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

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

Tuesday, March 06, 2018

What does reduced ejection fraction in elete athletes mean?

Some NBA  and  professional European cyclists (1) have been shown to have reduced cardiac ejection fractions (EF) and some NFL players(2 )have EFs in the lower range of normal. In regard to the cyclists this observation has , at least in one review, been used to bolster the argument that "too much exercise" is harmful , i.e. support for the  "U-Shaped" curve theory."Too much " exercise certainty can be harmful  (maybe that is what "too much" means) but reduced resting EF in elite . athletes is not proof of that contention.

The wisdom of the body may dictate that maintenance  of stroke volume a priority and not EF. These athlete have large preloads ( aka end diastolic volumes) so that a smaller percentage can be ejected to maintain the resting stroke volume. These basket ball players had a normal increase in stroke volume  and EF with exercise as did the NFL players.I believe the exercise EF was not measured in the cyclists.

1.Abergel, E. Serial left ventricular adaptations in world -class professional cyclists.J AM Coll Cardiology July 2004.
2. Abernethy,WB Echocardiographic characteristics of professional football players.JACC Jan 2003 p 280
3)Engel,D Athletic cardiac remodeling in U.S. professional basket ball players. JAMA Cardiol 2016, (1) 80-87 

Monday, March 05, 2018

Reversing cardiac aging-maybe some but it isn't easy

More about cardiac aging and aerobic exercise  from the Institute for Exercise and  Environmental Medicine  is found  the January 2018 issue of Circulation. Howden et al(1) report the results of a two year trial of a vigorous exercise program on various physiological measurements.

They were able to show some improvement in cardiac compliance ( i.e. a decrease in myocardial stiffness) in a group of middle aged,otherwise healthy subjects over a 2 year period but the exercise required was considerably more than frequent brisk walks or slow jogs around the park.Rather , part of the exercise program involved a vigorous high intensity interval program using the "4 by 4 " Norwegian Skier technique twice a week and later in program only once a week.

Dr. Ben Levine, the Director of the Institute, and his team seemed to be able to recruit subjects who would persevere in a demanding exercise program over a 2 year program  and   to also permit right heart catheterizations which were done to give the investigators a index of compliance of the left ventricle.The bottom line is that they were able to demonstrate a reduction in cardiac stiffness with their exercise program .

This study is the most recent in a series of publications which have demonstrated that there is some level of prolonged endurance exercise that can at least to some degree mitigate the age related loss of cardiac compliance . Previously they had attempted to improve cardiac compliance in older subjects (in their 70's) and were unsuccessful. In this study they hoped they could find a "sweet spot", a time frame in which it was not loo late to reverse the age driven stiffness and they seemed to have , at least to some measurable degree succeeded .

Levine characterizes the sedentary heart as a "small, stiff heart" versus the endurance athlete's heart as larger,slightly thicker and more compliant.

Levine describes the stages in the aging of the heart :1) loss of relaxation ,2) stiffening ( beginning in middle age), and finally 3) remodeling. The hope is that adequate exercise might mitigate  or significantly delay stage 2 which may be the precursor or  a prerequisite for heart failure with preserved diastolic function. Years of endurance exercise does not seem to prevent the first phase but Levine's data suggest that exercise may counteract the stiffening and remodeling.

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

Wednesday, February 21, 2018

diastolic heart failure-do we need a two (or more) hit theory?

Warning The following represents the musings of a non-cardiologist,clearly unqualified by training to speak with much credibility on this subject.

The earliest recognizable phase (s) of diastolic dysfunction seems to happen to everyone if they live long enough and late middle age may be long enough. This phase is labelled, in the jargon of echocardiography, as "impaired relaxation" and  according to the latest expert guidelines technically as " E/A ratio less than or equal to 0.8 and E  wave velocity less than or equal to 50 cm/sec."These values are obtained by measuring blood flow with Doppler technique across the mitral valve. Relaxation occurs simultaneously with elastic recoil (aka restoring forces) from which there is no current method to distinquish it.Authors addressing this topic seem fond of the spring analogy and it has been suggested that the world's largest protein molecule,titin,functions like a spring.

 To perhaps overly simplify a complex process,let us consider diastole or ventricular filling as a three phase event, pre-early, early and late.See end note 1 Pre-early is the phase after the aortic valve closes and before the mitral valve opens (the isovolumic relaxation phase),early is the phase when blood flow rapidly into the ventricle ( as  depicted by Doppler technique as the E wave) ,late is when blood is pushed from the atrium by contraction and represented a the A wave. In the young E is greater than A and remains so probably until about late middle age.when the E wave is no longer higher than A, the echocardiographer  now usually says "impaired relaxation"

The party line current theory describes the early phase of diastole as being driven by relaxation and diastolic suction. Extensive data show that several indices of  diastolic function change in the process of healthy aging. The ventricle takes longer to relax which is signaled   by a prolonged isovolumic relaxation time or IVRT. There is also slowing of the early flow across the mitral valve  depicted by a lower E wave velocity and a lower E/A ratio.

The early mitral velocity of blood flow decreases and the IVRT lengthens- changes believed to represent impaired relaxation and is reported as such on echo reports. (Even though it is generally agreed that there is no way to partition the relative effects of relaxation and diastolic suction as they occur at the same time.)  Simplistically diastolic suction function can be thought of elastic recoil,the release of the stored energy created by contraction. This is also referred to as restoring forces.  The late phase of diastole is influenced by the stiffness or compliance of the ventricle and the contractility of the atrium.

One of the missions of echocardiography is non-invasively estimate the "filling pressure" of the left side of the heart. Filling pressure is the  pressure at the end of diastole also referred to as preload.
Elevated filling pressure can be used to confirm or support the diagnosis of heart failure (HF) and is believed to correlate strongly with shortness of breath on exercise.

Since every one is thought to develop  a decrease early diastolic function but everyone does not develop diastolic heart failure ,could those patients with decreased ( or more decreased) ventricular compliance-which exerts its effect in late diastole- be the HFpEF candidates?

The story of the changes detected in the aging heart as depicted by the Group from Southwestern (1) goes like this:

Early on there is impaired relaxation.Left ventricular stiffening occurs during the transition period between youth and middle-age and "become manifest between the  ages of 50 to 64", This is followed by left ventricular volume shrinkage and remodeling ( wall thickening) after age of 65. So the sequence is impaired relaxation, stiffening and then remodeling.

There are data indicating that about 1/4 patients with stage 2 or 3 diastolic function    progress  to HF.(Impaired relaxation is stage 1, as ventricular stiffness builds up so does the pressure in the atrium and this is reflected with an increase in E ,and E/A increases , a pattern often referred to as pseudonormal (although the most recent ASC guidelines no longer use that term) , as things get worse the LA pressure increases more and values change appropriately earning the designation of restrictive pattern (again this is the older terminology banished by the 2016 revised guidelines)

So maybe a second hit is needed. One such hit could well be prolonged hypertension and the resultant concentric hypertrophy of the heart leading  to decreased ventricular compliance, or at least "ventricular chamber compliance".Left ventricular myocardial changes seen in obesity and diabetes could also represent a second hit and could contribute to both diastolic dysfunction and systolic dysfunction.

Myocyte apoptosis occurs with aging is accompanied by hypertrophy of the surviving myocytes and increase in fibrosis, all of which could conspire to stiffen the ventricle  as well as impairing relaxation.

The group from  Dallas (2) has presented data that a sedentary lifestyle can cause concentric cardiac hypertrophy and that prolonged aerobic exercise  ( at levels as least twice that of the standard exercise prescription which would be about 5 hours of moderate exercise per week) if started by early middle age may prevent the age related loss of ventricular compliance It should be noted that there are data and interpretation of data that contradict that hypothesis. See here  and here for commentary regarding the observations that more aerobic exercise is required to prevent diastolic heart failure that is sufficient to decrease the risk of coronary artery disease.

Diastolic heart failure is a well recognized companion of diabetes .Several possible second hit suspect mechanisms  have been described  in diabetes including deposition of glycation products and increase in myocardial cell tension.

Of course there is much more to it than that. Normal healthy aging per se has been associated with apoptotic loss of heart muscle cell,compensatory hypertrophy of remaining muscles cells and fibrosis leading to some stiffening of the ventricles with the only apparent "hit" being aging. But again that seems to happen to everyone and everyone does not develop diastolic heart failure.Maybe a second hit is needed and again according to the Dallas group a sedentary lifestyle may be one such second hit second hit.See here for commentary on effect of sedentary lifestyle on cardiac remodeling .

In broad, non specific terms the "second hit" is anything that increases cardiac stiffness.

1) Fujimoto,N. Effect of ageing on left ventricular compliance and distensibility in healthy sedentary humansThe Journal of Physiology2012 590 (pt 8)1871 (see end note 2)

2) Dr Benjamin D Levine N Fujimoto Paul Bhella and others have published extensively examining the effect of ageing,exercise and the lack of exercise on various aspects of cardiac function and age related impairment. They posit that long term endurance exercise begun at lest by middle age may prevent the loss of compliance that is common in sedentary human evens in the absence of the usual suspect heart problems (HBP,diabetes,obesity)

end note 1.I know there are "really 4 stages" I left out "diastasis"
end note 2. If anyone can explain to me the difference between compliance and distensiblity please comment.

Addendum 3/16/18 A few more additions to try and get this thing right.

Monday, February 05, 2018

Might meta analyses and meta data dreging gaslight everyone

Two dueling meta-analyses come to mind. There was a widely quoted meta analysis regarding Vitamin E which concluded it increased the risk of death. Soon after that article appeared in the Annals of Internal Medicine , letters to the editor claims that using a different statistical technique on the same data base, there was no increase in death risk.

Large data bases and multiple comparisons between outcomes and variables seem to always show that some factor becomes a risk factor for something often with relative risk values less than 2 and often less than 1.5.RR.Values in this range are unlikely per se to  unearth a causative factor.This activity is sometimes referred to as "data dredging"  or looking for a positive correlation to rush to print and press releases.

The prudent researcher usually emphasizes that these finding are "hypothesis generating" and not game changing breakthroughs although  the less prudent and the lay press and astro-turf propaganda outlets may suggest the latter. When apparently contradictory data then appears in the medical (and then the popular) press what is one to believe. This seems to be a cousin of "gas lighting" even though no one is plotting to make anyone doubt their ability to reason and analyze medical  data but  tons of data and sounding alarms on the findings of many  of them may have a similar effect of "not knowing what to believe".

Friday, January 19, 2018

Has the modern electronic medical record made many physicians accomplices to lying?

In the last few  years I have the opportunity to read my medical records  and those of  some extended family members. After reading these documents, I wondered has the electronic medical record (EMR)  made doctors liars? When they sign off on a record that filled with erroneous statements and claims that something was done and it was not done and the physician knew it had not been done ,why would not lying be an accurate description ? I suggest it would be.

When I reflect back on the emphasis of the importance of accurate medical records that was  embedded into my nascent physician  mind as a medical student and house officer and  as I read the repetitive useless information, erroneous entries and pages of useless cut and past repetitions  and even fabrication of what transpired I cannot believe what the medical recored has become. So in some ways this is one of the saddest and most disillusioned  blog entries I have ever posted. In some cases the medical record has been useless and misleading and often inaccurate garbage and certainly potentially capable of harming the patient and likely a fertile field for plaintiff attorneys.

I read the medical records ( fairly easily obtained through the clinic's patient portal). I read that the patient had a physical exam ( describing normal finding for various parts of this phantom exam which she never had). No one listened to heart or lungs. Reading the medical history I find that she was said to have hyperthyroidism ( she had hypo) said to be on Armour thyroid  ( she is not) .Reading another orthopedics record ( again from the patient portal ) I learn that the summary sheet described the wrong leg bone as having the issue of concern i.e. tibia rather  than femur.

A few years ago I read on my own  colonoscopy report that my physical exam was normal. This was another phantom exam, this was being signed off by one of my former partners.

So would it be fair to describe this type things as publishing a false medical record or simply put lying. Court room scene. Doctor, your records on Mrs X indicate you performed a physical exam prior to her endoscopy?. Did you in fact do such an exam? Mrs X has testified that she did not have such an exam.

Do the physicians even know what is contained in the medical record that they sign? Is that any excuse if they sign the record?

Addendum:  2/8/18 Still more. Having  a pacemaker in place I take part in a "remote interrogation" of the PM every three months.This includes a summary done by a PM tech at the PM center at a local hospital. Each report ends with "the patient had no complaints". At no step in this process has anyone ever asked me how I am doing.

Wednesday, January 17, 2018

Mayo study: higher cardiorespiratory fitness associated with lower risk of atrial fibrillation

Data and analysis continues to address the issue of exercise level and risk of atrial fibrillation (AF)-sometimes referred to as the U-shaped curve controversy.

Hussain et al (1) published a follow-up study on 14,094 selected subjects who had been referred to Mayo Clinic for exercise stress testing. These were from a much larger group from whom those with a history of heart failure, atrial fibrillation or flutter or stroke were excluded.The average follow-up was 14 years and the outcomes of interest were incident atrial fibrillation ,stroke and death.
They divided the subjects into 4 groups based on functional cardiorespiratory capacity as estimated by their performance on the Bruce protocol stress test.

Those subjects in the highest exercise performance category showed no increase in the risk for AF.

The authors concluded:

"...better cardiorespiratory fitness is associated with lower risk of incident AF, stroke and mortality. Similarly risk of stroke and mortality in patients with AF is also inversely associated with cardiorespiratory fitness."

They also commented that the reduction in these risks with increasing exercise capacity  "may be a direct physiological effect of exercise and physical activity or a consequence of a lower burden of cardiovascular risk factors" I would add "or both".

This is  another coarse grain study which will not settle the U shaped curve argument.I think often these "controversies " just dwindle away rather than get settled. The etiology of AF and stroke with AF involves a complex array of numerous possible input variables and here we look at the effect of  only one such variable ( exercise capacity-as a surrogate for exercise level) on the outcome (s) but at least  long time endurance exercisers may find some solace here. Critics can justifiably point out that a number of potentially confounding variables were not available  for analysis including, smoking history,alcohol use,and actually exercise habits.

Again quoting  Simon (2) ".. a man hears what he wants to hear and disregards the rest"

1) Hussain,N Impact of cardiorespiratory fitness on frequency of atrial fibrillation , stroke,and all cause mortality. AJC Jan 1, 2018. vol 121 issue 1, p 41-49

2) Simon, P .Lyrics from the song ,The Boxer, 1969

H/T "notes from DR RW"

Monday, January 15, 2018

Not your father's internist any more

This a very lightly edited version of a commentary that I made 12 years ago. Nothing has happened in the last 12 years to change my views and from the point of view of a very over the hill internist, things are even worse and are not likely to get better.

"The current data are clear.There are fewer docs going into general internal medicine.Lower pay, less prestige are two of the reasons offered and an increasing amount of onerous,often counter productive computer driven requirements may for some be the final straw.

A  "op-ed" like piece in the ACP Observer by the President D. Anderson Hedberg is entitled "Finding the Art within the science of internal medicine". My gut reaction to it is " wouldn't it be nice if it were [still] true.?"The internist he portrays does resemble the internist I thought I was training to be. But I doubt if it is possible to be that type physician today.(see end note )

Dr. Hedberg quotes a 1998 article by Dr. Robert L. Wortmann, chair of IM at the U. Of Oklahoma in Tulsa. Dr. Wortman said the four distinguishing characteristics of internists are: 1) the ability to be a diagnostician ( internists were once called that) who can practice the deductive scientific process that leads to therapy. 2) the ability to provide care of complex acute and chronic problems. 3) the ability to be a consultant for generalists, specialists and subspecialists and 4) curiosity. One comment he made re "curiosity" does resonate with my IM training. He said that to the internist it is important to consider the "links between disease and pathophysiology as well as between the therapy and its mechanism of action"

These comments definitely had more currency at a time when: 1) there was no competition in primary care save for GPs. and there was a clear distinction between GPs and internists. There were no family doctors-from whom the distinction between them and internists is harder now to draw- and no competitor from nurse practioners. 2) there was the reasonable likelihood of being able to spend enough time with a patient to play out those characteristics and patients did not have to be seen every 10-15 minutes to either meet the clinic or HMO quota or generate enough income to keep the practice going. 3) there was no need to worry and try and determine if the recommended therapy was approvable by the HMO, Insurance company or pharmacy management company.4) there was no hospitalists to compete with you. You were the hospitalist. 5) there was time and opportunity to pursue efforts to satiate your curiosity.

Only about 25 % of internists consider themselves general internists and more and more subspecialists refer back to the general IM doc or the FP problems not clearly linked to their subspeciality.Hospitalists are growing in numbers and the arrow points in the direction of at least some general IM docs pulling back from their roles in the hospitals making them more like FPs than internists.

In short, in today's environment how realistic are the comments of the two physicians quoted above? I think not very. I am afraid their comments were more relevant in an earlier era.It is hard to say what are the distinguishing characteristics of internists in the current practice of medicine.
I believe it is a confluence of factors and forces that are leading to the demise of the general internist.

Another major determinative factor is the following:A few decades ago the internist (there was no "general" preceding the designation) was the recognized expert in diseases of the heart, lungs, and kidneys as well as the expert in endocrinology and hematology. Tremendous growth and development of the subspecialist domains of expertise has changed the landscape. Cardiologists are now called in to treat coronary syndromes, pulmonary docs for respiratory failure, etc etc. Oncologists take care of the cancers, kidney doctors the ESRD cases and it is the rheumatologists now giving the disease modifying treatments for rheumatoid arthritis .When emergent or semi-emergent medical issue arise after hours the patient is likely seen in the ER by an ER doc and if hospitalized, then seen by a hospitalist who more likely than not calls in specialists.In short, the areas in which the internist was the expert have largely disappeared and the experts are the IM subspecialists and it is the ER docs and hospitalists who sort out the problems of sick patients summoning subspecialists as needed.

To a large degree many internists are left with office treatment of the same conditions managed by FPs and nurse practitioners ( hypertension, type 2 diabetes,annual check ups, elevated cholesterol,URIs etc, annual "check ups" )

How many internists would want their myocardial infarction treated by an internist? I want a cath cardiologist.

end note: I do not deny there are exceptions. I have been a big fan of the blog ," db's medical rants" by Dr. Robert Centor,an academic internist who as best  I  can tell from his writings continues to function in the manner described by Dr. Worthmann.However he does not seem to  work primarily  in a private practice setting the landscape of which , in the last few decades ,has become a completely different game.

Addendum: 2/9/18 My own internist who is also my former partner finally decided to find a internist for his medical care.The one he chosen has an excellent CV board certified,good med school,good residency site etc. He said he liked him, he seemed nice  but it was "sorta funny" that he did no physical exam at all.