You are only as young as your legs

A high school friend once told me that one of his football coaches told him that wind sprints were important and you were only as young as your legs. I think that this is a physiological insight on the same lofty level as Woody Allens' maxim (1).  The time honored wind sprints have apparently morphed into high intensity interval training which is supposed to be good  for things ranging from improving glucose tolerance to improving 02 uptake and exercise tolerance in heart failure with or without reduced ejection fraction.

The stylized story about muscle loss with aging can be told like this:

From age 40 to age 70 there is 8 % per decade decrease in muscle mass and a 10-15 % decrease in muscle strength. Around age 70 the rate of decline for both increases so that there is a 10-15% decrease in muscle mass per decade and a 25 to 40% decrease in strength.

There is a greater loss in the fast twitch or type 2 fibers with some of the  fast twitch fibers being replaced by type 1.This observation helps explain the greater loss in strength relative to muscle size as type 2 fibers are larger and can generate more force and to some degree they are being replaced by smaller less forceful type 1 fibers.

Decreasing levels of exercise for various reasons accompany aging but not  all  muscle loss can  be blamed on decreased activity. There is to varying degrees loss of the anterior horn cells in the spinal cord which seem to target horn cells that serve type 2 fibers. as well as multiple other changes in muscles that seem refractory to continuing exercise.

 So why should we call the numbers stylized? The estimates of percentage per decade losses are of course averages  which are largely derived from longitudinal studies  and individuals have been noted to vary greatly. Further one study showed that various sample sites from the lateral thigh muscle  which investigators prefer for biopsy studies on muscle fiber type often give rather discrepant fiber distribution counts.




1) As you get older everything that  should be soft gets harder and everything that should be hard get softer. We can all think of examples.

Which master should physicians serve-Dr.Martin Samuels' thoughts

I have written before about what I believe the wrong headed and dangerous views expressed in the Physician Charter.See here.

http://mdredux.blogspot.com/2016/07/is-new-professionalism-and-acps-new.html

Dr.Martin Samuels ,Harvard neurologist, master teacher and lecturer,  expresses his views regarding the issue of who does the physician serve. Which master? See here.

Is the patient or "society" the master? Dr Michel Accad dissects  the related dangerous  notion of population medicine here.


h/t Notes from Dr. RW blog  See here.

Inadequate warfarin dosing may be worse than no warfarin in regard to stroke severity

Sokomoto et al (1) investigated the relationship between adequacy of warfarin dosing and severity of stroke in patients with atrial fibrillation. Inadequate was defined as INR less than 2.0 ( less than 1.6 for patients older than 70 years.)

They studied 477 patients with atrial fibrillation (AF) and acute ischemic stroke,53 of whom were undertreated. Inadequate or insufficient dose of warfarin was present in 53 patients and the odds ratio for a severe stroke was 2.7. The numbers in the study were fairly small but  other research had demonstrated a similar pattern.

The authors suggested that underlying pathophysiology or pharmacologic explanation related to the vitamin K dependent anticoagulant protein,Protein C. Protein C levels decrease earlier and with lower doses of warfarin than do the other vitamin K dependent clotting proteins. So early on in warfarin therapy there may be a procoagulant effect. This was why  in the not-too-long ago-days physicians would treat thromboembolism with a few days of heparin along with the warfarin. Too little warfarin may be more of a pro than an anticoagulant medication.

So we have still another reason why the newer oral  direct acting anticoagulants are better than warfarin.




1) Sakamoto, Y et al, Insufficient warfarin therapy is associated with higher severity of stroke than non anticoagulation in patients with atrial fibrillation and acute anterior-circulation Stroke

Circulation Journal Official Journal of the Japanese Circulation society. 2017 December.

All Left bundle Branch Blocks are not the same

The vast majority of patients with an EKG pattern of LBBB have structural heart disease,that is myocardial disease as opposed to disease only involving the conduction system which  is found in a very small minority-usually estimated to be about 1 % of LBBB cases.

It has been  recognized that some patients with isolated or lone LBBB will over a variable period of time develop a cardiomyopathy.The few clinical reports of  this condition suggests delays of up to over twenty years and often dramatic resolution of heart failure with cardiac resynchronization therapy. ( ref 2)

LBBB is associated with  inter-ventricular and intra-ventricular loss of synchrony, the later being more deleterious to cardiac function. Normally the various areas of segments of the left ventricle contract in sync. In LBBB the typically described or stylized  pattern of abnormal septal motion is : there is early contraction of the septal wall with concomitant bulging of the lateral left ventricular wall followed by late contraction of the lateral wall and bulging of the septum.The delayed ventricular contraction is followed by delayed relaxation of the left ventricle.


Han et al  ( ref 1) using tagged cine cardiac MR described 2 different patterns of abnormal septal movement in patients with LBBB.Interestingly in 2 of the  10 patients there was no septal dyskinesia at all. In some cases ( 50%) of LBBB there was dyskinesia of the entire septum while in others only the anterior septum was dyskinetic.This may at least partially explain why some patients with LLLB have little if any exercise intolerance over many years while other notice a decrease in exercise capacity soon after the onset of LBBB as was the situation in my own case and two others with whom I have had blog level correspondence.


Also animal experiments inducing LBBB have shown a rapid and often significant decrease in left ventricular function soon after the onset of LBBB.Perhaps the key is the presence or absence of the normal left to right activation of the interventricular septum and the degree to which conduction across the septum is delayed.The abnormal septal movement is the basis for the echocardiographic finding of "septal flash"

Of course the real game changer element of LBBB story is the capability of His Bundle pacing to "fix" LBBB  , at least in a significant number of patients with LBBB.


1) Han Y et al Circumferential myocardial strain in cardiomyopathy with and without Left bundle branch block. J. of cardiovascular magnetic resonance .Jan 5 2010, doi:101186/1532-42.9x-12.7
full text available on line.

2) Vaillent C et al  Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J Am College Cardiology 2013 vol 61 1089

How often does the Evidence in EBM turn on statistical subtleties?

A few years ago I posted a piece about the effects of antioxidants on GI tract cancers.There was a reported small increase in Relative Risk (1.06) if one used a fixed effects statistical model but no increase if one used a random effects statistical model analysis.

Here the truth seemed to turn on the choice of statistical method used. How robust could the truth be when it depends on choices made by statisticians and importantly when experts disagree on the choice which was the case quoted above? For a critical reader to decide for himself in a rational way it seems he would have to be fairly conversant in the vagaries of regression analysis and analysis of variance which are the areas where these two competing statistical models live.

I have read that the fixed effect model in general is the one more commonly used and it is the one with lower standard errors and hence more power. I have read that in regard to meta-analysis the fixed effect model is appropriate when the data appear homogeneous and the random effects model when the data are heterogeneous. Then we run up against tests for heterogeneity in regard to which no one should be surprise if statisticians may differ as to the correct way to do that. It seems to me if I writing a paper and wanted it published and since positive studies are more likely to see the light of day in print I would want to use the more powerful fixed effects model.


It seems the deeper you plunge into the analysis of the data the less certain you may become regarding the robustness of the conclusion.But truth does not really turn on the basis of the choice of statistical technique for one meta-analysis.The results of any one study-even if that study is a meta-analysis-should not decide the issue.Prior context and biological plausibility must be taken into account.

How to survive under socialized medicine

Here is a quote which to me seems may have high titer of deep insight.(my bolding)

"In many areas of medicine, particularly those related to especially politicized areas like CVD and other "life-style" diseases, government-franchised practitioners are often dangerously ignorant of essential facts. Remember that the worst aspect of socialist medicine is that medicine as a rational science is epistemologically destroyed by eliminating the role of the doctor as a sovereign, independently thinking, professional. "

H/T to Dr. Paul Hsieh in his blog "We Stand Firm" who in turn found it in essay entitled "How to Survive under Socialized Medicine" which was re-published in another blog (ReasonPharm) which in turn credited it to a facebook entry by some one named Christian W. (Please excuse the rather lengthy attribution but I did not want to slight the person who seems to be the actual author.)

. .

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.

.  

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.

Before Obamacare it was 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.

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 of the 20 subjects  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 only  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

Cognitive dissonance and medical practice conformity and different visions

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

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

Norton Hadler wrote of this issue:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Definitions are in order.

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

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

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

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



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

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

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

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

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

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

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

The marked variability of subclinical atrial fibrillation makes risk assessment difficult

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

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

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


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


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






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

Detailed cardiac study on a group of really extreme endurance athletes

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

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

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

addendum 0ct 21 2017.Typo in headline corrected.

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

The story goes like this:

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

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

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

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

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

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

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

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



 1. Morganroth, Jet  al. Comparative left ventricular dimensions in trained athletes.Ann Int Med. 1975,82(4), 521-524
 2. Spence,A et al A prospective randomized longitudinal study of left ventricular adaption to endurance and resistance training in humans. J Phys 2011 589, 543
 3.Brinker, SK et al. Association of Cardiorespiratory Fitness with Left Ventricular Remodeling and diastolic dysfunction. JACC Heart Failure.Vol 2, no.3, 2014, p238

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

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

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

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

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


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

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

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

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

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

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

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

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


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