a dilated cardiomyopathy and that P syndrome has some diagnostic,generally agreed upon differentiating features.

Dr. Justin Tivaxx reported a case of a 50 year old  half  marathon  runner who collapsed with and was resuscitated from ventricular fibrillation some 12 hours after a running workout. His MR showed a focal area of late gadolinium enhancement in the basal anterior septal said to not be a coronary artery distribution. This was suggested to be the focus of the previous ventricular fibrillation episode. Dr. Tivaxx presented in his paper an "hypothesis" concerning pathophysiology relevant to endurance exercise cardiac dysfunction and also said "considerable research is needed for to mature into an accepted understanding in clinical practice." Amen, yet some investigators write as if P. Syndrome is an accepted entity and that the general medical audience knows what it is.At the point I don't see how.

A third condition sometimes refers to as P syndrome is the putative clinical entity of exercise induced ARVD.At least two group of researchers  have presented some evidence that such an entity exists.



So what is P syndrome, a dilated cardiomyopathy in a endurance athlete, a runner with an area of delayed gadolinium uptake or  a person with ARVD who exercises.?

Tuesday, September 26, 2017

Does long time aerobic exercise mitigate age related heart stiffness by altering titin isoforms?

Well, with a topic title like that, I expect an overload of hits.

In 1977 Maruyama described a muscle protein that he named connectin, now more commonly referred to as titin.

Titin is responsible for the passive elasticity of muscles and to prevent muscle over stretching. It is the largest protein in nature and is appropriately  encoded by the largest human gene,  the TTN gene. The titin molecule is the length of the sarcomere stretching from the Z line to the M band in the sarcomere.

Lalande et al (1) describe the link between exercise and titin's properties, specifically passive stiffness.The are a number of titin isoforms, some are long and thin associated with less stiff muscles , while others seem more likely to be related to stiffer muscles.. The authors present animal experiment data  that suggest titin stiffness  can by modified by such post translational mechanisms such as  phosphorylation.

They suggest that "cardiac passive stiffness (k )may be a unifying mechanism "that links the benefits of long time aerobic exercise and the negative cardiovascular effect of sedentary lifestyles.

They review the work of the Dallas group (2) that demonstrated long time endurance athletes have ventricular stiffness similar to that of young sedentary subjects and their meta-analysis (3) that suggested that exercise levels above the US guidelines ( which is 150 minutes of moderate level exercise per week, or 500 Met minutes per week) significantly reduced the risk of diastolic heart failure presumably by mitigating the age and inactivity related increase in cardiac stiffness,

They review animal models that demonstrated exercise induced changes in cardiac passive stiffness that may be related to alterations in titin. To date there are no human data demonstrating that relationship but perhaps post translational alterations in titin offers a mechanism by which endurance exercise maintains cardiac compliance.Anyway it is nice to think so.


1) Lalande, S et al  The link between exercise and titin passive stiffness.Exp Physiology 2017 p 1-12

2)Arbab-Zadeh, A Effect of aging and physical activity of left ventricular compliance. Circulation 110,1799

3)Pandey,A Dose-response relationship between physical activity and risk of heart failure: a meta-analysis. Circulation 132 ,1786








Will the new war on opioids make patients with pain collateral damage.

Warren Meyer who writes the blog Coyote got it right. He said in part in commenting on Arizona's governor Ducey's announcement of guidelines regarding opioid control:


"Consider that many legitimate users will need more than the legal maximum dosage to control their pain, and thus the issue becomes whether we want to essentially torture innocent sick people by forcing them to remain in excruciating pain in exchange for (possibly) reducing the number of accidental deaths from abusers of these drugs (I say possibly because over the last 40 years the government war on drugs has had such a super stellar track record in reducing narcotic usage)."


CVS Caremark in getting in the act as well with more of their nanny-style pharmacy practices.Their "opioid utilization management" plan includes in part:

 This program will include limiting to seven days (the Arizona guidelines mandate 5 days) the supply of opioids dispensed for certain acute prescriptions for patients who are new to therapy; limiting the daily dosage of opioids dispensed based on the strength of the opioid; and requiring the use of immediate-release formulations of opioids before extended-release opioids are dispensed.

Who would know better how much pain pill to prescribe and at what dosage than a large pharmacy-pharmacy management company aided by guidelines from the CDC , an organization in which one is unlikely  to find many folks who actually treat  patients for pain or anything else for that matter.

If the results of the decades of the war on drugs offer any forecast of the success  of this latest surge it may be well be that there will be significant collateral damage to the patients who most need pain control.







never should have made pain which is a symptom into a sign

Monday, September 25, 2017

Sadly we will not get to see how fast Ed Whitlock could run a marathon at age 90.

This year the legendary marathoner Ed Whitlock died at age 86  on March 13 2017 of prostate cancer.

Famous in the running world Whitlock at 72 was the first at age 70 or older to run a marathon is less than 3  hours . What I find perhaps most amazing was the fact that his running speed in marathons changed so little in the age range when typically  a person's  O2 max decreases rapidly.See  ref 2 below for description of how the decline in aerobic capacity accelerates with age which seems to contradict the literature than has shown a constant linear decline until about age 70 at which time a more rapid descent appears.

At age 70 he ran a 3:00. 23 marathon and at age 76 he ran 3:04.53 and at 80 he ran a 3:35 54.Over a six year period beginning at age 70 his marathon time decreased only about 4 minutes- a time difference easily attributable to varying weather-temperature and wind- and terrain differences over a 26.2 mile course or an extra bath room break.

Physiological testing was done on Whitlock at age 81 and his measured  02 Max was 54. This , as best I can find, is the highest recorded value for a man in his eighties.  Earlier, Karlsen (3) reported a value of 50 in an 80 years old Norwegian in 2015.

Trappe et al(1)studied nine  80 years old endurance athletes ( they had exercised regularly for fifty years) and found their O2 max to be from 34-42.

 The authors  reviewed data from the literature and reported that in a total of 195 non athletic  men   in their  eighties the measured  O2 max  ranged from 17 to 25.

One can speculate that Whitlock would have been able to run at least a sub 2:10 ( and probably better) marathon  in his late 20s or early 30's as his 02 max would have probably been in the 80s which is the range measured in the typical world class marathoner.

While speculation about what some folks who are far out on the normal curve of aerobic capacity are able to do is interesting what can the typical,healthy non-lifetime athlete in his/her eighties do physically. Here we are talking about people whose V02 max ranges from 17 to 25.

They should be able to finish Stage 1 on the Bruce protocol treadmill tests as this is thought to require a 17.5 02 uptake and be roughly comparable to a 15 minute per mile walk. Some would be able to actually finish Stage 2 which corresponds to a 15 minute per mile run.  (It requires only 70% as much 02 uptake to walk a fifteen minute mile as it does to fun a mile in fifteen minutes.)According to the data from the CDC and ASM ,walking at less than 5 mph , golfing and ball room dancing would  well be in the range of activities easily done by folks in this aerobic capacity range as well as light house work and all activities of daily care.


1)Trappe,S et al New records in aerobic power among octogenarians lifelong athletes. J.A. P 2013, 114 3-10

2) Fleg,Jl Accelerated longitudinal decline of aerobic capacity in healthy older adults. Circ.2005;112;674-682

3) Karlsen T. How to be 80 years old and have a v02 max of a 35 year old.Case reports in Medicine vol. 2015. id no 909561

Friday, September 15, 2017

The new "medical professionalism"-the dogs bark and the carvan moves on

Five years ago a push back to the new medical professionalism was a frequent topic on the medical blogs.Now I hear or read little about it. On several levels it seems to be a fait accompli as least in academic writings and in appropriate politically correct speech. How practicing  physicians think about may be another matter.

I was reminded of one of my earlier blog postings by a letter from  CVS CAREMARK who wanted to be sure that I was still taking my BP meds as their records indicated that I had not refilled my prescription on time.

The origin(s) of the phrase " The dogs bark but the caravan moves on " is unclear, but the point is that the barking did not significantly impede the caravan on its journey. I suspect out barking did little.

I repeat a lighted edited version of a posting I offered 5 years ago in the hope that interest may be rekindled and to not let folks forget about the chilling  philosophy expressed the book "New Rules".  Some of the links may well be broken by now.


"
Kudos to Doug Peredina  at the blog roadtohellth with this commentary on medical nannies,the activities of CVS Caremark alone those lines and the broader topic of the problems with the new medical professionalism, also known as the "new ethics", a topic of considerable concern to me and one about which I have ranted repeatedly.See here and here.

Dr. Peredina discusses a lawsuit filed against CVS . Dr. Troyen Brennan is the CMO and executive vice-president of CVS Caremark. The following is a quote from the book "New Rules" which was written by Dr. Brennan and the current head of CMS Dr. Donald Berwick. They are discussing the physician patient relationship and say the following:

"Today, this isolated relationship is no longer tenable or possible… Traditional medical ethics, based on the doctor-patient dyad must be reformulated to fit the new mold of the delivery of health care...Regulation must evolve. Regulating for improved medical care involves designing appropriate rules with authority...Health care is being rationalized through critical pathways and guidelines. The primary function of regulation in health care, especially as it affects the quality of medical care, is to constrain decentralized individualized decision making.”

In 2007,Dr. Brennan,then the executive vice president of Aetna cowrote an article in JAMA entitled "Managing Medical Resources. A return to the medical commons" which I blogged about ( see here) and I said in part:

"They speak of an abstract hypothetical " medical commons" and how the current emphasis by the physician on the welfare of the individual patient will spoil the commons much as the farmer who selfishly grazes his cattle on public land without regard for depleting the resource will destroy the resource.Physicians are implored to "reconstitute the medical commons" and think in terms of resource conservation and allocation so at the end the greatest medical good can be done for the greatest number of patients.They admit there is not currently such a commons. There never has been so I am unsure how a return is possible."

With this increasing constraint of decentralized individualized decision ( translation-individual docs advising individual patients about a course of action) someone else must make those decisions. Do you think the folks at insurance companies and pharmacy management companies might enjoy that role? Isn't it interesting that the head of CMS and the vice-president of a pharmacy management company share the same view of the "proper"role of the physician?

Also kudos to DrRich at his blog, which sadly is no longer active, Covert Rationing Blog with this thoughtful and important criticism of the new medical ethics, in which the traditional physician patient relationship with its fiduciary duty of the physician is being replaced with a nebulous duty to society . Also DrRich-in his real life persona of Dr. Richard Fogoros- hosted a discussion on Sermo which from my vantage point was well received and he did an admirable job in fielding a variety of questions. It is instructive and worrisome that a number of the physicians writing in had not even heard about the New Professionalism. If you have not, go here to read about it in the original.

Also kudos to Dr. Beth Haynes at the blog Blackribbonproject for this entry concerning various aspects of the attack on the traditional physician-patient relationship.

This important topic deserves all the attention it can get.

Saturday, September 02, 2017

ESPN football commentator quits-Football too dangerous

I have blogged aabout head injury and football several times. What a former player and now former TV football analyst,Ed Cunningham had to say has much more limbic valence.

I refer to what he wanted to say to some football coaches after one of the more meaningless post season Bowl games after watching one the QBs being repeatedly pummeled.

Paraphrased - Dudes, what are  you doing- these are just kids.

http://bleacherreport.com/articles/2730459-espn-analyst-ed-cunningham-resigns-due-to-concern-over-head-injuries-in-football?utm_source=cnn.com&utm_medium=referral&utm_campaign=editorial

H/T CNN

addendum 9/4/17 Another quote I had to add. This from a George Will column regarding NFL football. He quotes college football coach Jim Harbaugh who said [football]" is the last bastion in America for toughness in men". Will added ..that thought must amuse Marines patrolling Afghanistan's  Helmand province.

Tuesday, August 22, 2017

Coarse and fine grain distinctions in medicine

 



Coarse Grain,Fine Grain distinctions in Medicine.

Jacob Bronowski in his "The Origins of Knowledge and Imagination" speaks of  what he considers a basic problem in the brain's mechanism namely how to  achieve fine  discriminations with a coarse apparatus.Further, he says that in many ways "about all" human problems..in science or in literature..center around the same problem.How do you refine the detail with an apparatus which remains at bottom coarse and grainy?"
 
Consider the randomized clinical trial (RCT) currently thought to be at the apex of the hierarchy of  the mechanisms we use to find  medical truth.We are left with aggregate data, groups numbers that are relevant , strictly speaking, to patients having the characteristics of those in the trial but is freqently extrapolated to include many other patients.

Compare this grainy-ness with the progress made in the following example.
Consider the use of MRI in a patient with the clinical picture of optic neuritis.
The finding of white matter abnormalities of a cetain type provide valuable information regarding likelihood of progression to multiple sclerosis. The coarse grain category of optic neuritis has been fine grained a bit by sorting out those patients with a high risk of subsequent development of multiple sclerosis.

But fine tuning is not a feature the RCT. We can break the aggregate data into sub groups but we loose power to see differences and at the same time we increase the likelihood of Type I errors by cranking out many comparisons. So basically the RCT is a coarse grain apparatus and cannot get any finer, remaining coarse and grainy.
 
One way to fine tune the aggregate data is to determine the relevant pathophysiology.The example of TPMT deficiency comes to mind. Before the details of this deficiency were mapped out, we could only say that a certain percentage of children treated with a thiopurine type drug developed serious bone marrow failure. Once we learned what the pathophysiology was , testing could be done to see who comprised that percentage and the coarse grain became fine.
 
 
Disclosure: This is a lightly edited and revised essay that I originally posted years ago on a now defunct blog.

Monday, August 21, 2017

The perfect country-western song -the perfect medical article

The Perfect Country and Western Song-The perfect Medical article
In the David Allan Coe song, "You never even called me by my name" we are told some of the essential components of the " perfect" country song. Things that should be mentioned are: trains, trucks, mama,prison and getting drunk.
There are also essential components of the perfect medical article and should appear in the introduction and/or the discussion and summary sections. They include: mention of evidence based medicine (this is required even if the article has little if any evidence actually presented), mention of the disease at issue being "a public health problem"(saying it is common is not enough), a word about "quality" and perhaps most importantly stating that "we must be good stewards in this era of scarity of medical resources ". Unlike the essential elements of C&W music, which are timeless, the medical article sine qua nons are of recent vintage.
Non C&W fans may claim that tired cliches populate some country songs. It could be claimed that "floating abstractions" and politically correct comments are the fluffy fillers of the perfect medical articles.

Sunday, July 30, 2017

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 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.







Tuesday, June 13, 2017

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 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)

Monday, June 12, 2017

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

Monday, June 05, 2017

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.

A new 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 .

Friday, May 12, 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