Featured Post

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, May 16, 2019

Does a high coronary calcium score in long time endurance athletes mean greater mortality

Another article (2)  has  been published regarding the proposed relationship between high level endurance exercise and coronary calcification.

 We get this comment from the chief science officer and CEO of the Cooper Institute , Dr. Laura DeFina :

" The key question addressed in the present study was whether the presence of a high CAC associated with high levels of exercise training as typically practiced by masters marathon runners is associated with greater mortality.For this question,the answer is clearly no"

During times when I am influenced by Lily Tomlin's observation (1) I tend to think - perhaps unfairly-of studies such as these as coarse-grain,multi-comparison, big "n" small "RRs" fishing trips.

It is big n  study with 21,758 men followed for about ten years. The significance of n size is that with large numbers,small differences may be statistically significant but not clinically important. The point of saying multi-comparison is that sometimes researchers will do many regressions that may or may not be mentioned in the article searching for a p value of statistical significance. ( I ,of course, am not accusing authors of this article with that practice.)This article cannot be considered fishing as earlier work has suggested that high or very high levels of endurance exercise are associated with more coronary calcification but no increase and possibly a decrease in cardiac disease mortality.This article seems consistent with that notion.

We also get this quote from Dr. Carl Lavie : " Despite the fact that this type of high volume physical activity and exercise may promote calcific coronary atherosclerosis, it appears to still be associated with safety and possible lower mortality risks" Dr. Lavie has written several articles with Dr. James O'Keefe arguing that some relatively low level of exercise described as "excessive" would increase one's risk of death but has subsequently softened views what is excessive.

The analogy with the more potent statins and more coronary artery calcifications and lower C-V mortality seems obvious



1) Lilly Tomlin: No matter how cynical you become its never enough.


2)DeFina, LF et al ,"Association of all cause and cardiovascular mortality with high levels of physical activity and concurrent coronary artery calcification. JAMA Cardiol 2019 4 (2)174


Saturday, May 11, 2019

Is it possible for experts to determine objective high value health care

Is value objective or subjective?

A common, though oversimplified and exaggerated view,  is that Adam Smith was the father of economics. His views were published in 1776 in his Wealth of Nations.He along with several other early giants of classical economists,David Ricardo,John S. Mill, promoted the Labor theory of value. Karl Marx continued that line of thinking in 1867 in his magnum opus Capital  in which he said " If a pair of shoes usually takes twice as long to produce as a pair of pants,for example then..the competitive price of shoes will be twice the price of pants."

Lawrence H, White , in his book The Clash of Economic Ideas talks about what he describes as the fundamental flaw in the labor theory of value is "its supposition that the price of a good reflects an intrinsic feature of the good,...rather than something in the minds of its buyers". The belief was that input costs determines the selling price rather than the reverse.

It was not until 1871 that the labor theory  of value was displaced by what is known as the subjective or marginal utility theory of value. Karl Menger one of the three co-founders of this idea,who worked independently, said in his Principles of Economics , "Goods always have value to certain economizing individuals and this value is also determined only by those individuals."

Simply put the value of a good or service is the subjective evaluation of the buyer.

In fact,it is this subjective value that underlies exchange-Fred values the apple more than dollar he give the grocer who in turn value the dollar more than the apple.Both party typically thank each other as exchange is mutually beneficial.


So since the late 19th century economists of almost all stripes have agreed that value is subjective.
If this is the overwhelming consensus views of economists what is the rationale or justification for organizations such as the American College of Physicians and others to  claim to be able to determine which medical procedures and treatments are "high value". Are they claiming that value is objective,that they can determine scientifically the real value,and further determine which value are high enough to merit the designation "High value"

First how is value determined by health outcome experts and how is a value determination judged to be "high". Is the process objective and scientific all the way down or is it the case that at some point someone's subjective value is inserted .

Through clinical research it is possible to determine if the outcome of treatment X versus treatment Y is better in terms of survival.So one could talk about life years saved by treatment X versus treatment Y-this is clinical effectiveness research.X is better-more effective than Y in terms of simple survival. But to determine value cost has to be injected into the analysis.How much did X cost versus how much did Y cost.,then one could look at life years saved per dollars and compare X  and Y in that way.

Obviously  years lived  per se is not the only relevant outcome to consider.How one lives (pain,mobility,level of cognition etc) are all important and those and other elements are lumped under the heading "quality of life" (QOL). Measuring quality to transform life years into quality adjusted life years is a difficult and ambiguous slippery  area and we will defer a discussion about whether than can ever be done for later but for discussion we'll assume that something called quality adjusted life years(QALY) can measured. (I seriously doubt that it can be measured  because in part I do not believe you can aggregate quality of life.I doubt that it is meaningful to add Frank and Fred life quality of life and transform that some aggregate of quality years.)

After the QALY are determined for procedure X and Y then in theory one can sum the cost of the two procedures and then derive a ratio of QALY s per dollar spent. Ignoring for the moment the difficulties and ultimately the arbitrary nature  of teasing out cost from charges in the context of what is certainty not a free market unencumbered by price control  but rather one whose costs exist behind a veil of various variable negotiated prices between providers groups and third party payers with an even more opaque series of subsidies and discounts.


When you brush past the bewildering display of statistical artifacts and step to view the overall landscape what you see is another utilitarian procedure. Some new wine is there but the bottles are stamped underneath with the imprint  "utilitarian analysis" A joint resurrection of Benthams "greatest good for the greatest number." in the form of a cost benefit analysis done in the tradition of and with the tools of Neo-classical economics.




Tuesday, April 09, 2019

Has the movement to debase medical ethics become a done deal now


In 2013,  when I posted the essay found below in a slightly revised version found ,there was still considerable resistance to the "New Medical Professionalism" which had been introduced in 2002 by the American College of Physicians and the European Federations of Internal Medicine. and published in the Annals of Internal Medicine in an article entitled  "Medical Professionalism in the New Millennium: A Physician's Charter." Numerous medical blogs protested and there was some public debates.Now I find little comment or concern about what I believe was a effort to destroy traditional medical ethics.
Here is my earlier essay entitled "The Great Linguistic Coup of 21Th Century Medical Ethics"

"George H. Smith in his book "The System of Liberty" in the chapter entitled "Liberalism,Old and New" discusses how the concept of liberalism and its advocates were victims of a linguistic coup in the latter part  of the nineteenth century.

 The classic liberals considered freedom as the absence of coercion.They championed   limited government whose function was to secure the rights of individuals.Enter a group of thinkers who proposed a " new liberalism" , one that would,in their view, correct this inadequate,limited definition of freedom.To the newcomers liberty without equality was freedom in name only  and true freedom involved equal opportunity and power to enjoy one's life. They wanted to replace the idea of "negative freedom" of the classical liberals with what would become  the focus  of  the welfare state.True freedom in their view was more than mere removal of compulsion or coercion.  The new liberals were paternalistic and believed  the state should do much more than secure the people from internal and external predators but rather protect them from the effects of their own uncoerced actions.The classic liberals defended their position in part by asserting that the new liberalism was old wine in new bottles, with the wine being advocacy for a paternalistic government.The new liberals continued to dispense rhetoric that seemingly supported liberty but they had redefined the word liberty.

The new liberals won the day and the old or classic liberals lost much influence  but re-appeared in the 20th century with a new label, libertarian. The new liberals were simply known as liberals and later referred to by some as progressives.

I argue analogously that the traditional ,classical medical ethics and its advocates ( physicians themselves) were victims of a similar linguistic coup. Throughout most of the 20th century and earlier the core of medical ethics was primacy of patient welfare and respect of the autonomy of the patient,the later gradually replacing an older paternalism of medicine.Physicians were considered to have a fiduciary duty to the patient.

At the end of the 20th century and the early years of the 21th century a new medical ethics emerged,one in which -while  its proponents claimed nothing had really changed-there was a radical sea-change in regard to the duties of the physician.This was accomplished by nothing more rhetorically solid based  or intellectually justified  than a simple gratuitous assertion.The notion of social justice was simply declared to be part of medical professionalism and medical ethics.The degree to which this bogus concept has been accepted and endlessly repeated in medical publications is a tragic shame.The victims of this linguistic coup are the physicians themselves but to a greater degree the patients are the real losers as they have lost their advocates at a time when they may need them the most."


Monday, March 25, 2019

Will the quality crusade be the final corruptor of the medical record?


 File this under "The corruption of the medical record".

  The topic today is the " After visit summary"(AVS).

In my case this was a collection of mistakes,misstatements and falsehoods all neatly printed out in a manner that  may facilitate the physician getting credit for various quality measures.  After reading the AVS I asked myself do I really want a serious medical problem that I may develop to be  overseen by someone who signs off on such a pile of crap.

Recently I saw my primary care physician (PCP) for an annual check up.

Several aspects are worth a blog entry. Today it is the "After visit Summary" (AVS) which was available the next day on the practice's web site .Actually it is the hospital web site's patient portal,
This group of internists is "hired" by the hospital under the guise of being a practice group somehow affiliated with the hosptial.

Mt particular  AVS is a sleek  , multicolored document replete with little icons by such entries as your weight (icon of a dial),pulse ( icon of a valentine style heart). etc.

Under the "Today's Visit" we see small head shot photo of the physician and a listing of the addressed issues.This was a collection of mistakes,misstatements and outright falsehoods which are now part of my permanent record.

I was said to have atrial fibrillation. I do not have AF. The diagnosis of AF was erroneously placed on the  chart by the EP clinic but was later ( 8 months) corrected and removed from by problem list. I mentioned to my PCP that do not have AF and that the earlier entry was the results of a error in the EP clinic.This was the second time I explained about the diagnosis of AF to him and his scribe.

I was also said to have "osteopenia of both hips" .WTF. I have had no imaging of my back or hips at that facility .

I was said to have "hypercalcemia"  and "hypergammaglobulinemia "When  first seen by this PCP one issue was a metabolic profile done by my previous PCP that was stuffed with errors, namely elevated, calcium,elevated K and elevated globulin ( all likely the results of hemolyzed blood sample). These were all repeated and found to be normal but some how the diagnosis of hypercalcemia and elevated globulin level remain.

Nevertheless, on my AVS I was told that those issues were addressed.

What is the AVS all about? it is about "meaningful use".It is one of the eligible professional meaningful use core measures. It all began in 2009 with the HITECH act that was designed to "encourage physicians" to use an EHR.There were monetary carrots and sticks. Neither of which seem to me to be much more than chump change particularly after considering the care and feeding of a EHR .

Kaiser Health News and Fortune Magazine have a detailed article describing what a utter disaster the EHR has become.The title is "Death by A Thousand Clicks"










Monday, March 18, 2019

Recent changes in AHA/ACC atrial fibrillation guidelines

One of my favorite EP cardiologists, Dr. John Mandrola,gives his thoughts regarding the 2019 focused update on  atrial fibrillation (AF)  from the AHA/ACC ,Heart Rhythm Society task force.

Here are some of the highlights and the entire article by Mandrola (full text is available) is recommended.

Aspirin is no longer recommended for low risk AF patients. As Mandrola says , just like that, without much of an explanation .

Both the FDA and CMS have approved percutaneous left atrial appendage closure with the Watchman device  and the panel gives it. a class 11b recommendation. Apparently, the panel did not see fit to comment on the 4% risk of device associated thrombosis reported with Watchman.

DOACs now is  officially preferred over warfarin. Not mentioned by Mandrola is the observation that the fewer strokes with DOACs versus warfarin is driven by the fact there  are fewer hemorrhagic strokes with DOAC while there is little if any difference in the number of ischemic strokes.

The task force stated that female sex alone is no longer considered  a risk factor  for stroke in an AF patient per se.

The guideline writers gave a class 11 b (additional studies are need-procedure may be considered) recommendation for AF ablation in heart failure.Mandrola believes the data supporting AF ablation in HF patients is sufficient for the panel to have given a higher recommendation quoting the positive results of the CASTLE-AF trial that showed a 12% absolute risk reduction in death and in heart failure admissions in the ablation cohort.


Mandrola shares my views on the CHA2DS2VASc score . It is "simple to use , but at its core distills a decidedly continuous risk for a future event down to an integer." He references D. R. Quinn's 2017 review of 34 studies of AF ( reference can be found in Mandrola's review) that illustrate the large variation in the baseline risk of stroke in untreated AF patients. Quoting Mandrola " Translation: We have no idea of the risk in untreated patients.",and yet every day cardiologists and other docs crank out the CHA2DS2VASC and mater-of-factly tell their patient that they have x% annual risk of stroke and suggest how much that risk will be reduced by oral anticoagulation.


I have written about Quinn's study before and quoting from Quinn's article "' The majority of cohorts did not observe stroke rates that would indicate a clear expected net clinical benefit for anticoagulating AF patients with a CHA2DS2-VASc score of 1 or 2."

Monday, March 11, 2019

Left anterior fascicular block-comments on epidemiology and ventricular function

Left anterior fascicular block (LAFB) was previously known as left anterior hemiblock (LAH) .The earlier designation can be attributed to the widely accepted   writings of Maurico Rosenbaum whose work ( 1967) seemed to indicate that in humans the left bundle divided into a left  and   a right branch.

This "trifascicular" concept (right bundle branch and the two branches of the left bundle) was widely accepted and persisted  even though  work in 1972 by Demoulin and Kulbertus  make it clear than there was also frequently a septal branch of the left bundle and more importantly that the anatomy of  left bundle is much more complex that simply consisting of two (or three) branchs, i.e. more of a spiderweb or fan.There is great variation in the interconnections and  in few of the 49 careful dissections by Demoulin can a simple pattern of 2  or even 3 fascicles be seen. (the patterns can be seen on page 283 of reference 1, full text is available)

Realizing that all models are wrong but some are useful ( George Box, circa 1978),it may be that the LAFB model has some value.

LAFB is diagnosed on EKG when the frontal plan axis is between minus 30 and minus 90 with QRS duration less than 120 msec and the patient does not have an inferior wall myocardial infarction,LVH  or WPW syndrome.So, typically LAD equals LAFB in the EKG reading context.

Mandyam et al ( 2) from UCSF studied long term outcomes in patients with LAFB who at the beginning  of the data collection did not have evidence of heart disease. Using data from the Cardiovascular Health Study (CHS), they compared 39 subjects with LAFB with 1625 patients without LAFB over a 19 year period.The average age of the control groups with 71.4 and the age of LAFB group was 74.9

They report LAFB was significantly associated with atrial fibrillation (AF) Heart failure(CHF) and death with the following p values-AF .02,CHF .02, and death .001.

This was a small  ( 39  patients),coarse grain study.The authors point out that although CHS tries to exclude preexisting disease on entry to the program hypertension or asymptomatic coronary artery disease may have been missed. The authors referenced no corroborating studies .

This UCSF article received considerable medical press coverage in part as it offered some suggestion that the previously accepted notion that LAFB was a  "benign" finding might not be correct but within a year their findings were seeminly contradicted by research from Copenhagen.

JB Nielsen (4) studied the cardiovascular outcome of 222,227 subjects with a 5.7 year  follow-up period. They did find a statistically significant correction between LAFB and AF, HF and both all cause and cardiovascular mortality. However, after adjusting for age and gender only the all cause risk retains statistical significance.

Quoting the authors: "current EKG definition of LAFB is not always clinically important marker of cardiovascular morbidity and mortality beyond what can be expected by age and sex."

What is the effect of LAFB on left ventricular function?

Leeters and colleagues from The Netherlands studied 28 patients  with RBBB,LAFB and heart failure with 2D speckle tracking regional strain measurements as well as healthy controls and 28 LBBB patients. This is not a study of "lone LAFB" as the patients had RBBB and HF and a number of them had scars detected by CMR. Since the RBBB per se would  not affect Left ventricular activation sequence it is reasonable to assume the delay in activation of the anterior LV is due to the LAFB.The study indicated wall motion abnormalities between the anterior wall and inferior wall of the LV analogous to the classic pattern of septal and lateral LV wall dyssynchrony characteristic of LBBB but apparently less disruptive of cardiac function.


1) Fisher,JH Hemiblocks and the fascicular system:myths and implications. J. Of Interventional cardiac electrophysiology 2018 52: 281-285

2)Mandyam, ML Long-term Outcomes of left anterior fascicular block in the absence of overt cardiovascular disease, JAMA 2014 309 (15)1587

3)Leeters IP, et al Left Ventricular regional contraction abnormalities by echocardiographic speckle tracking in combined right bundle branch block with left anterior fascicular block compared to left bundle branch block.J Electrocardiol 2016 49 (3) 353

4)Nielsen, JB et al Left anterior fascicular block and the risk of cardiovascular outcomes.
JAMA Int Med June 2014, 174(6),1001-1003











Tuesday, February 19, 2019

More data on lifelong exercisers-this time from Ball State

Scott Trappe and colleagues (1) from Ball State Human Performance lab  studied 7 women and 21 men all in their 70's who were lifelong ( fifty years or more) exercisers and compared them to elderly,apparently healthy sedentary  subjects and to heathy young exercisers (average age 25)

The lifelong exercisers exercised 5 days/week with a weekly hourly total of 7 hours. for the past 52 =/- 1 years.

Maximal oxygen uptake was measured on a maximal cycle test and muscles biopsy done to determine a "muscle aerobic profile" (MAP for short). MAP refers to the degree of capillarization and metabolic enzymes eg. Citrate synthase,B-HAD and glycogen phosphorylase  were determined by muscle biopsy in the lateral thigh.

While the MAP was the same as in the young exercising controls the 02 max  of course was not .The set of long time exercising women was small, but rounding up women who have exercisers for fifty years is no small feat.

Comparing the 02 max in young women,exercisers and elderly control women we find: 44,26 and 18 .

The authors conclude : " the data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than the more central aspects of the cardiovascular system."

The authors mention the fragility index and quote that the value for men is 17.5 ml/kilo/ min and make their educated guess about what it is for women giving 14 ml/kilo/min as the value. I am not sure why women would have a lower number since the index is corrected for weight. Folks fortunate to have values well above those numbers are said to have more physiologic reserve to withstand and survive various homeostasis challenges whose frequency is a function of age.

This index should not be confused with another fragility index which gives an indicator of how robust are the results of a clinical trial.See here for more on that.  (A clinical trial would have an FI of 1 if the hypothetical movement of one patient from the success column to the failure column would make the study no longer statistically significant ( at the p of 0.05 level)

.

1) Gries,J et al Cardiovascular and skeletal muscle health with lifelong exercise
JAP 125: 16736 2018 (full text available on line)

Wednesday, February 13, 2019

In the long run ( or ride) do runners wear out sooner than cyclists?

 Tim Noakes, the MD, PhD exercise physiologist from South Africa has suggested that perhaps many years of running and the gravity assisted  pounding might accelerate the aging process at least as regards muscles and tendons.

If that is the case, might a comparison of the decrement in performance over time between long time runners and long time cyclists be useful  tend to confirm or deny that hypothesis.

Noakes and colleagues made that comparison (see here) and things look better for the cyclists.








Tuesday, February 12, 2019

We knew all along who would be the collateral damage from the "war" on opioids

This NYT article puts faces on those who bear the collateral damage. No satisfaction from "I told you so" here

Anyone remember "Cure sometimes,treat often,comfort always."

Sunday, February 10, 2019

All cases of LBBB do not have the same ventricular contraction pattern or same response to CRT

The block in left bundle branch block (LBBB)-and this can apply to right bundle as well-may not be actually in the left bundle branch, as least as it has been traditionally described.And  the "block" may not mean complete disruption of the electrical cardiac system perhaps just a delay.Further amazingly, at least sometimes,electrical stimulation of the His Bundle can "fix" LBBB obtaining a normal QRS complex.

The traditional text book electrical  anatomical pathway is from sa node to av node to His bundle and then a division into  left and right bundle branches and then to branching purkinje fibers out to the myocardium.

Anatomical work at least as early as 1971 and physiological studies in 1977-1978 demonstrated in both the canine and human heart that the right and left bundles were actually anatomically distinct within the bundle of His.This was described as longitudinal dissociation.

It has been known at least as early as 1978 that stimulation of the his bundle can normalize the ekg pattern of LBBB and RBBB,Presumably-according to the longitudinal dissociation model - in these situations the lesion or block in the bundle  branch was in the His bundle and that stimulation distal to the lesions resulted in a normal ekg.

In other words the left and right bundles are organized longitudinally and separate within the His Bundle.So a lesion in the His bundle could cause LBBB and could be corrected by stimulation distal to the block.

The work done in the 1970s did not really apply to clinical situations  until  cardiac resynchronization (CRT) was proven effective in the treatment of heart failure in the 1990s.  About 30% of patients did not seem to respond to CRT and it was soon realized that the presence of LBBB was a favorable prognostic factor and that , in a sense it was  the impaired electrical conduction system which was the culprit that caused  mechanical dyssynchrony that could markedly impair cardiac function and in some after a variable lag period  lead to disadvantageous cardiac hypertrophy, chamber enlargement and remodeling and heart failure

Further it has been suggested ( Strauss et al ) that the  traditional ekg criteria for LBBB need to be replaced with critieria that make the diagnosis much more specific  and therefore useful in predicting response  from CRT.The QRS duration should be 0.14 seconds for men and 0.13 for women and there should be a double humped QRS either in lead i and AVL or V5 and V6 ( i.e. 2 contiguous leads) .Using the old criteria,according to Strauss, lead to overdiagnosis of true LBBB and included patients who actually had LVH ( left ventricular hypertrophy) and left anterior hemiblock). It was suggested   that patients with "true "LBBB" by EKG are the ones who are likely to benefit from cardiac resynchronization therapy (CRT).

However, results from Denmark and Pittsburgh by Dr. Niels Risum (2) indicated that the sine qua non of "true" LBBB is not necessarily the EKG pattern but rather the mechanical activation pattern ( basically delayed left ventricular activation )which they described in terms of 2D strain echocardiography and that  neither the supposedly specific Strauss criteria nor the traditional criteria   always would  indicate which patients would have that contraction pattern and  would therefore be more likely respond to CRT.See end note # 1for Risum criteria:

Risum and colleagues content that all patients with LBBB diagnosed on EKG do not have delayed left ventricular activation which correspond to their criteria for "classic" LBBB activation pattern.

Risum's work offers an explanation for  at least some of the widely quoted 30% CRT poor response rate .Interestingly, as early as 1979 several different patterns of septal movement were described on echocardiogram in LBBB.( Fujii et al )

Their data demonstrated that during a 4 year follow-up 40% of patients without the classic pattern had an adverse event (combined end point of death,need for LVAD,or heart transplant) versus 14 % in the group with the classic pattern.So since it is not 100% versus 0 % the presence or absence of Risum's classic pattern does not explain all cases of CRT failure.



 It would not be expected, on mechanistic grounds, for Bi-Ventricular pacing to improve cardiac output in patients with right bundle branch block since in RBBB the electrical activation and the contraction pattern of the left ventricle would not be abnormal.There is considerable clinical data that CRT results in RBBB are definitely worse than in LBBB; However, there may be an exception.

Rosenbaum described an RBBB pattern in which there is left axis deviation and broad slurred r waves in I and Avl which was termed LBBB masquerading as RBBB in which an argument has been made that Bi-V pacing might be on benefit.(1)


1)Auriccho, A Does Cardiac Resynchronization therapy have a role in patients with right bundle branch block.irc. Arrhymia Electrophysiol 2014 pg 532

2)Risum,N et al, Identification of typical left bundle branch block contraction by strain echocardiography is additive to electrocardiography in prediction of long term outcomes after cardiac resynchronization therapy. Journal American College of Cardioogy  2015 vol 66 no 6 pg 632

3)Fujii, J K, et al  mode and cross sectional echocardiographic study of left ventricular wall motions in complete left bundle branch block. Brit Heart Journal 1979 42 (3) 255

end note 1
Risum 2d strain echo criteria:
1)early shortening of at least one segment of the septal wall atnd early stretching of at least one segment of the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure


Thursday, February 07, 2019

Lone Left bundle branch block and increased afterload -bad combination

I have commented before on functional impairment associated with LBBB. See here.

J Aalen and colleagues  (1) see here demonstrated that  cardiac output in asymptomatic patients with isolated LBBB is very sensitive to afterload as  in elevated arterial pressure as would also occur with strenuous exercise.  (Full text is available on line,)

Dr Aalan studied the effect of increasing afterload on left ventricular ejection fraction (LVEF) in 11 asymptomatic patients with isolated ( or lone) LBBB. Afterload was increased not by exercise by increasing blood pressure (increase of 38 +/-12 mm Hg) by pneumatic extremity constrictors and handgrip exercise .

The controls subjects decreased their LVEF from 60 to 54 while the LBBB patients decreased their LVEF from 56 to 42. The increased heart rate and after load accentuated the effect of the left ventricular dyssynchronous contraction which consists of early septal contraction with bulging of the lateral left ventricular wall and delayed lateral wall contraction and bulging of the septum.

The severity of cardiac functional impairment is not reflected by the resting LVEF. Most studies have indicated at most a mild decrease. On a personal note, when I developed a LBBB my decrease in running speed was by about 20% -close to the 25% decrease in LVEF note in Aalan's paper. (decrease from a fairly comfortable 12 minute mile run  to a difficult 15 minute mile with unusual calf discomfort)

I received 2 comments on the blog post mentioned in the first paragraph from readers indicating their exercise history after LBBB onset was similar to mine.

Lone LBBB is often considered asymptomatic and  often is at rest.  A person not doing strenuous exercise would likely not notice any problem and probably for that reason many texts describe LBBB as asymptomatic. For example, Mayo Clinic Patient website -" in most people BBB does not cause symptoms " and Up to Date "LBBB can also be seen in  asymptomatic patients with structurally normal hearts."(Both accessed on 2/6/19) The key here is "with structurally normal hearts". Patients with already reduced EFs may experience significant worsening of exercise ability with onset of LBBB.




1) Aalen J  et al Afterload hypersensitivity in patients with left bundle branch block . Jan, 2018 JACC Cardiovas imaging.

Thursday, January 31, 2019

Is the link between atrial fibrillation and obesity epicardial fat?

The epicardial fat pad image on chest x-rays was long regarded as nothing more than a barely  interesting incidental finding of no clinical importance. That no longer appears to be the case.

The epidemiologic data having   established a  sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists  began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes,  and more recently  detailed scrutiny of  the role or roles  of epicardial fat to which has been assigned the ironic designation, of  EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.

At least as early as 2003 cardiac fat  acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could  possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.

Now EAT is accused of playing a role in the genesis of AF.

Dr, Mahajan and co-workers from Australia  studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left  atrium adjacent to EAT.

Author quotes:

" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "

"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"



1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.

2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128



Monday, January 28, 2019

Did a third randomized trial for PSA screening reconcile the conflict betwen the first two?

Did the third RCT settle the issue of the efficacy of PSA screening for prostate disease?  The short answer is no - that settling purportedly was   achieved by another statistical analysis. ( see reference # 2 for that) at least for a while .

There are now three large RCTs (1) that have addressed the subject.

1) the PLCO
2) The ERSPC
3) the Cluster Randomized Trial of PSA testing for Prostate Cancer.

Only the ERSPC demonstrated reduction in cancer in an "invitation to screening"  with PSA setting.

So did the two out three being negative settle the issue? Not even close.

In 2012, faced with two conflicting RCTs the USPSTF decided to recommend against screening with PSA.Then a third RCT was completed showing no difference in mortality in the PSA screened group.

So if the score was 2 to 1 showing no benefit for PSA screening why did the USPSTF recant and return to their recommendation of "shared decision making" in 2018?

 The answer seems to be that Tsodikov from the University of Michigan ( and 21 other authors from various institutions)   did some adroit statistical footwork (2) in an effort to reconcile the disparate findings. Their work appears successful with the conclusion
being that when the proper type analysis is done (taking into account mean lead time) both the PLCO and the ERSPC both demonstrated approximately the same decrease in mortality with PSA screening.
Note the original analysis did not show a benefit to screening .

So now the score is two RCTs in favor of screening with one against and the current USPSTF recommendation is for shared decision making.


1)A blueprint for cancer screening and early detection :Advanced screening's contribution to cancer control. Wender RC et al . Ca,A Cancer Journal for Clinicians, Vol 49, no 1 Jan/Feb 2019 ( This is an excellent review of screening for cancer detection in average risk, asymptomatic adults including breast,cervix,colorectal,endometrial,lung and prostate.}


2)Tsodikov, A Reconciling the effects of screening on prostate cancer mortrality in the ERSPC and PLCO trials, An Intern Med. 2018, 168 608


"Life is short,art long,opportunity fleeting, experience treacherous,judgment difficult."Hippocrates.


Sunday, January 27, 2019

Left bundle branch block -a really big deal part 2

Left bundle branch block (LBBB) is associated with a contraction pattern(s), that are dyssynchronous in regard to the pattern of left venricular (LV) relaxation and contraction.

The first "big deal " I commented on was the observation that the ventricular dyssynchrony associated with LBBB per se can lead to heart failure. See here.

The next big deal is that the pattern of ventricular dyssynchrony typical of "true" LBBB is determinative of a favorable clinical response to CRT and the presence of a LBBB EKG pattern does not necessary indicate a underlying LBBB dyssynchronous pattern.


Risum et al (1) list 3 criteria for the typical contraction pattern of a "true"LBBB
(these apply to description of a longitudinal stain curve in a 4 chamber 2-D strain echocardiogram)

1)early shortening of one or more segment in the ventricular septal wall and early stretching in one or more segments in the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure

The early shortening of the septum is recognizable on standard echocardiography and referred to as "septal flash". "Apical rocking" is another echo finding in which there is a rocking motion  of the LV apical  myocardium perpendicular to the long axis. These two findings seem to be the findings on routine echo exams that correspond at least to some degree  (possibly large degree) to the Risum's criteria from strain echocardiography and  perhaps share to some degree the predictive power as regards outcomes of cardiac resynchronization therapy (CRT).

Those patients with a ekg pattern of LBBB and these findings on strain echo are much more likely to have a favorable clinical response to CRT.

Not all patients with a typical LBBB EkG pattern have what Risum refers to as the typical LBBB contraction pattern which is predictive of likelihood of favorable response. to CRT.This seems to hold true in regard to both the standard criteria for LBBB and the newer Strauss criteria .


Quoting Risum : "It seems reasonable to believe that the main mechanism underlying the differential effect from CRT according to QRS morphology is whether a significant activation delay is present in the LV". ( my underlining)

Question: Does the presence of septal flash and apical rocking predict likelihood of success with CRT as good or better than Risum's criteria? Have the two set of criteria been directly compared? While I could find no direct comparison ,Stankovic et al (2) published data that indicated apical rock and septal flash could predict reverse remodeling with a sensitivity of 84 % and 79% and the absence of both was associated with unfavorable long term survival.

Bottom line from Risum's work is that a patient may have EKG criteria for LBBB  (either the standard criteria or the new criteria proposed by Strauss) and not have the mechanical dyssynchrony pattern described by Risum do not respond well to RCT.

So is the evidence strong enough to recommend pre-implantation 2d strain echo and not proceed with Bi-V pacing if the Risum criteria are not met? Is the absence of apical rock and septal flash reason to not proceed with Bi-v (or His Bundle) implantation?



1) Risum , N Identification of typical left bundle branch block contraction by strain echocardiography is additive electrocariography in prediction of long-term outcome after cardiac resynchronization
J Amer Coll of cardiology, 2015, vol 66, no. 631-641

2)Stankovic, I Relationship of visually assessed apical rocking and septal flah and long term survival following cardiac resynchronization therapy (PREDICT-CRT) Eur Heart J Cardiovasc Imaging. 2016,Mar 17 (3)262-9

addendum 1/30/19 reference to the Stankovic paper added
s

Thursday, January 24, 2019

Once I thought I knew how to advise people how to eat to reduce heart disease risk , Now....

Read this recent brief overview of diet and fats and carbs and and cholesterol levels  and heart disease risk and see if you would presume to advise patients on how to eat. I am glad that I am out of that business.

I have written several times on medical hubris . In light of what we think we "know" now and what I advised ten years ago,I think "who is without sin....." I believed I had the answer while having answers was little more than parroting the recommendations of boards and organizations.

You have to remember the lawyer's classic query "Doctor, where you wrong then or are you wrong now/"

Neither the pre-operative beta blocker debacle nor the post menopausal use of estrogen and progesterone missteps seem to be a teaching moment for the population medicine devotees. The pop med folks , as explicated here would presume to take funds away from the treatment of some to fund preventive program to others which would "after a few generations" bring about a utilitarian gain by some metric even as some might suffer now.

At the time of this writing serious doubt has been cast on the previously widely disseminated advice about how to eat to avoid heart disease and who should take aspirin for primary prevention of coronary artery disease and who , if anyone, shovel be screened to detect low vitamin D levels, just to name a few of the ever changing array of medical recommendation to prevent disease and death. 

The internist who once upon a time was thought to be the physician trained to diagnose and treat complex complicated medical conditions has to extent  that she is now a ambulist ( at least those who are not now hospitalists) sends her time in part giving advice about how to prevent disease. How to eat,how often to get a cervical cancer screening test or a colonoscopy , who should take statins of aspirin or vitamins  and how much to exercise. For this you did not need to study four years in medical school and then three of more years of internal medicine training.You just need to subscribe to a service ( an app on your IPAD) to keep you up to date on the latest, and every changing, recommendation of various panels.

Friday, January 18, 2019

"Some people do not deserve health care reform?what would Maimonides have said?

The notion of someone "not deserving medical care reform" has appeared at least twice in writings by physicians. KevinMD taked about it here as he called attention to a commentary by Dr Edwin Leap. Dr.Leap is a long time medical blogger and ER physician and submitted this essay to an online version of a newspaper.

My first cursory reading of the essay and KevinMD's comments I erroneously read it to say " "Do some people not deserve medical care"


Sometime ago I wrote about a wonderful essay by Dr. Lawrence J. Hergoff published in JAMA which seems to address this line of thought.


Near the end of his current manuscript he quotes part of the Oath of Maimonides:

"May I never see in the patients anything but a fellow creature in pain."
I added:

Not as someone who deserves his dyspnea because of cigarette use defying years of advice to quit, not as someone whose ascites is his just due from profligate use of alcohol, not as someone who should not be in this country at all, not as someone who would not be having the myocardial infarction at all if he had done what his doctors told him to do and not as someone who is taking "scarce medical resources" from someone who deserves them more or for whom the treatment could be more cost effective but as a fellow human whose is in need of what physicians spent so many years of their lives preparing themselves to be able to offer.

The oath ( Maimonides) should remind us that being face to face with a fellow human in need

..makes judgment beyond the biomedical not only unnecessary but inappropriate.


Tuesday, January 15, 2019

Comments on the "Extreme Exercise Hypothesis"

Dr. THM Eijsvogels  from the Netherlands has written extensively about the relationship between endurance exercise levels and various cardiovascular outcomes and findings.

His  recent (1) review with an annotated references list  is available in full text on line.

Maybe the first question should be "what do you  mean "extreme'?

U.S. National and WHO guidelines  recommend 250 minutes of moderate exercise per week or 125 minutes of vigorous ( greater than 7 METS) per week based on in part a well established  reduction in cardiovascular mortality and morbidity as well as numerous other health benefits. However ,US guidelines also state that exercise above that levels is associated with added benefits. But how far "above" should one go. Can you go too far?

Is there a U-shaped curve when you plot health risk of the Y axis and exercise training volume on the x axis? If so, can the inflection point be defined?

Arem (2015) combined data from six prospective population based cohorts ( 661,137 individuals).Maximal all-cause mortality risk reduction was noted at exercise level of 3-5 times current recommendations and even  those exercising at 10 times current recommendation had a lower mortality risk  ( HR 0.69, 95% CI 0.59-0.78). But at the highest level the degree of risk reduction was  less than that achieved by lower exercise levels,

Ten times would be 25 hours ( one full day) of moderate exercise per week,I suggest very few exercise at that level while many preparing for a marathon would likely exercise 7 or 8 hours a week (3-5 the recommend levels).The relatively few exercisers at the highest volume make the confidence intervals for HR estimation at that exercise level so large as to not be reliable or useful.

Eijsvogels summarizes the quest for "what do mean by extreme" with this understatement:

" Based on limited current evidence and numerous potential confounders, it is difficult to delineate an upper limit for the for the benefits of physical activity at this time."

So there is no epidemiologic support for a U shaped relationship between exercise volume and health risk at least as measuring all-cause mortality. But what about certain medical conditions that have been reported to be increased in long time endurance athletes at levels said to be higher than those who exercise less.

The usual suspects include 1) atrial fibrillation 2)cardiac fibrosis 3)coronary artery calcifications.

I have commented on atrial fibrillation before ( see here) and will likely have more to say later and have blogged about the coronary  calcification paradox before( see here).

Cardiac or myocardial fibrosis (MF) is detected by cardiac MRI imaging with injection of gadolinium  and  is referred to as late gadolinium enhancement (LGE).There is a recognized pattern of LGE designating the  localized fibrosis following a heart attack. The  LGE pattern at issue in endurance athletes is something different-, i.e. a non-ischemic pattern. .

Van de Schoor et al did a systematic Pub Med search (2) and identified 65 athletes with MR imaging. A subgroup (30 subjects) were identified in an MRI study of 509 athletes.

The most frequent pattern was that located near the interventricular septum  and right ventricular insertion points. The significance of this type of myocardial fibrosis is unclear.

Levine (3) et al have suggested that LGE in endurance athletes may not represent irreversible fibrosis and note that a similar pattern of LGE at the insertion points is seen in hypertrophic cardiomyopathy and also pulmonary hypertension.

Chan et al (4) described the histopathology in patients with hypertrophic cardiomyopathy (HCM). In a multi institutional study of 1293 HCM 10% demonstrated small areas of LGE in the area of  ventricular insertion into the ventricular septum. Biopsies showed " greatly expanded extracellular space" with intestinal fibrosis and disorganized myocyte patterns." The authors emphasized the pattern was not that of myocyte death and replacement fibrosis.

Perhaps a similar histologic pattern would be found in the endurance athletes but to my knowledge that information is not available.

LGE has been reported in participants in various sports , the first case was a soccer player. Its significance and underlying mechanism  ( repetitive microtrauma, transient pulmonary artery pressure over load ??) are  not known.

 I have to agree with Eijsvogels' summary statement :  )"There is limited evidence that supports the "extreme exercise hypothesis",the most compelling relating to the increased risk of atrial fibrillation at high volume of exercise. 2) cardiac abnormalities may be present in a small proportion of the most active veteran athletes …"






1)Eijsvogels, TMH, er al The "Extreme Exercise Hypothesis:Recent findings and cardiovascular
health Implications. C"urr Teat Options Cardio Med 2018 20:84

2)Van de Schoor, F ,et all Myocardial Fibrosis in athletes . Mayo Clin Proc 2016,2016

3)Abdullah, Sm Lifelong Physical Activity regardless of does is not associated with myocardial
fibrosis. Circ Cardiovas Imaging. 2016 9,:e005511 (ful text)

4)Chan R, et al Significance of late gadolinium enhancement at right ventricular attachment to ventricular septum in patients with hypertrophic cardiomyopathy. Am J cardiol. 2015:116 436

Monday, January 07, 2019

The concept of medical commons is a bogus and dangerous concept

A fundamental concept of the various types of egalitarianism is. neither coherent,correct and operationally meaningful. .. That concept is : Individually possessed  resources or assets should be considered as part of a collective pool owned by everyone and that all have an equal right to some share of the pool.

In regard to a private property system the rights of the owner in general terms are clear. The owner has the right to use his property,exclude others from us of the property and dispose of the property through sale,gift or inheritance.

 In contrast , the rights are in a common ownership system are vague and indeterminate. Feser said it is not clear how one can be said to "own" something if no one in principle is excluded from making a claim on that something.

Even a  cursory survey of the twentieth century reveals how tragic and unsuccessful were attempts to build a society based on the notion of common ownership and the abolition of private property. The Bolshevik revolution promised peace,freedom ,equality and prosperity and delivered mass murder and starvation.Communist China's attempt in that regard were no better .The dramatic nighttime photograph of the Korean peninsula showing darkness in the north and countless points of light in the south tells the story of the difference between the two systems of ownership..

Yet the movement to consider medical or health care resources as a central pool or a medical commons has had surprisingly wide acceptance in certain medical organizations and medical academia and among health care planners and policy wonks.

Even though the concept of a collective pool of individually possessed resources is basically void of meaningful operational content a derivative metaphor-that of the physician as a steward of the mythical medical resources-has been promulgated and to some a surprising degree accepted and has become part of a major  and growing effort to control medical care and has become part of the discourse about health care policy.

The rules by which a collective of healthcare resources  would be allocated are not defined, but  those who advocate the physician as steward of these resources have several things in mind to make the metaphor operationally meaningful, the most important of which is the purported ethical requirement of physicians to adhere to guidelines which in their most at least superficially justifiable  analytical form are based on a cost benefit analysis and in their least evidence based form , expert opinion.

Cost effective analysis has been smuggled into the professionalism package in the trojan horse of social justice. This is bogus as well.he The utilitarian mantra of the greatest good for the greatest number is not necessarily a part of the concept of social justice.The basis of social justice is equal respect for all humans while utilitarians would favor policies that benefit the aggregate though some individual may loose. The prominent egalitarian John Rawls rejected utilitarian allocations because they ignored the separateness of individuals and in his mythical behind- the- veil contract he believed that individuals would not sign up for a society that would sacrifice them for some aggregate benefit.









High value? Fuzzy concept? who gets to decide?

"Some measures are golden, but mostly those that we have tested. We have a responsibility as a profession to challenge this concept without seeing clear evidence that patients benefit from labeling some measures as value. Value and quality are fuzzy concepts. How can one oppose using value and quality? No one opposes the concept, but we all should demand that the implementation of measures does improve patient outcomes. We should all worry." From a blog commentary by Dr. Robert Centor. Yes, we should all worry.

Value and quality have be become buzz words-  to be blended into "value statements" and purported goals .

Classical economists ' notion of value as something imparted into a good by the labor expended in its production was overturned by economists in the late 1800s when Menger and others introduced the idea of  marginal subjective value. The value of a good or service was subjective,that is in the eye of the beholder, and was made "at the margin".The value of the tenth piece of apple pie is less to a person than is the value of the first piece. Great effort and artistic skill might be expended in the production of an artistically beautiful pogo stick but labeling it a high value product would not  bring about large sales of such a product. Few potential consumers would value such a product.

Marx 's labor theory of value is  resurrected in the payment system  for medicare "The doc fix" carried that archaic misconception  further. The Medicare payment scheme contains elements likely to be admired by the old time Soviet Union central planners".

Third party payers embrace the notion of high value medical care . The words quality and high value are  loose, vague and indeterminate  but seem to have considerable rhetorical value . They are found to a degree making them worthless in myriads of value and missions statements of various organizations whose actual activities and goals have nothing to do with those statements.
Some measures are golden, but mostly those that we have tested. We have a responsibility as a profession to challenge this concept without seeing clear evidence that patients benefit from labeling some measures as value. Value and quality are fuzzy concepts. How can one oppose using value and quality? No one opposes the concept, but we all should demand that the implementation of measures does improve patient outcomes. We should all worry.
- See more at: http://www.medrants.com/archives/8118#comments
Some measures are golden, but mostly those that we have tested. We have a responsibility as a profession to challenge this concept without seeing clear evidence that patients benefit from labeling some measures as value. Value and quality are fuzzy concepts. How can one oppose using value and quality? No one opposes the concept, but we all should demand that the implementation of measures does improve patient outcomes. We should all worry.
- See more at: http://www.medrants.com/archives/8118#comments
Some measures are golden, but mostly those that we have tested. We have a responsibility as a profession to challenge this concept without seeing clear evidence that patients benefit from labeling some measures as value. Value and quality are fuzzy concepts. How can one oppose using value and quality? No one opposes the concept, but we all should demand that the implementation of measures does improve patient outcomes. We should all worry.
- See more at: http://www.medrants.com/archives/8118#comments

Thursday, January 03, 2019

What happens to your heart in you train really hard for a year or two may depend on your age

First -what happened to the hearts of young men and women who trained intensively for one year in preparation for a marathon.See below for changes noted in older subjects.

Dr.Benjamin Levine (1) and colleagues at the Institute for Exercise and the Environment performed extensive physiologic studies on 12 such  subjects ( aged 29 +/- 6 years) and provided valuable insight into the functional and structural change in their hearts over  one year.

The training program was intensive and progressive and was divided into four 3 months periods or segments. The third quarter included 2 hour long runs and 4 th quarter involved 7 -9 hours per week  with 3 hour long runs and interval training.

The cardiovascular system of the trained endurance athlete differs in a number of ways from the untrained person.These include:
1.increased red blood cell mass and blood volume
2.increased numbers of mitochondria and capillaries in leg muscles.
3.lower peripheral arterial resistance
4.lower systolic and diastolic blood pressure during exercise.

What distinguishes the elite endurance athlete's heart from other equally well trained athletes is the very large stroke volume which in turn depend on a very large end diastolic left ventricular volume (LVEDV). A  very compliant left ventricle is the key (.It may be more accurate to state "compliant heart" as that would include a more easily stretched pericardium facilitating diastolic filling.)

The maximal 0xygen uptake increased from 40.3 =/-1.6 to 48.7  =/-2.5. (The 02 max for elite marathoners is typically 70 to 80 plus).  Maximal stroke volume increased from 98 to 113 ml.

A key finding was that both right and left ventricular mass increased to levels similar to those seen in elite athletes but the LV volume did not change until six months of training. In the first 6 months of training when training did not include significant high intensity training the left ventricle remodeling was concentric and eccentric remodeling ( i.e. increased LV volume) did not occur more intense exercise was part of the regimen.The right ventricle began "eccentric" hypertrophy early on. Question -is the eccentric pattern dependent on the addition of some HIT or interval training in addition to the moderate intensity exercise.

Cardiac catherization data derived measures of LV compliance improved but did not approach those typically observed in elite athletes. The "Starling Curves" which plot pulmonary capillary wedge pressure (PCWP) which is an index of left ventricular filling pressure on the x axis versus stroke volume on the y axis shifted up and to the left suggesting an improvement in left ventricular compliance, i.e a ventricle more easily filled.


Their morphology measurement which  were done by cardiac MR ( generally thought to be more accurate than echocardiographic measurements) did not conform with the Morganroth hypothesis (1975) which stated that endurance exercise lead to eccentric hypertrophy which is a balanced increase in wall thickenss and ventricular volume while strength training leads to concentric hypertrophy with an increase in wall thickness with no significant change in cavity size.

Levine's subjects first had a LV concentric pattern and only after more intense ( volume and intensity) exercise was part of the program did the classic endurance athletes eccentric pattern become evident. A certain level of  intensity of exercise seems to be necessary for aerobic exercise to cause eccentric hypertrophy. This seems to run contrary to the notion  that endurance exercise is simply a "volume overload event".

Levine's group has also reported on a similar project (2) involving older ( age 68-74) subjects and although their training program was vigorous it was less intense than the young subjects.The 02 max increased on average by 19%,arterial elastance decreased, LV mass increased with no change in the mass volume ratio ( i.e physiologic remodeling) but the Staring curves did not indicate a more compliant left ventricle.So good things happened but improved LV compliance was not one of them.

The third publication (3) in Levine's hat trick involves similar measurements of  heart function and structure in middle age subjects over  a two year period.The details are complex and interested readers can find details in ref 3 which has  entire text without firewall.

The two year training program involved at least 30 minute session of moderate exercise 4-5 times  per week with at least one high intensity exercise session ( the Norwegian 4x4).
The authors were able to show an improvement in compliance using the techniques ( The Starling curves) mentioned above .The data offer the hope that "middle age" is not too late to start .

Levine suggests that sedentary aging effect of the heart has 3 stages; 1) loss of relaxation 2)loss of compliance or stiffening of the myocardium and 3) remodeling.This sedentary aging may predispose  to heart failure with preserved ejection fraction (HFpEF) perhaps when confronted  by another "hit" such as hypertension,obesity,and diabetes. Levine's data suggests that some doable amount of endurance exercise might retard or mitigate the process . (Whether high intensity exercise is a necessary component is still an open question)

t





1) Arbab-Zadeh, A  "cardiac remodeling in  response to 1 year of intensive endurance training.
Circulation 2014, 130 (24) 2152

2)Fujimoto,N Cardiovascular effects of 1 year of progressive and vigorous exercise training in previously sedentary individuals older than 65 years of age. Circ. 2010, 122 (18), 1797

3) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized 
trial.Circulation,2018 137; (full text available on line without firewall)

addendum 2/17/19 Comment about pericardium added.