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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 ...

Thursday, October 19, 2017

Biggest changes in medical practice in 40 years-loss of physician autonomy and physician 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?

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  observed in the fit person from that if  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

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. 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 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 about 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 approximate prediction equation relating the estimation of a person 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 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.

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 statin 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)  suggested 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 is conflicting data and the magnitude of the putative risk is a open question]

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.

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.



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

Tuesday, May 09, 2017

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

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

 How so?

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

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

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

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

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

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

Sunday, April 23, 2017

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

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

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

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

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

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

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

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

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

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

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

Friday, April 14, 2017

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

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

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

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

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

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

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

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

Thursday, March 23, 2017

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

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

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

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

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

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

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

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

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

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

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

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

Sunday, March 19, 2017

Do low levels of cardiovascular fitness predispose to cardiac hypertrophy?

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

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

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

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

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

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

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

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

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

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

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

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

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

Wednesday, February 22, 2017

Cardiac remodeling -some old and new theory and some data

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

The story goes like this:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Wednesday, February 01, 2017

Parameters on Utopias-something politicians don't want

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

"Economics put parameters on Utopias".

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

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

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

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

Professor Gruber has been late in providing some parameters .

Monday, January 30, 2017

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

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

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

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

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

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

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

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

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

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