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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 ...

Sunday, December 16, 2018

Milton Friedman's " 4 ways to spend money" and health care spending

Milton Friedman spoke of the four ways people could spend money based on the funding source and the recipient of the goods or services and the associated mind sets,incentives and constraints that each arrangement supports. In his book "Free to Choose" he presented a four quadrant diagram, a version of which can be found here.

The left upper quadrant  represents the situation in which you spend your own money on yourself, a situation where one typically exerts some degree of prudence a thought not found to same degree in the other arrangements.

In the RUQ you spend someone else's money on yourself.

Much (most ?) health care spending seems to be in the RUQ which is clearly the case with Medicare and Medicaid spending and from one view point employees spending their employer based health insurance money.Although you could consider that type of insurance basically part of the employee's compensation so maybe that should be in the LUQ ,folks tend to act as if they are spending someone else's money so I'll leave that in the RUQ.

The LLQ denotes your spending their money on someone else, such as Aunt Hattie buying a birthday gift for her niece in which getting what the niece really wants may not be the determining factor.

The RLQ represents you spending some one else's money on someone else.Think of a welfare program dispensing money .

The concern over high and rising health care costs is sometimes (and in my view correctly) focused on the governmental spending on health care. However, increasingly pundits and health care policy wonks and "thought leaders" frame the issue as one in which total health spending is a threat to nation's fiscal solvency. .

The argument that government spending is out of control, relies on foreign funding and the national debt is growing to a dangerous level resonates across the political spectrum of views. Regardless of the validity of various elements of that sentiment how would spending in the LUQ relate those concerns?

Would not individual spending their own money on things (even medical care)for themselves increase the C part of the GDP formula? Would not increase in spending be exactly what economists of the Keynesian view prescribe to bolster a economy lacking in the right type of "animal spirits"? Why would policy wonks want to limit personal spending? Are they really basing their proposal for more control over individual actions on legitimate concerns for the future economic safety on the country? Or is it the progressive view ( as well the NeoCons view) that society is best managed by wise leaders ?

Wednesday, December 05, 2018

If there is increased coronary calcification in some long time endurance atheletes,is that a good or bad thing?

If there is increased  coronary calcification in long time endurance athletes,is that a good thing or a bad thing? Also if true is it true only in white males? The Cardia Study (1) found an increased risk of coronary calcification in white men ( depending on what statistical model was used) but not black men.

 Funnily enough a similar question can be asked in regard to the use of statins with  more calcification reported in users of the more potent ( in terms of LDL lowering power) statins.(I am aware of no racial differences reported in that regard)

So is the absolute worse thing you, as a white male could do would be to run excessively for 30 years and take the most potent statin ever?

1) Laddu DR 25-year physical activity trajectories and development of coronary artery disease as measured by coronary artery calcification.

Tuesday, December 04, 2018

Is the key to prevention of post ablation atrial fibrillation risk factor modification?

Dr. Rajeen Pathar (1) and co researchers from Adelaide Australia seem to think so.

Hypertension,diabetes,obesity, sleep apnea and smoking are recognized risk factors for the development of atrial fibrillation (AF).The authors reasoned that the same risk factors might predispose to  recurrence of AF after a successful atrial fibrillation ablation and that aggressive risk factor reduction just might decrease the recurrence rate. Their published data (1) tends to support that hypothesis.

A excellent discussion of risk factor importance in AF  by Dr. John Mandrola on Medscape can be found here.

1) Pathak,RK Aggressive risk factor reduction study for atrial fibrillation and implications for the outcome of ablation.The Arrest-AF study. JACC2014 Dec 2;64 (2) 2222

Monday, December 03, 2018

kids fredquently getting hit the head is not a good idea

More data accumulate indicating MR changes in the brain are associated with sub concussive blows in youth football in a single season.

Functional MR studies (fMr) have shown changes in both gray and white matter correlated with the number of blows  to the head  as measured by impact detecting systems placed inside football helmet's.

The immediate and long term effect on the young brain is not known and the relationship to CTE is speculative.

Maybe the developing brain is more vulnerable to harm from multiple mini traumas or maybe it is more adaptive .

Meanwhile the  experiments continue in youth football leagues and under Friday Night Lights.

Murugeson from Southwestern Medical School in Dallas  presented data at recent  RSNA  meeting demonstrating functional MR changes in a single season of high school football correlated with sub concussive head blows. Data from a Wake Forrest study indicated majority of sub concussive blows occurring during practice.

Monday, November 26, 2018

will regular exercise help keep your thymus from shrinking keeping immune system "younger"

Researchers (1) from University of Birmingham present evidence supporting that proposition. 

Remember  the T lymphocytes,they arise from the bone marrow and trek to the thymus where they multiply and prosper then traveling to the lymph nodes and play a essential role in immune function.Decreased immune function and shrinkage  of the thymus are well known effects of aging.

The authors studied immune function in 125 subjects aged 55-79 who had exercised regularly ( cycling) for many years.These were not elite athletes .They also studied age matched non exercisers and young adults.

The active group had higher T cell levels and higher levels of something called RTE which stands for recent thymic emigrants than did the less active control group and these levels were the same as the healthy young controls .

This finding lead some of the lay press to hype the findings in terms such as having the immune function of a 20 year old when you are 80 but only a selected aspect of immune function seemed well preserved and the authors found other aspects of the immune system (including numbers of B Cells) were the same in the active and the inactive group and not similar to the young controls.

So, 80 year old  master cyclists may not have the immune function of a 20 year old but do have some aspects of immune function better preserved than the age matched sedentary controls and there is still another reason why active aging is different from sedentary aging .

1)Duggal NA, Major features of immunosenescence including thymic atrophy are ameliorated
by high levels of physical activity in Adulthood. Aging Cell 2018 Apr 17(2) Online published March 8 2018

Monday, November 19, 2018

20 years from demonstration of AF origin in pulmonary veins to a clincal trial with controversial results

 In 1998, Haissaguerre et al (1) described atrial ectopy or premature atrial beats within the pulmonary veins as the trigger for atrial fibrillation.It seemed to be a particularly attractive theory for the origin of paroxysmal AF (PAF) and has also been proposed as a facilitator of continuation of AF to persistent AF.

This lead to the idea that electrical isolation of the pulmonary veins by burning atrial tissue would keep the ectopy from reaching the rest of the atrium .

And so Pulmonary vein isolation (PVI) really caught on being used for not only PAF but for persistent AF as well  and ever since  the electrophysiology world has awaited a randomized clinical trial answering the question does PVI decrease mortality in atrial fibrillation (AF). It is accepted dogma,backed by considerable experience that PVI is superior to medication treatment in suppressing AF and there is general agreement that restoration of sinus rhythm improves quality of life .A  unanswered question was does PVI decrease risk of death associated with AF.

The Long-awaited CABANA trial was supposed to  or at least hoped would  provide an "Answer" to that question.

When the results of this large (2204 subjects) multi-center,multi national (https://www.acc.org/latest-in-cardiology/clinical-trials/2018/05/10/15/57/cabana) were announced there was no widespread celebration in the EP community. When the data were analyzed according to the standard statistical method used in randomized superiority clinical trials ( namely the "intention to treat" (ITT)) method), there was no difference in the primary outcome which was the combined end points of death,disabling stroke,serious bleeding or cardiac arrest  between the ablation group and the treated with drugs group.Further using ITT analysis there was no significant difference between the two treatment arms for each of the components of the combined end point .

For ablation versus drug therapy :8% vrs. 9.2%  with a hazard ratio of 0.86 (0.65-1.15, ) p=0.3 in regard to the primary endpoint.

There was no difference in death nor in serious stroke between the two arms of the study.

However looking at secondary outcomes- In regard to the category of death or cardiovascular hospitalization  there was a significant difference.

 There is more than one way to analyze data and results of the "per protocol " analysis gave  consolation to the EP cardiologists.

The per protocol analysis showed: a significant decrease in the composite primary end point with ablation  -ablation 7% versus  drug10.9 %  ( HR 0.57 , 0.50 -0.89) and decrease in all cause mortality in the ablation group , 7.5 % for drugs versus 4.4 % for ablation.

So intention to treat analysis indicated that ablation was not superior while per protocol analysis indicated that ablation was superior.Something for everyone.

Though heralded by some as a "game changer", I see nothing in the results changing any game. EP cardiologists are not likely to change their practice in any meaningful way  Just look at the final sentence in the Conclusion slide presented at the American College of Cardiology meeting in August 2018:

"Ablation is an accepted treatment strategy for treating AF with low adverse event rates even in higher risk patients."

 Since the study confirms what other data have shown namely that ablation converts AF to sinus rhythm more often than drugs and the results are more durable why would EP docs  change the way they are practicing ?

 1)Haissaguerre M, Jais P, Shah DC, Takahashi A, Hocini M, Quiniou G, Garrigue S, Mouroux AL, Metayer PL, Clementy J. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med.1998;339:659

Wednesday, November 14, 2018

Is aerobic endurance training even better for the muscles than the heart?

Aerobic exercise capacity is strongly linked to 02 max which is the product of the cardiac output ( stroke volume X heart rate) multiplied by the A-v 02 difference.

Five middle aged men who underwent aerobic training at age 20 in 1966 participated in a 6 month endurance training program in 1996.Their average 02 max increased 14% but there was no change in their maximal cardiac outputs. Their A-V 02 difference did increase by 10% accounting for the  entire improvement in their aerobic power.

The increase in mitochondrial function brought about by aerobic exercise is well documented and the more mitochondrial the higher the 02 uptake by the exercising muscles.

1)McGuire, DK et al A 30 year followup of the Dallas Bedrest and training Study11Effect of age on cardiovascular adaptation to exercise training. Circulation2001 Sept 18 104 (12) 1358-66

Friday, November 09, 2018

Endurance exercise,aortic stiffness,Windkessel effect

The beneficial effect of prolonged endurance aerobic exercise on the aortic and great vessels may be as  important or more important that its effects on diastolic function and favorable remodeling. 

First the aorta is not  a stiff pipe. One  model used to explain aortic function and the shape of  the aortic pressure waves is the Windkessel effect model which considers the aortic and large elastic arteries as if it were an elastic buffering chamber which provides a cushioning or reservoir effect providing blood flow during diastole and damping the pulsatile flow. This reservoir effect flow is said to be as much as 40% of the stroke volume. The large elastic arteries act as capacitors , storing energy during systolic while bulging  a bit and then pushing back  or recoiling during diastole maintaining  a more or less steady flow of blood and offering protection to the vulnerable arterial vessels of the brain and kidney to which excessive pulsatile flow may be harmful. The capacitance effect does not eliminate pulsatilty,of course ,the textbook normal diastolic blood pressure is 80 and  not zero which is what it would be if  the aorta were a lead pipe. 

With aging,and arguably more so with sedentary aging,the elastic vessels become less elastic, stiffer and provide less of the Windkessel effect reflected in higher systolic blood pressure, lower diastolic blood pressure (increased pulse pressure) and more rapid blood flow. This   can measured  by noninvasive measurement of pulse wave velocity with an higher velocity indicating stiffer arteries.Loss of the reservoir  function. i.e.. a stiffer aorta and other great vessels  increase the left ventricular afterload predisposing to left ventricular wall thickening. 

It is easy to find data supporting the claim that exercise will improve aortic compliance.As early as 1973 a report from the Baltimore  Longitudinal Study on Aging (BLSA) (ref 1) indicated improved pulse wave velocity ,augmentation index and systolic blood pressure in older endurance athletes as compared with sedentary controls.

Other more recent detailed physiologic studies have confirmed that finding. Gates et al(2) studied men with varying exercise histories in three different age groups and reported that the regular endurance trained subjects has lower large artery stiffness as measured by a reduced aortic pulse wave velocity.

An excellent, detailed exposition of the physiology of the adaptation of the aorta to endurance exercise can be found in full free text in reference 3.

1)Vaitkevicius, PV et al Effect of age and aerobic capacity or arterial stiffness in healthy adults.Exp Physiology 2005:90.645-651

2)Gates PE,Left ventricular structure and diastolic function in human aging. Europen Heart Journal 2003,24, 2213-2220

3) Montero, FJC Adaptation of the aorta to training.Physiological perspective.
Apunts,Medicena de L'esport. 2017:52 (193): 3-9

Thursday, November 08, 2018

Football lineman may be damaging hearts as well as brains

Dr. J Kin along with Dr. Aaron Baggish, who directs the Cardiovascular Performance Program at MGH, studied a group of NCAA Div.1 college football lineman and compared results with non-lineman over the course of a single season. (1)

They reported that the lineman were all normotensive preseason while post season , 30% had developed Stage one hypertension and 60% developed pre-hypertension. The non-lineman improved their Global Longitudinal Strain measurement (as determined by speckle echocardiography)while the lineman worsened theirs.Concentric hypertrophy was noted in the lineman while the non-linemen displaced eccentric hypertrophy.

This was after a single season.Consider that many high school player play for four years and a number then have a college career.

The authors concluded:
... participation at a lineman field position may lead to a form of sport-related myocardial remodeling that is pathologic rather than adaptive. Future study will be required to determine if targeted efforts to control blood pressure, minimize weight gain, and to include an element of aerobic conditioning in this subset of athletes may attenuate this process and translate into tangible downstream health benefits."
I have blogged before about the occurrence of CTE in collegiate football players quoting a study from the Boston University CTE center. The authors reported 48 cases who only played high school and college ball.

There have also been several articles reporting imaging abnormalities in young players with both concussive and subconcussive head trauma.Now we seem to have evidence of subclinical heart damage  that like subconcussive blows might lead to downstream health problems.

1)Lin, J Blood pressure and left ventricular remodeling among American style football players.
JACC,vol 9, number 12 dec. 2016.

Friday, October 26, 2018

Cleveland Clinic article says the more fit live longer

Dr. Kyle Mandsager and colleagues at the Cleveland Clinic reported on the long term mortality  ( median followup of 8.4 years)  on 122,007 patients who were referred for symptom limited exercise treadmill testing.They were stratified by age and sex  into five cardiorespiratory  performance groups .(low,below average,above average,high and elite expressed as metabolic equivalent units (METs) which is 3.5 ml 02 uptake/kilogram/minute) which was estimated by treadmill incline and speed.

The 25th, 50th,75th and 97.7 percentiles were tabulated for age and sex .Low is defined as less than 25 th percentile and elite as greater than 97.7 th percentile.

They found that cardiorespiratory fitness (CRF) was "inversely associated with long term mortality with no observed upper limit of benefit. Cardiorespiratory  fitness is a modifiable indicator of long term mortality …"

We have another coarse grain study that could be used to support  the thesis that exercise is good and lots of exercise is better and you will live longer. I don't believe it is that simple.

 This study does not correlate exercise history with longevity as it correlates exercise performance with longevity. Admittedly exercise performance or capability does correlate with exercise history but they are not exactly the same thing.  Further, while it may well be the case that CRF is modifiable and  that one can actually improve mortality by improving one's CRF their data does not direct address those point although I like to believe that proposition is true.

What is shown impressively in their Figure 1, is  the 10 survival probability for the above average or the high group is about 95% ( just by my eyeballing the chart) versus the low group where the survival probability is slightly less than 80%

So how low is the low group in terms of exercise capability.For example in the 70-79 year age group the low group had a MET of less than 6. Some one in that category could likely walk a mile in 15 minutes or complete Stage 1 of the Bruce treadmill protocol. 

A 70-79 year old in the high group could likely complete stage 3 on the Bruce protocol and run a 12 minute mile. METs from the high group had METs in the 8.5 to 11.4 range and about 9 METS is needed to complete Stage 3.

What about a 40 year old? Subjects in the 40-49 year old group had a MET levels of less than 9.8. This corresponds to being able to finish Stage 2 and a bit into Stage 3 and be able to run a 12 minute mile.
Someone in the high category would have a MET value of 12.5 to 14.6 which corresponds to being able to reach Stage 5 on the Bruce  protocol and run a mile in 9 minutes.

The authors made comments that are headline attractors.  "The increase in all cause mortality associated with reduced CFR (low versus elite:adjusted HR,5.04:95% CI, 4.10--6.20;p<.002) was comparable to or greater than traditional risk factors." See figure 2 in their artcle for details of that comparison.<0 .001...was="" 2="" comparable="" compared="" diabetes="" esrd.="" factors.="" factors="" figure="" greater="" hypertension="" nbsp="" or="" p="" risk="" see="" smoking="" than="" the="" their="" to="" traditional="">

Skeptics of the thesis that there is a "U -shaped"curve relating risk of death to exercise level will perhaps find some comfort in their finding : "There was also no evidence to suggest relative harm associated with extreme levels of fitness in these subgroups of patients"In fairness I should add that no one has claimed that excessive fitness is deleterious but rather the claim has been that excessive exercise may be harmful, again realizing that fitness levels and exercise levels are highly correlated. 

Nitpicking aside, their data provide more fuel to the argument that exercise ( or at least CRF) is good and apparently the more the better.

1)Mandsager,k et al "Association of cardiorespiraory fitness with long-term mortality among adults undergoing exercise treadmill testing" JAMA Network open, 2018 1 (6)Oct 19


Friday, October 19, 2018

Changing status for use of aspirin in primary prevention of heart disease

In the not too distant past based in part  on the results of the Physicians Health Study (1989) and the Women's Health Study (2005) it seemed reasonable to recommend aspirin for cardiovascular disease prevention. Recommendations were typically based on various guidelines that were estimates of a person's risk based on various risk factors such as cholesterol level,Blood pressure, smoking status, family history, etc. Since age is a major risk factor many of elderly are taking low dose aspirin with or without a physicians's advice.Is that still a good idea?

Dr. Paul Ridker in a editorial in the NEJM (1) questions whether the old advice is still justified in light of more recent clinical trial data  and perhaps a changing risk baseline for the population in general. More people now are on medication for blood pressure,fewer smoke and many more now are taking statin drugs than they were at the times of the PHS and WHS.

In the same issue of NEJM 3 primary prevention trials were published. Only the trial in diabetic patients (the ASCEND trial) was there shown to be a statistically signficiant reduction in vascular events. A 12% reduction is vascular events was countered by a 29% increase in major bleeding and the all-cause mortality was the same in the control and the treatment groups.

The ARRIVE trial was  a primary prevention trial in"high risk " subjects The intention-to-treat analysis showed that the primary outcome was the same in the control and aspirin groups. The primary outcome was a composite of stroke,heart attack,unstable angina,TIAs and death from CV causes.Gi bleeding was twice as common in the aspirin group.

The ASPREE trial was a primary prevention trial in subjects 70 years of age and older who were free of CV disease ,dementia or disability on entry into the study. After five years of 100 mg aspirin a day versus placebo there was no CV benefit .There was more GI bleeding with aspirin ( Hazard ratio of 1.39).

So unlike aspirin's well established  role in secondary CV disease prevention the benefit-risk ratio in primary prevention is ( in Ridker's words) "exceptionally small" . Dr. Ridker has been an advocate of statin use and it is not surprising  that he end his commentary with: "Thus beyond diet maintenance,exercise, and smoking cessation,the best strategy for the use of aspirin in the primary prevention of cardiovascular disease my simply be to prescribe a statin instead."

1) Ridker, PM Should Aspirin be used for primary prevention in the post-statin era? NEJM 379;16 oct 18 2018. 1572

Saturday, October 13, 2018

More physical activity may be needed to prevent HF than some other CVD events

 The title is a reworded version of the title of the article which is designated as reference 2 in the footnotes.

There are  2 (at least 2) epidemiologic studies that indicate a linear dose-response relationship between physical activity (PA) and the risk of heart failure. While one study ( Pandy et al see below) does demonstrate a "modest" reduction in HF risk at a lower levels of PA, both studies how a more robust reduction in HF at higher exercise levels.

Pandy et al (Circulation 2015,, see ref 1 below) did a meta-analysis involving about 370  thousand subjects , 20 thousand of which developed HF over a 13 years period.They compared the HF risk in 3 categories based on level of exercise, namely 500 MET-min per week ,1000 MET-min per week and 2000 MET-min per week.

500 MET-min per week is equivalent to 2.5 hours of "moderate" exercise per week or 1.25 hours of "vigorous" exercise per week.Moderate is defined a exercise requiring 3-5.9 MET and vigorous as about 7 METS. (It requires about7 METS to run a 15 minute mile or to finish Stage 2 on the Bruce protocol treadmill exercise tests. One should be able to walk a fifteen minute with a 02 consumption of 5 METS.)

1000 MET-hrs per week is 5 hours of moderate or 2.5 hours of vigorous exercise per week and 2000 as twice that or 10 hours of moderate exercise per week. Yes, that does seem like a lot,

Both the 2008 US exercise  guidelines and the 2018 guidelines recommend at least 500 but state that more benefits accrue with higher levels .

Pandy reported a linear,dose response with a "marked reduction in risk at very high doses of PA ( about 35%) at 2000 MET-min per week".

Their data:
exercise level                                HF RF

500 MET hrs per week                  0.9 (0.87-0.92)
1000 "  " " " " " " " "                       0.81(0.77-0.80
2000 "  "   "   "" """""                     0.65 (0.58-0.73)

Quoting the authors; "Only a moderate reduction ( about 10%) risk in HF noted at the minimal ( US guidelines) recommended level,"

The authors offer a mechanistic explanation namely that CAD event risk occurs at a lower level of exercise by reducing the usual suspect Risk factors (BP,Lipids,blood sugar control) while HF risk reduction occurs at a higher levels of exercise perhaps  by altering cardiac function and structure, i.e beneficial remodeling.

An earlier article Patel K, (Int J Cardiol 2013 see ref 2) had reached generally similar conclusions regarding the levels of exercise needed to decrease HR risk versus the amount adequate to  reduce general  CV risk, e m.gyocardial infarction.

Patel et al studied 5503 patients age 65 and older
During the 13 years of follow up incident HF developed in:
26% of those with little or no regular exercise
23% of those with "low"level of exercise
20% of those with "moderate"
19 % of those with high .

Low was defined a 1-499 Met-min per week
medium as 500-99
high as greater than 1000

The HRs for incident HF were:
low level exercise     0.87 (0.71-1.06)
medium                     0.68 (0.54-0.85) stat sig 
high                            0.60 (0.49-0.74) stat sig 

All exercise level groups had reduced HR for incident MI, stroke, and cardiovascular mortality but the lowest level group did not have a statistically significant  decrease in HR risk.

These 2 studies indicate that more exercise is associated with greater reduction in HF risk, although some HR HF decrease was noted in the lowest exercise group in the Pandy study.

Now for something completely different. A different type of study published by CR de Fillippi from the Cardiovascular Health study ( reference 3) provides an interesting  insight regarding possible mechanism(s) by which more exercise is better in terms of HF risk reduction. 

They studied 2, 9333 subject free of HF at the onset and  who had normal values for two biomarkers, NT-Pro BNP and cTnT (troponin).They then measured these markers every 2 to 3 years and compared incident increase in those markers in groups divided by their exercise levels.(They quantitatedle exercise using  a particular system and used numerical scores to define groups and I was not a to translate those values in to MET hrs to compare with the other 2 articles)

 They found compared with the participants with the lowest PA activity scores those with the highest (i.e. more exercise) had an low odds ratio of 0.50 (0.33-0.77) for a significant increase in NT proBNP and an OR of 0.3 for and increase in troponin.  Quoting  the authors "increased levels of NTProBNP and cTnT may reflect pathological precursors of hemodynamic stress and injury that are prevented by PA at some as yet more precisely defined level.

So how to put all this together.

An  appealing ( at least to me) mechanistic explanation is that an overall decrease in CV mortally and arguably a slight reduction in HF risk  can be brought about by modest exercise and even  perhaps slightly less  than modest levels  by reducing the usual suspect,traditional CVD risk factors.Modest here refers to about 500 MET hrs per week. but some studies have shown a decreased heart attack risk at even lower exercise levels.

A more robust risk reduction in HF risk (perhaps 20-35%) seems  to require higher levels of exercise  ( in the 1000 Met-hrs per week range and higher) by perhaps bringing about an advantageous remodeling of the heart or at least a mitigation of the deleterious remodeling of the heart than occurs with sedentary aging which in turn may predispose to the development of heart failure with preserved ejection fraction (HFpEF).

To the extent that CVD risk factor reduction can decrease heart attacks and the  accompanying reduction in   heart function some reduction in HF risk would be likely, i.e.some reduction in heart failure with reduced ejection fraction ( HFpEF). But at least half of cases of HF are not associated with decreased systolic function ( at least as measured by the ejection fraction  (EJ) but by the echocardiographic finding of decreased left ventricular compliance and distensibility which according to the work of Dr. Ben Levine and others at SW  Medical School in Dallas predispose to diastolic heart failure  (HFpEF) .That group suggests that at least 30 minutes of exercise 4 to five times a week might be sufficient to prevent that age related loss of cardiac compliance. ( see ref 4 below for more on this argument) and perhaps prevent at least some cases of HFpEF.

1)Pandy,A "Linear,dose dependent inverse association between PA(physical activity) and heart failure risk Circ. 115.132 p 1786-1794

2.Patel K. "Prevention of heart failure in older adults may require higher levels of physical activity than needed for other cardiovascular events." Int J Cardiol. 2013, Oct 168 (3) 1905-1909)

3)de Fillippi, CR "Physical activity, change in biomarkers of myocardial stress and injury, and subsequent heart failure risk in older adults. JAm Coll Cardiol.. 2012 Dec. 18;60 (24), 2539-47

4) Bhella, PS  "Impact of lifelong exercise "dose" on left ventricular compliance and distensibility"J Amer coll cardiology. 2014 , 64, no 12,p 1267  

Tuesday, October 09, 2018

2018 U.S. exercise guidelines-or how exercise is good for just about everything

The 2018 Physical Activity Guidelines Advisory Committee issued its report to the Secretary of HHS in February 2018.See here for link to full report.

Their prescription for exercise was unchanged from their 2008 recommendations.  They recommend 2.5 to 5 hours of moderate to vigorous exercise per week. This can also be expressed as 500 to 1000 Met-minutes per week. "Moderate" is defined as exercise requiring between 3 and 5.9 METS and "vigorous" as greater than 6 METS.

To put those numbers into perspective , consider than it would require about 7 METS to run a fifteen minute miles and about 5 METs to walk a fifteen minute mile and about 9 METS to run a 12 minute mile. It requires about 7 METS to complete Stage 2 on the Bruce treadmill protocol .A MET is 3.5 ml of oxygen per kilogram weight per minute. 

Now, about how exercise (physical activity or PA) is good for just about everything. 

The 2008 exercise guidelines reported that PA could lead to a reduction in risk of breast cancer and colon cancer . The 2018 reports adds the following cancers to those whose risk is reduced by PA :
bladder, lung, esophagus, endometrium and stomach.But reduction in heart disease risk is the major selling. point for an exercise program as well as decrease in diabetes and hypertension risk. 

The publication also offers evidence of a risk reduction for dementia and depression.

If the benefits of exercise could be achieved by a daily  pill, everyone would be taking it.

Thursday, September 13, 2018

The impressive and alarming success of the American Board of Internal Medicine Foundation

The American Board of Internal Medicine Foundation (ABIMF) is not the largest,most heavily endowed nor the best known of the many non-profit organizations who  function as advocates for various aspects of health care and medical practice. However, its success in promulgating concepts and influencing medical practice and health care seems disproportionately greater than one might expect based on its size. ABIMF's "greatest" achievement is the development and promulgation of the notion of Medical Professionalism and its major tenets: patient welfare,patient autonomy and social justice. The insertion of the later tenet into medical ethics is a major departure from traditional ethics and is destructive to the physician patient relationship

The first two tenets were long standing pillars of medical ethics and practice and dealt with the relationship between the physician and patient but in 1992, their efforts along with the ACP Foundation and a European Group proclaimed that part of medical professionalism included what they believed was the proper relationship between the physician and society

This  manifesto was published in the Annals of Internal Medicine in 1992 in a paper entitled Medical Professionalism in the New Millennium-A Physician Charter. The ABIF has continued after the 1992 paper to promote the primacy of patient welfare,patient autonomy and social justice and to advocate for "a just and cost effective distribution of finite resources".

 The notion of a co-duty,one to the patient and one to society,was not previously a part of western medical ethics.The 1991 edition of the AMA ethical code did not mention social justice or stewardship of society's resources. Cost effective care is the major thrust of the foundation's recent initiative called "choosing wisely" .  By 2012 over 100 other medical professional organizations had signed on to the Charter and education along those lines apparently is taking place in a number of medical school according to a 2012 article in the Annals of Internal Medicine.

It is the ABIM's MOC  ( Maintenance of Certification program ) that has caused the most angst for internists and reliable reports of its very questionable financial activities have triggered an unprecedented uprising  which surprisingly has had more than a little success.( Much credit for this is due to Dr. Wesby Fisher who on his blog has reported activities of the ABIM and the ABIMF that are  egregious and arguably illegal.)

Yet the sea change in the discussion about medical ethics and professional behavior importantly driven by the same folks who gave us MOC  may in the long run be even more damaging.

Thursday, September 06, 2018

Is the minimal level of recommended exercise sufficient to decrease the risk of heart failure?

In January 2017, I posted a blog commentary entitled " The minimum exercise levels of  the 2008 guidelines won't prevent heart failure". See here.

The gist of that commentary   was that the adherence to the minimal exercise levels indicated by the guidelines had been demonstrated by ample epidemiologic studies to reduce the incidence of cardiovascular disease (CVD) but  exercise at that level had not been demonstrated to reduce   heart failure (HF) incidence and that a higher amount of exercise was needed.

Since then I have more carefully studied a 2015 epidemiologic paper  by Pandy,which I had read before but obviously not with adequate attention , and a detailed physiologic comparison of cardiac function by Bella et al  in 4 groups of healthy subjects who varied  in their long term exercise levels to which I also had not paid appropriate attention. 

These considerations   resulted in a major revision my 2017 headline to " Adherence to the 2008 guideline will reduce HF incidence but more exercise will reduce HF risk significantly more"

Note: I have added an addendum to the 2017 posting  stating the headline is simply wrong 

So now to try and clean up the earlier erroneous  commentary .

First a review of some background:

The 2008 US and WHO guidelines recommend a minimum of 150 minutes of moderate exercise per week or 75 minutes of vigorous exercise. This corresponds to 500 MET minutes  per week or 8.3 MET hours .The US panel also said that further gain could be made by increasing that level to twice that amount. Moderate intensity was defined as requiring between 3 and 5.9 METS and vigorous greater than 6 METS.Note-the panel was addressing the risk of cardiovascular disease in general and not heart failure risk per se .

There is universal agreement that aerobic exercise will decrease heart disease risk ( and according to some studies-dementia,some cancers and type 2 diabetes) but there is disagreement as regards how little exercise  might be  sufficient to reduce cardiovascular risk  and how much exercise might be harmful. I leave those 2  questions  to another time.

In regard to HF:

Patel et (1) published a 2013 review of 5503 subjects age 65 and older from the Cardiovascular Health Study .They divided participants into inactive ,low level exercise ( 1-499 METS),Medium (500 to 999 METS )and high was defined as  greater than 1000 METS 

The hazard ratio (HR) for the low group was a non-statistically significant 0.87 (0.71-1.06,p=0.170.
The medium groups HR 0.68 (0.54-0.85)p=0.001
The high group HR 0.60(0.49-0.74, p=0.026<0 .001.="" p="">

Note that  the low and medium groups overlap the 500 level so  no conclusive verdict regarding HF risk reduction with 500 MET level can be made. You can say that the lowest exercise group enjoyed no reduction in HF risk but we do not know how many subjects were closer to the 1 than to the 500 level. We can say that the medium and high level  did demonstrate a HF  risk reduction but can conclude  nothing about the value of exercising at the 500 MET min level,which is the minimal level recommended by the 2008 panel. 

However, from Pandy's 2015 meta-analysis (2) that there demonstrable risk reduction  in HF in a group of subjects exercising at the 500 MET level. The authors examined data that included over 20 thousand HF events among 370 thousand participants in some 12 prospective cohort studies. 

The 500 MET-min  per week group had a reduction in HF risk ( HR-0.9 (0.81-0.92). However, a greater risk reduction was found in the 1000 MET Min per week group ) HR-.81 (0.77-0.86) and even greater reduction 0.65 (0.58 -0.73 ) in the group at the 2000MET min per week which corresponds to 10 hours of moderate exercise per week or 4 times the minimal amount suggested by the 2008 guidelines.

So the epidemiology  data indicate  that the lower level of recommended exercise will cause a measurable decrease in HF risk but in that regard more does seem to be better.Now to consider Bella's (3) physiological data which is consistent with Pandy's analysis.

 The following  2 paragraphs are copied from my earlier blog commentary.

" Dr Paul Bhella and his  associates  did extensive physiological studies on four groups of healthy volunteers over the age of 64. Four groups were designated   on the basis of their exercise history for the preceding 25 years. (not a typo) 1) sedentary-no more than one exercise session per week  2) casual exerciser-2-3 session per week 3) "committed" exercisers-4-5 session per week and 4)competitive master level athletes -6-7 session per week and competed regularly.  All had normal systolic function ( as defined by a normal resting ejection fraction) but groups one and two has decreased left ventricular compliance while the committed and competitive groups had left ventricular pressure volume curves and left ventricular masses similar to young healthy controls. ( see here for my  further comments and a few caveats regarding this paper including reference to Tanaka's work that challenges the notion that long term endurance exercise  does in fact preserve  ventricular compliance)

Quoting Bhella ". . at least 30 minutes of dynamic exercise per session for 4-5 days per week over a lifetime can  sufficiently prevent most of the decreases in LV compliance and distensibility observed with sedentary aging"

It appears that training at triathlon or marathon levels is not necessary to decrease long term risk of heart failure but the exercise has to be persistent. The term "lifelong "used by Bella may be an exaggeration but his subjects had a 25 year history of regular aerobic exercise.

Bella's data seems to confirm the notion that the 2/12 hours per week recommendation just might decrease the risk of HF with the caveat " if done over a long period of time". The same  group has subsequently published data showing that beginning a  more intense exercise program in a person's 60s or 70's will not result in improved left ventricular compliance but , of course, one would expect  health benefits.

I quote a key paragraph from Bella:

"This study's key finding is the novel observation tcompliance that at least 30 minutes of dynamic exercise per session 4  to 5 days per week over a lifetime can sufficiently prevent most of the decrease in and distensibility observed  with sedentary aging.
This finding holds important implications for global health as ventricular stiffening has been implicated in the pathophysiology of many common CV conditions affecting the elderly."

Contrary to my earlier commentary the minimal levels of exercise may well be enough to decrease the risk of HF but exercise at about twice that levels is likely to bring about a more significant reduction. Note that Bella's comment of 30 minutes 4-5 days a week corresponds to the minimal recommendation of 150 minutes of moderate exercise per week.

1)Patel,K et al Prevention of heart failure in older adults may require higher levels of  physical activity than needed for other cardiovascular events.Int j Cardiol 2013 1905,-1909.

2)Pandy, A Dose Response relationship  between physical activity and risk of heart failure.A meta-analysis. Circulation 2015 132 1786-1794

3)Behlla,P Impact of lifelong exercise "dose"on left ventricular compliance and distensibility. JACC 64 1257-1267 2014  

Wednesday, September 05, 2018

Does the notion that people have a duty to be healthy shatter traditional medical ethics

First lets define what we mean by traditional medical ethics.This would include the medical ethical precepts that constituted medical ethics before the announcement of the "New Professionalism" by the ACP and others. Basically and stating it informally it is that the physician has a fiduciary duty to the patients, and he should place the patients interests before his and of course first do no harm.

Keeping those precepts in mind, consider the following statement which is typical of a growing trend in medical commentaries .

People ( patients) have a duty to be healthy ( practice "healthy behaviors" and eschew "unhealthy behaviors") and comply with medical advice for the good of healthy population.

Drs. JF Wharam and D. Salmasy, writing in the Jan. 14,2009 issue of JAMA. In their discussion of P4P arrangements they state:

...policy makers, health care executives,disease advocates, and scientists with clinical or epidemiological expertise effectively choose population-level goals and thus impose obligations in a manner that
might ( my italics) infringe on patient and physician autonomy. Without fair deliberation,such goals, however wise, cannot claim legitimacy

I suggest that the word "might" be deleted from the above quote. It will infringe. Further, it is not clear what would constitute "fair" deliberation.When someone begins to talk about being fair,watch out.So with "fair deliberation " such claims ( if wise) are , according to the authors therefore  legitimate.

When physicians get some of their income by meeting certain population based goals( e.g. have x% of patients with a hemoglobin A1c under some number) patients who might seem to eat too much or not always take their medicine or whatever else might  be perceived  by the physicians as getting in the way of the population based goals and keeping  the doc from her bonus.Again it is issue of serving two masters,the real life patient in the exam room  versus some insurance based collective construct.

Friday, August 10, 2018

Many Kudos for the anti-MOC warriors and glimmers of hope

Dr. Wes Fisher ,an EP Cardiologist from the Chicago area, has waged what was  for a long while a
one man crusade about the questionable activities of the American Board of Internal Medicine and its own foundation the ABIM foundation and the harmful effects of  their maintenance of certification  (MOC) program. I have blogged a bit about that before and now a number of other physicians have joined in the fray.

Now it seems his prodigious work in that area is beginning to pay off.He recently took part in a very instructive  podcast with Dr. Michel Accad. Fisher is now working with a law firm doing preliminary work hopefully leading to a law suit against the ABIM possibly involving anti trust  issues and fraud.

Money is need for the litigation to move forward.To aid in that effort , Dr. Accad has offered a copy of his brilliant book, "Moving Mountains" to folks who contribute to a fund for the litigation.

Go to the pod cast to learn in details about the antics of the ABIM that catalyzed Dr. Fisher's efforts. See  this link for episode no. 17 of the Accad and Koka Report and links are available there for a GoFundMe link for Fisher's law suit and to the organization he founded, Practicing Physicians of America.

Incidental note. For the last 2 days I have been unable to link to Dr. Fisher's website. I enter drwes.blogspot.com and am diverted to www.widgetserver.com .I was able to backdoor into his site from his Twitter feed.Has his web site been hacked? Coincidence? Addendum , two days later Dr. Fisher's web site was up .

Thursday, July 12, 2018

How well do the Echo guidelines work to estimate cardiac filling pressures ?

Elevated filling pressure is thought to define heart failure as it is thought to be the driver for exercise intolerance and shortness of breath.

Filling pressures can be invasively determined by catheters in either the pulmonary artery wedge position or in the left ventricle.

One of the major aims of echocardiography is to provide reliable estimate of filling pressures .It is generally accepted that echocardiographic indices are more effective in determining  filling pressures in patients with reduced ejection fraction (EF) and is more problematic in patients with preserved EF

The 2009 echo guides  for determination of diastolic function were revised in the 2016 guidelines and both  have been the target of some criticisms.

IMO a 2015 article ( 2) from the Cleveland Clinic offers data that raises reasonable concerns about the estimation of filling pressure in patient with preserved EF.It should be noted that the classification system of degrees of diastolic dysfunction (DD) used by the authors is not the exact system proposed by the 2016 guidelines. but rather those of the 2009 guidelines.(1) and the authors' criticism relate specifically to the 2009 system.However I believe their conclusion ( see below) regarding the basic underlying paradigm holds regardless of tweeks made to the 2009 guidelines.

The authors reviewed 460 consecutive patients who underwent echocardiography within 24 hours of elective left heart catheterization.

Their figure 5 plots left ventricular diastolic pressure (LVEDP) against normal and the 3 grades of DD in patients with EF greater than 50 % and those with EF less than 50%.In both groups there was no difference in LVEDP between normals and those with Grade 1 and Grade 2. The only statistically significant difference was that between normals and those with grade 3  DD who had EF less than 50%.

The authors conclude: "the findings of this study question the notion that DD is a predictable, progressive process beginning with impaired relaxation followed by reduced compliance and increased filling pressures. The prognostic value of echo graded DD may relate more to its reflection of intrinsic properties of the left ventricle, or to exercise hemodynamics  than to its correlation with resting hemodynamics alone. "A Mayo Clinic study  of 467 patients ( 3) by Kane et al found  no higher pulmonary artery systolic pressures at rest  or on  exercise in those patients with the echo diagnosis of impaired relaxation.

 1) Nagueh, SF Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echo 2009, 22, 107

2) Grant A, Grading diastolic function by echocardiography:hemodynamic validation of the existing guidelines. Cardio Vascular Ultrasound 2015.

3)Kane, GC et al Impact of age on pulmonary systolic pressure at rest and with exercise.Echo Research and Practice, 2016,3(2) 53-61

addendum 8/1/18 spelling errors corrected and several poorly worded sentences revised.

Sunday, July 08, 2018

The great social justice bait and switch courtesy of ACP,ABIM and RWJF

Certain members of the leadership of the American College of Physicians,the American Board of Internal Medicine and the Robert Wood Johnson Foundation authored a manuscript designed to permanently change the physician patient relationship.The paper is entitled "Medical Professionalism in the new millennium: A Physician Charter.",.which I will refer to in this commentary as "The Charter" .  It was a project of  the  foundations of the ABIM and ACP and the European Federation of Internal Medicine.See here for the document.

The documents simply asserted that physicians are the stewards of a [collectively owned] store of medical resources and that physicians have a professional obligation to work for social justice. While they did not explicitly deny the fiduciary role of the physician to the patients in effect  they declared that there was a co duty to conserve the "limited" medical resources as well as the duty  to the individual patient.Contrary to the biblical warning about serving two masters the Charter's authors urge a stewardship of medical resources which subsequent publications by ACP,ABIM and others  said will best be made operational by physicians  following guidelines.

In my opinion this publication is a poster child for the use of gratuitous assertions.

Quoting from the Charter" essential to the contract [medicine's contract with society] is the public trust".

The Charter was published in the Annals of Internal Medicine  and Dr. Harold Sox, the then editor of the Annals of Internal Medicine, offered an introductory commentary. He said in part "the condition of Medical Practice are tempting physicians to abandon their commitment to the primary of patient welfare....the Charter call physicians to promote fair distribution of health care resources"

 I suggest that the choice of the words "primacy of patient welfare" is significant in the omission of the modifier "individual" in front of the word patient. Subsequent promotion of the Charter has made it clear that patient welfare will be defined in terms of the aggregate not in terms of the individual patient.  A subsequent publication ( JAMA: November 13,2013) by Dr. Sox advocating  "population Medicine " made it clear what type of patient welfare Dr Sox favored. See here.

A brief quote from Sox; "

"Perhaps the de facto organizing principle for US health care,approaching each patient strictly as an individual is obsolete.The population health approach is an alternative." (I have added the bolding)

Dr. Sox makes explicit what is hinted at and glossed over in the charter,namely the sacrifice of the individual to the group, the individual patient to the aggregate, or at least  to some aggregate metric claimed to represent the good of the group.

 The charter promised social justice and operationally that has been translated to following guide lines based on alleged aggregate benefit.

Friday, July 06, 2018

Medicine is increasingly dominated by collectivist ideology.

This commentary title is an truncated and slightly altered version  of the following quote from the brilliant essay by Dr. Michel Accad. "Medicine today is dominated by the collectivist ideology" . See here for the reference to his 2009 contribution. 

This is a theme I have thought and fretted about far too much.Many of the thoughts I have mulled over and occasionally expressed in this blog are far better expressed in Dr. Accad's essay. Here is a sample;

"In the broadest sense, medical collectivism is the belief that medicine cannot be left to voluntary and unrestricted transactions between individual patients and individual healers but must be improved, directly or indirectly, by the hand of government."

and another.

" Individuals and populations ,patients and society are conveniently conflated as a matter of fact."

And here is the real money quote.

"..hoodwinking physicians into practicing population medicine is of course the essential means to confuse practitioners into thoughtlessly carry out sweeping interventions whose primary benefit is the profit of third parties."

Docs who were trained in my era ( I know that was a long time now-MD-64) learned that the principle ethical precept was do what was right for the patient and there was ,with few exception.s no other obligations.  What was definitely not on the table was the notion that physicians had an obligation to conserve the nation's medical resources. Social justice was not on the table.

I believe the metaphor of the Bootlegger and the Baptist captures an important aspect of what is happening in  medical practice in the United States.

I do not envision a wide spread plot or conspiracy of third party payers and academic physicians and leaders of major medical professional organizations meeting regularly to further their long term dream of finally taming the physicians and disabusing them of their traditional role as a fiduciary of their patients. However, the third party payers certainty welcome the efforts of the academic medical elite in that regard and some times welcome them into their ranks .

The Baptists in this conception are those physicians who sincerely believe that in the age old conflict between the interests of the individual and those of society as a whole that the trump card would be held by society.The Bootleggers are the third party payers whose bottom line increases in proportion to the acceptance of those views.

Thursday, July 05, 2018

Is the Choosing Wisely campaign a giant flim flam benefitting the thrid party payers?

Is the choosing wisely initiative (CW) just a clever ploy to save money for the third party payer?
 or Is it just about a sincere effort by physicians who really care to eliminate to the extent feasible fraud and waste?

Is CW an extension of the New Professionalism movement?

I  argue that CW is a flim flam and a power grab jointly shared by the third party payers and the medical progressive elite who provide the academic cover and propaganda. I  argue that it is in fact about much more that elimination of fraud and waste and that it is a logical outgrow of a major element of the change in medical ethics that the New Professionalism movement is attempting to bring about.

It is a story about the ACP the ABIM and a foundation ( the ABIMF) established with money obtained from internists taking certifying exams whose fees greatly exceeded any reasonable cost of providing those examinations and about  another foundation  , the Robert Wood Johnson Foundation (RWJF)

I  argue that it is not just the CW ad campaign funded by ABIMF and RWJF but it is larger namely The New Professionalism-Choosing wisely-high value care flim flam.

The New Professionalism authored by folks from ACP,ABIM and the RWJF  provided the cover or alleged philosophical foundation for CW and the push for high value care.The follow the money rule continues to have great explanatory value.

Wednesday, June 27, 2018

Why did the greatest "ancient marathoner" slow down signficantly in his 70s?

Why did the greatest ancient marathoner of all time slow down so much in the decade of his 70s?

At age 73 Ed Whitlock finished a marathon in 2:54:48. Twenty-five years earlier he ran a marathon in 2:31:23. In a quarter of a century his marathon time decreased by only 23 minutes. See here for the blog Cannute's Efficient Running Site 's tribute to Whitlock.

Whitlock's 02 max was measure at 52.8 ml/kilo/min when he was aged 70 and 11 years later at age 82 a measured Ox max was essentially unchanged ( 54 ml/kilo/min).

A person's maximal oxygen consumption ( 02 Max) decreases with age. The per decade decrement is generally said to be between 5 and 10 Percent. The jury is still out regarding if the rate of decline in endurance athletes is more,less or the same as more sedentary humans. There is good evidence indicating that the rate of decline increases around age 70 and values as high as 15 % percent per year or more have been reported. Assuming the 02 Max measurements are correct, Whitlock's 02 max was essentially unchanged during his running trek through his  70s but his marathon times decreased significantly.

As commented on by Cannute, Whitlock in his 40s was a very good marathoner but was not setting world age marathon records . At age 48 he ran a marathon in 2:31:23- a very good time for age-actually any age- but not the record.  Ye,t by age 70 he was setting marathon records for age and continuing setting records until a few months before his death at age 86.He set the age 85plus marathon record in Toronto clocking in a 3:56:33

So what was his secret? Obviously his genetic endowment included a high 02 max. His marathon times did decrease between age 70 and age 80. He was running sub four hour marathon at 80 plus while running sub 3 hour at 70 plus while his measured 02 max seemed constant over that time period.

Of course there is more to running marathon than 02 max.

Whitlock's training in his 70s and 80 did not follow the current generally accepted marathon training  principles. He did no speed work except in races. In his 70s he is said to  have run up to 3 hours a day , almost every day at a very slow pace, described  by him as a "slow shuffle". He carried the LSD (long slow distances) program to a extreme.

Tim Noakes, noted exercise physiologists and long time endurance athlete, believes that a major reason than marathon times decrease markedly in the decade of their 70s is that most older runners cannot maintain the hours of training necessary to perform well in the marathon  in part because  there are too manyminor ( and major injuries), too many aches and pains. The muscles endure better than the "connectors", i.e the structures and tissue connecting the bones to the muscles and joints.

Yet it may be that even in the absence of significant injury or a nagging series of minor injuries and even with high level of training  a human's running speed for distance decreases significantly during the 8th decade of life. (about 25% decrease in marathon running speed for the world's greater old timer marathoner.) One suspect to consider is  muscle loss of "spring function" and the spring function of tendons and the arch of the foot. You figuratively and maybe literally loose the "spring in your step".