A few years ago I posted a piece about the effects of antioxidants on GI tract cancers.There was a reported small increase in Relative Risk (1.06) if one used a fixed effects statistical model but no increase if one used a random effects statistical model analysis.
Here the truth seemed to turn on the choice of statistical method used. How robust could the truth be when it depends on choices made by statisticians and importantly when experts disagree on the choice which was the case quoted above? For a critical reader to decide for himself in a rational way it seems he would have to be fairly conversant in the vagaries of regression analysis and analysis of variance which are the areas where these two competing statistical models live.
I have read that the fixed effect model in general is the one more commonly used and it is the one with lower standard errors and hence more power. I have read that in regard to meta-analysis the fixed effect model is appropriate when the data appear homogeneous and the random effects model when the data are heterogeneous. Then we run up against tests for heterogeneity in regard to which no one should be surprise if statisticians may differ as to the correct way to do that. It seems to me if I writing a paper and wanted it published and since positive studies are more likely to see the light of day in print I would want to use the more powerful fixed effects model.
It seems the deeper you plunge into the analysis of the data the less certain you may become regarding the robustness of the conclusion.But truth does not really turn on the basis of the choice of statistical technique for one meta-analysis.The results of any one study-even if that study is a meta-analysis-should not decide the issue.Prior context and biological plausibility must be taken into account.
Monday, November 27, 2017
Saturday, November 25, 2017
How to survive under socialized medicine
Here is a quote which to me seems may have high titer of deep insight.(my bolding)
"In many areas of medicine, particularly those related to especially politicized areas like CVD and other "life-style" diseases, government-franchised practitioners are often dangerously ignorant of essential facts. Remember that the worst aspect of socialist medicine is that medicine as a rational science is epistemologically destroyed by eliminating the role of the doctor as a sovereign, independently thinking, professional. "
H/T to Dr. Paul Hsieh in his blog "We Stand Firm" who in turn found it in essay entitled "How to Survive under Socialized Medicine" which was re-published in another blog (ReasonPharm) which in turn credited it to a facebook entry by some one named Christian W. (Please excuse the rather lengthy attribution but I did not want to slight the person who seems to be the actual author.)
. .
"In many areas of medicine, particularly those related to especially politicized areas like CVD and other "life-style" diseases, government-franchised practitioners are often dangerously ignorant of essential facts. Remember that the worst aspect of socialist medicine is that medicine as a rational science is epistemologically destroyed by eliminating the role of the doctor as a sovereign, independently thinking, professional. "
H/T to Dr. Paul Hsieh in his blog "We Stand Firm" who in turn found it in essay entitled "How to Survive under Socialized Medicine" which was re-published in another blog (ReasonPharm) which in turn credited it to a facebook entry by some one named Christian W. (Please excuse the rather lengthy attribution but I did not want to slight the person who seems to be the actual author.)
. .
Friday, November 17, 2017
The division of internist into hospitalist and "officist" and its demise.
It is the 20th anniversary of the birth of the hospitalist.A recent article describes what was presented as a fairly widespread feeling among hospitalists of "not getting no respect. ".
Some of the doctors interviewed spoke of the hospitalist being a gopher for various attending physicians,a clerk and paper work finisher for numerous physicians and thought of more or less as a intern or junior resident and one who often seemed not worthy of a return phone call.The duties of the hospitalist when I was briefly in the hospital last year with a pulmonary embolus seemed to fit that pattern. A very pleasant young physician mainly ushered the consulting cardiologist and pulmonary doc in and wrapped up the paper work as both of the consultants made the real decisions regarding testing and treatment. A colleague of mine who attended at that hospital said he made the decisions regarding patients he admitted while the hospitalist was useful in relieving him of paperwork. I realize that the above description does not apply to the situation of all hospitalists.
While the officist has become barely distinguishable from the FP or GP or even NP, the hospitalist , at least in some settings seems to have devolved into a junior house officer while the real management of the critically ill fall to the cardiologist, the pulmonologist and the intensivist.
In the 1970s and 80s in our internal medicine practice it was routine for GPs ( they were not FPs at the time) to refer complicated,sick patients to our groups. ( It seemed to more often than not happen late on Friday afternoons. The physician to whom the referral was made would personally care for the patient in the hospital often aided by his internist specialists partners.)
The sequence was that the patient or referring physician would call the physician in our group -if he was not on call one of the partners would admit the patient to the hospital and attend to him calling on other partner subspecialists as the situation warranted. Now the patient calls ,for example after hours and the recorded message advises the patient to go to the ER. He is seen by the ER doctor who may admit the patient and the hospitalist would see the patient and consult as needed various specialists. The internist, assuming the patient had one, would often learn of the event when the patient was discharged back to the internist who had nothing to do with his treatment and may or may not have received a copy of the discharge summary.
In describing that archaic situation to young house staff I would feel like describing the quaint rotary phone that I used when growing up in the 50s.
.
Some of the doctors interviewed spoke of the hospitalist being a gopher for various attending physicians,a clerk and paper work finisher for numerous physicians and thought of more or less as a intern or junior resident and one who often seemed not worthy of a return phone call.The duties of the hospitalist when I was briefly in the hospital last year with a pulmonary embolus seemed to fit that pattern. A very pleasant young physician mainly ushered the consulting cardiologist and pulmonary doc in and wrapped up the paper work as both of the consultants made the real decisions regarding testing and treatment. A colleague of mine who attended at that hospital said he made the decisions regarding patients he admitted while the hospitalist was useful in relieving him of paperwork. I realize that the above description does not apply to the situation of all hospitalists.
While the officist has become barely distinguishable from the FP or GP or even NP, the hospitalist , at least in some settings seems to have devolved into a junior house officer while the real management of the critically ill fall to the cardiologist, the pulmonologist and the intensivist.
In the 1970s and 80s in our internal medicine practice it was routine for GPs ( they were not FPs at the time) to refer complicated,sick patients to our groups. ( It seemed to more often than not happen late on Friday afternoons. The physician to whom the referral was made would personally care for the patient in the hospital often aided by his internist specialists partners.)
The sequence was that the patient or referring physician would call the physician in our group -if he was not on call one of the partners would admit the patient to the hospital and attend to him calling on other partner subspecialists as the situation warranted. Now the patient calls ,for example after hours and the recorded message advises the patient to go to the ER. He is seen by the ER doctor who may admit the patient and the hospitalist would see the patient and consult as needed various specialists. The internist, assuming the patient had one, would often learn of the event when the patient was discharged back to the internist who had nothing to do with his treatment and may or may not have received a copy of the discharge summary.
In describing that archaic situation to young house staff I would feel like describing the quaint rotary phone that I used when growing up in the 50s.
.
Monday, November 13, 2017
James Gailbraith combines a belief in perpetual motion machine with believe in there IS a free lunch in his economic advice
Dr. James Galbraith is the son of John Kenneth Galbraith and here the apple falls very close to the tree. See here for his thoughts published in the Nation. Here is discussion of those comments as formulated by Dr.Paul Hsieh and published on line at Pajamamedia.com blog.
Here are the major points as Dr. Hsieh summarizes them:
Think about what he said. Governments and banks can create something from nothing. Yes, I know that the government can "print money" and that banks create money in the fractional reserve banking system but you can't fool all of the people all of the time. The government and banks in Greece seem to have not understood that universal principle as they have made nothing out of something as they made tried to make something out of nothing Apparently the government in Greece has not consulted with Dr. Galbraith as they seemingly have run out of money. His perpetual motion money making machine is that you just keep rolling over debt which was the something that governments made out of nothing and there is no problem. So why did the Germans and the EU have to bail out Greece? Why could not the government just continued to make something from nothing?Why did we see hyper-inflation in Germany? Why are Not all countries made prosperous by this simple technique print more money and spend it.
Here are the major points as Dr. Hsieh summarizes them:
- The political push to reduce government deficits is economically misguided, based on an irrational “phobia” of deficits.
- If we want economic growth, we need more spending. Only banks and governments can stimulate spending because (in his words): “Governments and banks are the two entities with the power to create something from nothing.”
- We shouldn’t worry about the alleged impending bankruptcy of Social Security or Medicare — or of the U.S. government itself. Why? Because the government is the source of money and therefore can’t run out.
- Government debt is not really a “burden on future generations,” because it never has to be repaid. Each generation can just pass that debt onto the next generation, so there’s no problem.
Think about what he said. Governments and banks can create something from nothing. Yes, I know that the government can "print money" and that banks create money in the fractional reserve banking system but you can't fool all of the people all of the time. The government and banks in Greece seem to have not understood that universal principle as they have made nothing out of something as they made tried to make something out of nothing Apparently the government in Greece has not consulted with Dr. Galbraith as they seemingly have run out of money. His perpetual motion money making machine is that you just keep rolling over debt which was the something that governments made out of nothing and there is no problem. So why did the Germans and the EU have to bail out Greece? Why could not the government just continued to make something from nothing?Why did we see hyper-inflation in Germany? Why are Not all countries made prosperous by this simple technique print more money and spend it.
Wednesday, November 08, 2017
Before Obamacare it was other people's money effect -Afterwards more so
When something is being payed for with other people's money, more will purchased. This is also true if you merely think someone else is paying for it, as in the situation that exists with employer paid health care insurance.
Quoting myself from 2006:
Medical care came to be "managed " by the managed care sector because of the concept of "other people's money". To a large degree individuals pay for only a portion of their health care the remainder paid by either employers or the government. There was not much fuss made by these other people until the costs of health care rose to some threshold above which employers and other third party payers including CMS thought costs were getting out of hand. Then entered cost containment via the various cost savings actions of managed care.
The effect on the traditional fiduciary duties of physicians to patients by the duties of the for-profit corporation vis-a -vis its shareholders is the root cause of many ethical problems generated by managed care. Basically the HMO and third party payers generally strive to make money or save it and they introduce mechanisms to control physician behavior to that end even if that control involves abrogation of the fundamental duty of the doctor to place the patient well being and interests first. The efforts of the third parties in that regard weaken the physician-patient relationship and damage the trust element in the relationship.Ethical cover for this abrogation was provided by the introduction and unfortunate widespread acceptance by medical professionals organizations of the "New Professionalism" which alleged a physician's duty to society to be a good steward of society resources must somehow be balanced against the physician's duty to the patient.
With Obamacare, more people will be trying to spend other people's money.The biggest other people is CMS who along with HHS will have mandates to control costs. Mix in the decreasing number of primary care doctors to the number of patients seeking care with HHS/CMS moving to decrease health care providers reimbursements and you have a situation in which patient need more than ever an advocate. But patient advocacy will be not longer be the prime directive but merely a factor to be weighed against the imperative to be a steward of society's scare medical resource to the extent that physicians actually internalize the bogus arguments of the New Professionalism.
Monday, November 06, 2017
What is the evidence that prolonged endurance execise damages the conduction system of the heart.
In 1985, RJ Northcutt studied 20 males endurance athletes that were recruited from a Scottish Harrier's club. All were older than 45 years and ran for 25 miles per week or more. Stress testing and 48 hour Holter type monitoring were done.. He found that 9 had heart rates less than 35 beats per minutes,6 had a prolonged PR interval, 4 had Mobitz type ii heart block and three with complete heart block one of whom had a pacemaker implanted. With exercise all of the various blocks disappeared.
Northcott with co-author Stuart Hood (1,2) studied 19 of the 20 subjects twelve years later.Two of the group had pacemaker implantation in the interval, one for complete heart block with atrial fibrillation and the other for asystolic intervals up to 15 seconds. None of the others had any "bradycardic problems". 7 of the 20 in 1985 has systolic pauses greater than 2 seconds and 5 of those had none on follow-up. The other two had decreased the intensity of their running. ( not clear from the article if those 2 had pauses or not) Quoting the authors: "Our finding nonetheless suggest that clinically significant bradycardia symptoms are a real but rare potential complication of lifetime endurance exercise."
Baldesberger et al (3) studied 62 former professional cyclists who had long since (over thirty years) retired from active competition.Two had pacemaker implantation. None had complete RBBB or LBBB and two had EKG pattern of left anterior hemiblock.None had second degree heart block. Six had "sinus node disease which the authors defined as heart rate less than 40 beats per minute.
Andersen's 2013 article (4) is often quoted in support of the argument that there is an increased risk of atrial fibrillation in endurance athletes but it also has data on the risk of "bradyarrhythmias".The authors studied the records of over 52 thousand participants in a 90 km cross country race in Sweden (the Vasaloppet). They then compared those who raced more (five or more races) with those who only did one race and compared the faster skiers with the slower. The Hazard ratio (HR) for atrial fibrillation was 1.2 (0.93-155) while the HR for bradyarrhythmias was 1.85 (0.97--3.54). When comparing those who did more races with those who did only one they reported a HR for AF of 1.29 (1.04-1.61 and a HR for bradyarrhythmias 2.10 (1.28-3.47).The bradyarrrythmis were mainly type ii heart block but the ICD s codes used did not enable the investigators to separate type 1 and 2 second degree block, an important distinction as Wenckeback is usually considered much less serious that type 2 second degree block. No mention was made on any one requiring a pacemaker. The rhythm outcome endpoints were obtained from hospital records those race finishers hospitalized with rhythm disturbances.
Comment.This is a very "coarse grain" study.All that was known about the subjects was the race numbers and times ,ICD codes of those hospitalized with arrhythmias, and their age, education and occupational status. How much they exercised outside of this race and other pertinent health factors that could influence the outcome ( BP,diabetes,obesity,height,smoking history,alcohol use) were not known and the various hazard ratios were not all statistically significant. Incidentally, the HR for atrial fibrillation were much lower than the five times increased risk often quoted for AF in several case control studies.
1.Northcote R. et al. Electrocardiographic findings in male veteran endurance athletes. Br Heart J. 1989, 61: 155-160
2.Hood S and Northcote,R Cardiac Assessment of veteran endurance athletes;a 12 year follow up study. Br J Sport Med, 1999, 33: 239-243
3.Baldesberger S, et al Sinus Node disease and arrhythmias in the long term followup of former professional cyclists. Eur Hear J. 200829.71-78
4.Andersen K. Risk of arrhythmias in 52,755 long-distance cross country skiers: A cohort study.
Eur Heart J 2013 Dec 34(47) 3624-3631
Monday, October 30, 2017
Cognitive dissonance and medical practice conformity and different visions
Anyone who has practiced medicine for more than a week, or observed its practice as a medical student may recognize the truth of the following paragraph.
Medical science alone is inadequate to solve the contingencies of the day. Improvising is required.
The rules are riddled with exceptions and the world of caring for patients is a world of exceptions and the rules we devise are to generally point in the right directions at least some of the time.
Norton Hadler wrote of this issue:
"..for the most difficult critical and trying decisions involved in clinical care, the body of scientific information is inadequate,or incomplete or idealized....clinical truth is a contract between a physician and a patient based on trust."
The ambiguity and the inadequacy of medical science to solve every problem is so self evident that it is puzzling the degree to which guidelines and rules are not only promulgated but increasingly used to judge physician's practices and the quality of care given.
Dr. Atul Gawande in his 2004 commencement address at Yale Medical School said:
"...Information is inadequate.The science is ambiguous.One's knowledge and abilities are never perfect.The risks of the unforeseen consequences and terrible mistakes always loom."
Everyone seems to be quoiting Hippocrates one way or another. Life is short,the art long, experience fallacious and judgment difficult.
On an individual level and as applied to the patient it is widely recognized that rules designed to standardize a world that is dominated by exceptions will have limited application at best and at worse frequently send us down the wrong road and generate perverse incentives to treat the chart at the expense of patient care and yet there are increasing efforts and acceptance of the use of rules and guidelines to judge the quality of a physician's practice and perhaps impose monetary consequences based on adherence to guidelines.
One of my medical friends suggested we might have an example of cognitive dissonance.
Maybe so for some physicians, but more to the point is that there are two different visions-the population treatment vision and the individual patient treatment vision.The individual treatment vision is played out by most practicing physicians while those who are proponents of the other vision are unfortunately often those in policy influencing roles, such as in medical schools and IOM and ACP and various of the "non-profits" more than a few of which are funded largely by the Robert Wood Johnson Foundation.
Medical science alone is inadequate to solve the contingencies of the day. Improvising is required.
The rules are riddled with exceptions and the world of caring for patients is a world of exceptions and the rules we devise are to generally point in the right directions at least some of the time.
Norton Hadler wrote of this issue:
"..for the most difficult critical and trying decisions involved in clinical care, the body of scientific information is inadequate,or incomplete or idealized....clinical truth is a contract between a physician and a patient based on trust."
The ambiguity and the inadequacy of medical science to solve every problem is so self evident that it is puzzling the degree to which guidelines and rules are not only promulgated but increasingly used to judge physician's practices and the quality of care given.
Dr. Atul Gawande in his 2004 commencement address at Yale Medical School said:
"...Information is inadequate.The science is ambiguous.One's knowledge and abilities are never perfect.The risks of the unforeseen consequences and terrible mistakes always loom."
Everyone seems to be quoiting Hippocrates one way or another. Life is short,the art long, experience fallacious and judgment difficult.
On an individual level and as applied to the patient it is widely recognized that rules designed to standardize a world that is dominated by exceptions will have limited application at best and at worse frequently send us down the wrong road and generate perverse incentives to treat the chart at the expense of patient care and yet there are increasing efforts and acceptance of the use of rules and guidelines to judge the quality of a physician's practice and perhaps impose monetary consequences based on adherence to guidelines.
One of my medical friends suggested we might have an example of cognitive dissonance.
Maybe so for some physicians, but more to the point is that there are two different visions-the population treatment vision and the individual patient treatment vision.The individual treatment vision is played out by most practicing physicians while those who are proponents of the other vision are unfortunately often those in policy influencing roles, such as in medical schools and IOM and ACP and various of the "non-profits" more than a few of which are funded largely by the Robert Wood Johnson Foundation.
Thursday, October 26, 2017
Has medical care been reduced to Leave a message or call 911?
When I contact some medical practices by phone that is exactly what seems to be the situation.
Case in point- When recently I developed a rapid heart rate that seemed to be atrial flutter I called the medical practice where my EP cardiologist practices and the telephone prompts gave me the choice of "in an emergency call 911" or when directed to the cardiologist's nurse," leave a message " which I did and then waited and then waited.
Finally we decided to drive to his office and insist to be seen. It was about 2 hours after the initial call , as I was sitting in his waiting room,his nurse returned my call which we had forwarded to my cellphone . Even then I had to insist to be seen which I finally was, by which time I was back in sinus rhythm.
Medical care as is provided by physicians' offices seemed to have been simplified and reduced to go to the emergency room or leave a message. I wonder if this might be one of the factors leading to the increase in the number of urgent care centers as it offers a third way.
Case in point- When recently I developed a rapid heart rate that seemed to be atrial flutter I called the medical practice where my EP cardiologist practices and the telephone prompts gave me the choice of "in an emergency call 911" or when directed to the cardiologist's nurse," leave a message " which I did and then waited and then waited.
Finally we decided to drive to his office and insist to be seen. It was about 2 hours after the initial call , as I was sitting in his waiting room,his nurse returned my call which we had forwarded to my cellphone . Even then I had to insist to be seen which I finally was, by which time I was back in sinus rhythm.
Medical care as is provided by physicians' offices seemed to have been simplified and reduced to go to the emergency room or leave a message. I wonder if this might be one of the factors leading to the increase in the number of urgent care centers as it offers a third way.
Wednesday, October 25, 2017
The heart will remodel itself whether you exercise a lot or not at all
Remodeling of the heart will occur whether you do anything about it or not. What you do about it may determine what type of remodeling you get.
The prototypical remodeling that occurs with a sedentary lifestyle seem very different from that of a long term exerciser.
Studies from the cardiology group at Southwestern Medical School and the Cooper Center Longitudinal Study have described important aspects of the structure and function of the heart in the sedentary and the persistent aerobic exerciser. Higher levels of exercise directly affect heart function and structure in a way different from sedentary aging.
In a study of over 3000 healthy participants at the Cooper Clinic in Dallas, Brinker et al characterized the remodeling patterns of individuals as correlated with their "fitness" levels as determined by their levels of exercise achieved on a treadmill tests.
In a nutshell, the low fit individuals had smaller hearts,concentric remodeling/hypertrophy and poorer diastolic function while the fitter participants demonstrated a pattern of eccentric remodeling , larger hearts and normal diastolic function.
Definitions are in order.
Heart size for this purpose, refers to left ventricular volume at the end of diastole( left ventricular end diastolic diameter) typically determined by echocardiography. Concentric remodeling refers to increased wall thickness and normal ventricular mass while concentric hypertrophy means increased LV mass and increased wall thickness.Eccentric remodeling refers to increased LV diastolic volume (hence LV mass)with no significant increase in wall thickness.
The relationship beween LV chamber size and wall thickness is expressed by the relative wall thickness (RWT) and defined as 2 X posterior LV wall thickness/ LV diameter at end of diastole.
Concentric remolding has a RWT of greater the 0.42 while eccentric remodeling is less than 0.42. The range of normal is 0.32 -0.42
The distinction between concentric and eccentric remodeling of the heart dates back to the 1975 "Morganroth hypothesis" which described different stereotypic cardiac adaptations to endurance exercise and strength building or resistance exercise. The idea was that endurance training presents a volume overload while resistance exercise presents a pressure overload. Remember though it is called an hypothesis.Several studies have reexamined the concept and reported that every endurance athlete does not get eccentric hypertrophy and many weight lifters do not have concentric changes.Futher ,activities such a bike racing and rowing involve a considerable amount of both volume and pressure overload and both group have among the largest hearts.
The diastolic dysfunction , in the Dallas study, was assessed by the ratio E/e' ( e over e prime) where e is the the early diastolic flow through the mitral valve and e prime is movement of the mitral annulus.the ratio giving some measure of left ventricular compliance or stiffness.
The "Dallas hypothesis", my term as far as I know, is that the cardiac phenotype ( structure and function ) of the sedentary heart is a likely precursor of diastolic heart failure. aka heart failure with preserved ejection fraction ( HFpEF) . ( Note this designation is not the same as saying heart failure with preserved systolic function.EF is only one measure of systolic function. Some studies have shown decreased systolic function in HFpEF as measured by speckle echo exams measuring longitudinal strain.)
I have argued before that the lower level of the 2008 recommendation for exercise , while decreasing the overall risk of cardiovascular disease, is not sufficient to prevent heart failure. Exercise at at least twice that level seems to be needed. The minimum recommendation was for 500 MET min per week which would translate to 2.5 hours of moderate exercise per week or 1.25 hours of vigorous exercise ( where vigorous is over 7 MET)
The argument is that the reduction is diastolic heart failure risk may be brought about by endurance exercise induced structural changes in the heart and preservation of left ventricular compliance. How much exercise, at what level and for how many years remain to be determined.
The prototypical remodeling that occurs with a sedentary lifestyle seem very different from that of a long term exerciser.
Studies from the cardiology group at Southwestern Medical School and the Cooper Center Longitudinal Study have described important aspects of the structure and function of the heart in the sedentary and the persistent aerobic exerciser. Higher levels of exercise directly affect heart function and structure in a way different from sedentary aging.
In a study of over 3000 healthy participants at the Cooper Clinic in Dallas, Brinker et al characterized the remodeling patterns of individuals as correlated with their "fitness" levels as determined by their levels of exercise achieved on a treadmill tests.
In a nutshell, the low fit individuals had smaller hearts,concentric remodeling/hypertrophy and poorer diastolic function while the fitter participants demonstrated a pattern of eccentric remodeling , larger hearts and normal diastolic function.
Definitions are in order.
Heart size for this purpose, refers to left ventricular volume at the end of diastole( left ventricular end diastolic diameter) typically determined by echocardiography. Concentric remodeling refers to increased wall thickness and normal ventricular mass while concentric hypertrophy means increased LV mass and increased wall thickness.Eccentric remodeling refers to increased LV diastolic volume (hence LV mass)with no significant increase in wall thickness.
The relationship beween LV chamber size and wall thickness is expressed by the relative wall thickness (RWT) and defined as 2 X posterior LV wall thickness/ LV diameter at end of diastole.
Concentric remolding has a RWT of greater the 0.42 while eccentric remodeling is less than 0.42. The range of normal is 0.32 -0.42
The distinction between concentric and eccentric remodeling of the heart dates back to the 1975 "Morganroth hypothesis" which described different stereotypic cardiac adaptations to endurance exercise and strength building or resistance exercise. The idea was that endurance training presents a volume overload while resistance exercise presents a pressure overload. Remember though it is called an hypothesis.Several studies have reexamined the concept and reported that every endurance athlete does not get eccentric hypertrophy and many weight lifters do not have concentric changes.Futher ,activities such a bike racing and rowing involve a considerable amount of both volume and pressure overload and both group have among the largest hearts.
The diastolic dysfunction , in the Dallas study, was assessed by the ratio E/e' ( e over e prime) where e is the the early diastolic flow through the mitral valve and e prime is movement of the mitral annulus.the ratio giving some measure of left ventricular compliance or stiffness.
The "Dallas hypothesis", my term as far as I know, is that the cardiac phenotype ( structure and function ) of the sedentary heart is a likely precursor of diastolic heart failure. aka heart failure with preserved ejection fraction ( HFpEF) . ( Note this designation is not the same as saying heart failure with preserved systolic function.EF is only one measure of systolic function. Some studies have shown decreased systolic function in HFpEF as measured by speckle echo exams measuring longitudinal strain.)
I have argued before that the lower level of the 2008 recommendation for exercise , while decreasing the overall risk of cardiovascular disease, is not sufficient to prevent heart failure. Exercise at at least twice that level seems to be needed. The minimum recommendation was for 500 MET min per week which would translate to 2.5 hours of moderate exercise per week or 1.25 hours of vigorous exercise ( where vigorous is over 7 MET)
The argument is that the reduction is diastolic heart failure risk may be brought about by endurance exercise induced structural changes in the heart and preservation of left ventricular compliance. How much exercise, at what level and for how many years remain to be determined.
Tuesday, October 24, 2017
Can an individual's risk of a given disease ever be "determined"?
The risk assessment of an individual.that is determining a person's risk of a given disease has been described a peculiar,elusive,ambiguous process.
The statistician,Richard Von Misses ( Ludwig's brother ) said that it is only possible to speak of probability in terms of a collective ( ie. a group or a set ) and that to say , for example that Mr. Jones has the probability of 0.3 in the next five years of , for example, having a heart attack is nonsense.
Yet, physicians are encouraged ( and nowadays mandated in order to practice proper guideline driven medical practice) to do this in a variety of situations. The famous Framingham risk model is often used to assess the risk of a heart attack. For example,using an equation from the NCEP ( National Cholesterol Education Program) we find that a 67 year,non smoking man with a total cholesterol of 170 and an HDL of 75 would have a 10 years risk estimate of 9%. According to the Framingham data, there would be 9 deaths in a ten years period in a group of men with those characteristics ,but is it meaningful to say that a given member of that group has a 9% risk. Further, the risk number is not just something mentioned in the exam room but is often folded into guidelines from various organizations,for example the ACC .Someone with a risk of 10% ( or some committee derived cutpoint) might be advised to take a statin or aspirin.
What if we constitute another statistical collective since we can make up as many as our imagination and data allow.In a Framingham type study we could measure CRP,presence of absence of coronary calcification,results of a exercise stress test,blood sugar and whether or not the person takes daily vitamins. The person in the previous paragraph might now be determined to have a risk of 15%.So what is his " real " risk? Is there a real risk at all ? Is an elusive ,ambiguous risk number sufficient reason to recommend lifetime medications? I don't think so now; but that happens regularly in doctor's offices and I used to do it on almost a routine basis and thought I knew what I was doing. Frequently medical societies and committees will offer generic advice to generic patients by suggesting they complete a form or risk assessment tool but then consult with their physician /health care provider to discuss the issue and offer an "individualized" risk assessment. I wonder what sort of magical statistical tool the providers has at her disposal to achieve that result other than the same risk assessment tool the patient has already used.
What if we constitute another statistical collective since we can make up as many as our imagination and data allow.In a Framingham type study we could measure CRP,presence of absence of coronary calcification,results of a exercise stress test,blood sugar and whether or not the person takes daily vitamins. The person in the previous paragraph might now be determined to have a risk of 15%.So what is his " real " risk? Is there a real risk at all ? Is an elusive ,ambiguous risk number sufficient reason to recommend lifetime medications? I don't think so now; but that happens regularly in doctor's offices and I used to do it on almost a routine basis and thought I knew what I was doing. Frequently medical societies and committees will offer generic advice to generic patients by suggesting they complete a form or risk assessment tool but then consult with their physician /health care provider to discuss the issue and offer an "individualized" risk assessment. I wonder what sort of magical statistical tool the providers has at her disposal to achieve that result other than the same risk assessment tool the patient has already used.
Monday, October 23, 2017
The marked variability of subclinical atrial fibrillation makes risk assessment difficult
A post hoc analysis (1) of the TRENDS study concluded "significant temporal variability of AF burden exists when measured continuously with an implantable CRMD ( cardiac rhythm management device)."
The authors examined data from 394 patients who had a mean CHAD2DS.Vasc score of 3.7 (average) and divided AF burden into three categories: 1) No AF, 2) Low AF (less than 5.5 hours per day on any given day) and 3) High AF (greater than or equal to 5.5 hours per day).
They then determined how often that classification changed over time. What category in which the patient was placed was dependent on the time period over which the sampling was analyzed. One day they might have " no AF" another day be placed in the high AF category of greater than 5.5 hours per day.
So to what extent do these data invalidate the conclusion of the TRENDS study? Certainly one at least has to be much more skeptical of the findings. If a significant number of patients were considered to have no AF and then developed into either category 2 or 3 the calculation of the relative risk for stroke would likely be an underestimation of risk .So how good is the data regarding the question of the degree to which AF burden is an indicator of stroke risk at all?
The authors concluded: "The burden of AF is highly variable over time and cannot be accurately assessed by short-term monitoring. If burden of AF is shown to be an important variable to be considered when making decisions regarding long-term anticoagulation, perhaps continuous monitoring should be employed to follow changes in AF burden over time."
1 Kaplan RM et al Atrial Fibrillation variability on long term monitoring of implantable cardiac rhythm management devices. Clinical Cardiology 2017: 1-5 March June
The authors examined data from 394 patients who had a mean CHAD2DS.Vasc score of 3.7 (average) and divided AF burden into three categories: 1) No AF, 2) Low AF (less than 5.5 hours per day on any given day) and 3) High AF (greater than or equal to 5.5 hours per day).
They then determined how often that classification changed over time. What category in which the patient was placed was dependent on the time period over which the sampling was analyzed. One day they might have " no AF" another day be placed in the high AF category of greater than 5.5 hours per day.
So to what extent do these data invalidate the conclusion of the TRENDS study? Certainly one at least has to be much more skeptical of the findings. If a significant number of patients were considered to have no AF and then developed into either category 2 or 3 the calculation of the relative risk for stroke would likely be an underestimation of risk .So how good is the data regarding the question of the degree to which AF burden is an indicator of stroke risk at all?
The authors concluded: "The burden of AF is highly variable over time and cannot be accurately assessed by short-term monitoring. If burden of AF is shown to be an important variable to be considered when making decisions regarding long-term anticoagulation, perhaps continuous monitoring should be employed to follow changes in AF burden over time."
1 Kaplan RM et al Atrial Fibrillation variability on long term monitoring of implantable cardiac rhythm management devices. Clinical Cardiology 2017: 1-5 March June
Saturday, October 21, 2017
Detailed cardiac study on a group of really extreme endurance athletes
Much has been written about the issues of what is the point beyond which exercise is no longer health promoting but rather damaging to the heart or is there a point.
Larry Creswell writing on his blog Athlete's Heart Blog reviews a recent article that studied 33 endurance athletes with a history of prolonged intensive aerobic training. These guys trained so long and so hard that you might think that surely what they did would approach that limit and have evidence of cardiac damage. Yet that was not the case. (Dr. Creswell'sl blog continues to be a great source for issues involving what the blog title suggests.)
The data are interesting but finding 33 white swans does not rule out the existence of black ones.The fact that these athletes continued to be able to exercise at a prodigiously high level suggested that that did not develop some serious heart problem. Is there a survivor bias at play here?
addendum 0ct 21 2017.Typo in headline corrected.
Larry Creswell writing on his blog Athlete's Heart Blog reviews a recent article that studied 33 endurance athletes with a history of prolonged intensive aerobic training. These guys trained so long and so hard that you might think that surely what they did would approach that limit and have evidence of cardiac damage. Yet that was not the case. (Dr. Creswell'sl blog continues to be a great source for issues involving what the blog title suggests.)
The data are interesting but finding 33 white swans does not rule out the existence of black ones.The fact that these athletes continued to be able to exercise at a prodigiously high level suggested that that did not develop some serious heart problem. Is there a survivor bias at play here?
addendum 0ct 21 2017.Typo in headline corrected.
Thursday, October 19, 2017
Biggest change in medicine in 40 years-loss of autonomy and change in ethics
In regard to what has changed most in the last near half century some would answer medical advances, mainly in diagnostic techniques and therapeutics.For someone who has seen those happen they are incredible and marvelous but that is not what has changed the relationship between physician and patient. In the sixties, physicians used the tools of the day to diagnose and treat patient, so do they today even as the tools are much better and more varied. No relationship change there.
I submit that three factors acting alone and interacting with the other two have brought about a sea change. The factors are: 1) loss of physician autonomy, 2) a change in medical ethics (even the name has changed to professionalism) and 3) method of payment for physician services. I argue that the third has been a major factor in loss of autonomy and has triggered the ethical changes.
I submit that three factors acting alone and interacting with the other two have brought about a sea change. The factors are: 1) loss of physician autonomy, 2) a change in medical ethics (even the name has changed to professionalism) and 3) method of payment for physician services. I argue that the third has been a major factor in loss of autonomy and has triggered the ethical changes.
Tuesday, October 17, 2017
The basic narrative of medical collectivism as voiced by the ACP and ABIMF
The following two paragraphs are from a viewpoint commentary entitled "Resolving the Tension between Population Health and Individual Health Care " in the JAMA by Dr. Harold C. Sox, former president of the American College of Physicians and former editor of the Annals of Internal Medicine: See (JAMA November 13,2013,volume 310, number 18). Yes, I have written about this article before, obviously I find that commentary as disturbing as any I can remember reading.
"Throughout
history, codes of professional conduct have called on clinicians to
make each patient’s interests their highest priority. If resources
become limited, clinicians will find themselves unable to adhere to this
standard of practice for all patients. In 2002, a new code of conduct,
the Charter for Professionalism, addressed this conflict by calling on
physicians to consider the needs of all when treating the individual:
“While meeting the needs of individual patients, physicians are required
to provide health care that is based on the wise and cost-effective
management of limited clinical resources. The provision of unnecessary
services not only exposes patients to avoidable harm and expense but
also diminishes the resources available for others.
This
remarkable passage indicates that the physician has an ethical
imperative to balance the needs of the individual patient with the needs
of society. With this foundational principle of the population health
approach, the Charter, in effect, calls on clinicians to allocate
resources. However, it does not provide specific advice. Recent
programs, such as the American Board of Internal Medicine Foundation’s
Choosing Wisely campaign, are beginning to fill this knowledge gap, as
do some practice guidelines."
What constitutes fairness-equal treatment for all? less treatment for all?only treatment if it meets someone's definition of "high value" ,treatment based on considerations of "life years"? Who decides?
What constitutes fairness-equal treatment for all? less treatment for all?only treatment if it meets someone's definition of "high value" ,treatment based on considerations of "life years"? Who decides?
Remarkable passage indeed. "consider the needs of all when treating the individual." How to bring about a fair and equitable allocation poses a problem for the practicing physician? Would ordering a MR on Mrs. Jones somehow keep Mrs. Brown for having one? The answer was so simple. Follow guidelines.They will be written by people who know that medical care is too important and too complex to be left to the individual physician and her patient, which is just the medical care application of the progressive medical credo .
The alleged necessity of radically revising medical ethics was justified on the basis of "If medical resources become limited". The nature or magnitude of this limitation is not further explained nor is how this would come to pass.The conditional nature of the sentence implies that the author thinks such limitation has yet to occur. When have resources not been limited?
Later in the same article Sox seemingly justifies a scenario in which funds are shifted from the treatment of a sick person to fund some preventive program and in doing so admits there will be some short run harm to some for the greater benefit of a large group. This is much more than simply eliminating "unnecessary "provision of services. Sox never tells the readers who will make these decisions or how such an allocation of resources will be carried out. Amazingly in 2002 a relatively small group of internists affiliated with the American College of Physicians and the American Board of Internal Medicine ( and a few like minded European internists) proclaimed a new code of medical ethics.A ethical physician must consider the needs of all when treating the individual. The Charter (1) did not specify exactly how that new ethical imperative could be accomplished but the ACP and ABIMF subsequently revealed the way in which the new ethics could be practiced.It is called the Choosing Wisely Campaign which will offer specifics on things physicians should not do,certain tests and procedures that are deemed wasteful and/or harmful.Further certain practice guidelines which are based on cost effective considerations are or will soon be available.
Can a group of internists simply change medical ethics,ethics that had persisted for many years ? Well so far they have made much progress along those lines at least if ethical change proclamations by numerous professional organizations are an indication. I hope the typical practicing physician thinks otherwise .
The alleged necessity of radically revising medical ethics was justified on the basis of "If medical resources become limited". The nature or magnitude of this limitation is not further explained nor is how this would come to pass.The conditional nature of the sentence implies that the author thinks such limitation has yet to occur. When have resources not been limited?
Later in the same article Sox seemingly justifies a scenario in which funds are shifted from the treatment of a sick person to fund some preventive program and in doing so admits there will be some short run harm to some for the greater benefit of a large group. This is much more than simply eliminating "unnecessary "provision of services. Sox never tells the readers who will make these decisions or how such an allocation of resources will be carried out. Amazingly in 2002 a relatively small group of internists affiliated with the American College of Physicians and the American Board of Internal Medicine ( and a few like minded European internists) proclaimed a new code of medical ethics.A ethical physician must consider the needs of all when treating the individual. The Charter (1) did not specify exactly how that new ethical imperative could be accomplished but the ACP and ABIMF subsequently revealed the way in which the new ethics could be practiced.It is called the Choosing Wisely Campaign which will offer specifics on things physicians should not do,certain tests and procedures that are deemed wasteful and/or harmful.Further certain practice guidelines which are based on cost effective considerations are or will soon be available.
Can a group of internists simply change medical ethics,ethics that had persisted for many years ? Well so far they have made much progress along those lines at least if ethical change proclamations by numerous professional organizations are an indication. I hope the typical practicing physician thinks otherwise .
1) ABIM
Foundation, American Board of Internal Medicine; ACP-ASIM Foundation,
American College of Physicians-American Society of Internal Medicine;
European Federation of Internal Medicine. Medical professionalism in
the new millennium: a physician charter. Ann Intern Med. 2002;136(3):243-246.
addendum 12/30/2017. One minor wording change made to clarify meaning of one sentence.
addendum 12/30/2017. One minor wording change made to clarify meaning of one sentence.
Sunday, October 08, 2017
Is a sedentary life style and not resistance exercise a cause of concentric cardiac hypertrophy?
Following the 1975 echocardiographic study by Joel Morganroth of endurance athletes and resistance exercise athletes and several cross sectional studies that seemed to validate his work the "Morganroth's Hypothesis became the standard exercise physiology party line.
The story goes like this:
Endurance exercise brings about a volume overload or a preload stimulus to the ventricle that lead to eccentric hypertrophy which is an increase in ventricular cavity size and only slight increase in wall thickness. Resistance exercise brings about a pressure overload or an afterload stimulus which leads to concentric hypertrophy in which there is little change in cavity size but thickening of the ventricular wall.,The 2 types can be defined more precisely by the relative wall thickness (RWT) which is 2 x the posterior wall thickness dived by left ventricular diastolic diameter with the value greater than 0.42 indicating concentric hypertrophy.
Skeptics have argued that echo studies have inherent methodological errors ranges too great to separate groups whose absolute values are not that far apart and MR is a much more precise method and that cross-sectional studies have limited ability to sort out group difference that are due to training from other causes of individual differences.So what did a longitudinal study with MR imaging show?
A 2011 MRI longitudinal study provided interesting data from which one might conclude that endurance exercise does bring about eccentric hypertrophy but resistance exercise does not increase wall thickness-at least not in the small group of resistance exercisers who worked out three times a week for six months.
Spence et al (2) from Australia did a MRI study on a small number of subjects with one group undergoing endurance training and the other resistance training.
While Spence's study suggests that six months of resistance exercise does not lead to concentric hypertrophy,data from the group Southwestern Medical School indicate that a sedentary lifestyle can bring about concentric hypertrophy at least some of the time.
Brinker et al (3) studied cardiac function and structure in 2900 subjects from the Cooper Center Longitudinal Study. They found that the low fit subjects ( basically those with a sedentary lifestyle) had a higher prevalence of concentric remodeling as well as diastolic dysfunction that the fitter subjects. There was a 40% prevalence of concentric hypertrophy in the lowest fit group versus less than 20 % in the most fit group. So it is not an all of none thing.
The notion of volume overload exercise and pressure overload exercise may well be a oversimplification. A recent meta-analysis provided data to support the notion that there is some pressure overload in endurance exercise and there is apparently some volume overload in such resistance exercise. Further a number athletic endeavors are mixed, such as rowing and cycling. The rowers and cyclists had the greatest remodeling changes with both increased left ventricular end diastolic volume and wall thickness.
But it may also be the case to be the case there there is "inactivity remodeling", here referring to a sedentary lifestyle The ventricles remodel whether you exercise or have a sedentary lifestyle., you likely get a eccentric remodeling or hypertrophy with aerobic exercise and at least in some people without it you get concentric remodeling or hypertrophy.Further, they suggest as have others that the latter may well be a precursor to heart failure and the former may help prevent it.
1. Morganroth, Jet al. Comparative left ventricular dimensions in trained athletes.Ann Int Med. 1975,82(4), 521-524
2. Spence,A et al A prospective randomized longitudinal study of left ventricular adaption to endurance and resistance training in humans. J Phys 2011 589, 543
3.Brinker, SK et al. Association of Cardiorespiratory Fitness with Left Ventricular Remodeling and diastolic dysfunction. JACC Heart Failure.Vol 2, no.3, 2014, p238
"Humans are pattern-seeking, story-telling animals and we are quite adept at telling stories about patterns,whether they exist or not" Michael Shermer.
The story goes like this:
Endurance exercise brings about a volume overload or a preload stimulus to the ventricle that lead to eccentric hypertrophy which is an increase in ventricular cavity size and only slight increase in wall thickness. Resistance exercise brings about a pressure overload or an afterload stimulus which leads to concentric hypertrophy in which there is little change in cavity size but thickening of the ventricular wall.,The 2 types can be defined more precisely by the relative wall thickness (RWT) which is 2 x the posterior wall thickness dived by left ventricular diastolic diameter with the value greater than 0.42 indicating concentric hypertrophy.
Skeptics have argued that echo studies have inherent methodological errors ranges too great to separate groups whose absolute values are not that far apart and MR is a much more precise method and that cross-sectional studies have limited ability to sort out group difference that are due to training from other causes of individual differences.So what did a longitudinal study with MR imaging show?
A 2011 MRI longitudinal study provided interesting data from which one might conclude that endurance exercise does bring about eccentric hypertrophy but resistance exercise does not increase wall thickness-at least not in the small group of resistance exercisers who worked out three times a week for six months.
Spence et al (2) from Australia did a MRI study on a small number of subjects with one group undergoing endurance training and the other resistance training.
While Spence's study suggests that six months of resistance exercise does not lead to concentric hypertrophy,data from the group Southwestern Medical School indicate that a sedentary lifestyle can bring about concentric hypertrophy at least some of the time.
Brinker et al (3) studied cardiac function and structure in 2900 subjects from the Cooper Center Longitudinal Study. They found that the low fit subjects ( basically those with a sedentary lifestyle) had a higher prevalence of concentric remodeling as well as diastolic dysfunction that the fitter subjects. There was a 40% prevalence of concentric hypertrophy in the lowest fit group versus less than 20 % in the most fit group. So it is not an all of none thing.
The notion of volume overload exercise and pressure overload exercise may well be a oversimplification. A recent meta-analysis provided data to support the notion that there is some pressure overload in endurance exercise and there is apparently some volume overload in such resistance exercise. Further a number athletic endeavors are mixed, such as rowing and cycling. The rowers and cyclists had the greatest remodeling changes with both increased left ventricular end diastolic volume and wall thickness.
But it may also be the case to be the case there there is "inactivity remodeling", here referring to a sedentary lifestyle The ventricles remodel whether you exercise or have a sedentary lifestyle., you likely get a eccentric remodeling or hypertrophy with aerobic exercise and at least in some people without it you get concentric remodeling or hypertrophy.Further, they suggest as have others that the latter may well be a precursor to heart failure and the former may help prevent it.
1. Morganroth, Jet al. Comparative left ventricular dimensions in trained athletes.Ann Int Med. 1975,82(4), 521-524
2. Spence,A et al A prospective randomized longitudinal study of left ventricular adaption to endurance and resistance training in humans. J Phys 2011 589, 543
3.Brinker, SK et al. Association of Cardiorespiratory Fitness with Left Ventricular Remodeling and diastolic dysfunction. JACC Heart Failure.Vol 2, no.3, 2014, p238
"Humans are pattern-seeking, story-telling animals and we are quite adept at telling stories about patterns,whether they exist or not" Michael Shermer.
Friday, October 06, 2017
Will 2-3 hours a week of aerobic exercise keep your heart from getting stiff?
Will a few hours of aerobic exercise per week practiced over along period of time (years) prevent the ventricle from becomes stiff and could the current epidemic of diastolic heart failure be diminished if many people follow that practice. Does sedentary aging resulting in stiff left ventricles play a major role in the increasing numbers of older folks with heart failure (HF). If it does could the sufficient amount of exercise prevent it and what do we mean by "sufficient"?
Echocardiography and other imaging techniques have provided detailed information emphasizing the importance of diastole, the filling process of the ventricle priming the heart pump for systole or ventricular contraction.Indeed a key distinguishing feature of the endurance athlete's heart is its superior filling or diastolic function. The better diastolic function or ventricular filling the better is one's fitness or exercise level.
Knowledge of diastole has lead to a new concept of heart failure, one if which systolic function is said to be normal- at least at rest.Actually less than that is claimed as the systolic function is represented by one test of that function namely the ejection fraction done at rest. This has lead to the notion of "HFpEF" or heart failure with preserved ejection fraction and HFrEF, or heart failure with reduced ejection fraction. HFpEF is said to represent at least half of HF cases and other than exercise training there seems to be little evidence of an effective therapeutic approach. There are several echocardiographic tests used to assess diastolic function: EA ratio. E/E prime ratio,left atrial volume, etc .
Woody Allen's basic axiom of physiology can be paraphrased : as we get older everything that should be soft gets stiff and everything should be stiff gets soft. Aging certainly makes the left ventricle get stiff and the aorta as well.
The group from Dallas having the wealth of patient data available from the Cooper Longevity institute has published several articles claiming that long time endurance athletes are able to maintain a much more compliant left ventricle than matched persons with little on no regular aerobic exercise. Further their data suggest that a group with exercise levels lower than that of the competitive runner group ( about 2-3 hours per week of aerobic exercise) fare almost as well in regard to left ventricular compliance.This suggest that training or exercise far short of running marathon every year or doing the full Iron man type triathlon will suffice.
Ventricular compliance is one factor to consider in regard to diastolic function- another is the relaxation capability and in that regard long term endurance exercise does not mitigate the age related loss of optimal relaxation function. One way to measure relaxation is with the isovolumic relaxation time or.IVRT. This is the time interval after aortic valve closure and mitral valve opening. It is prolonged as humans age and the IVRT was no shorter in the fit group or the super fit group versus the sedentary group in the Dallas articles. .
The heart remodels itself. The remodeling pattern is different in the fit person from that in the sedentary person, the latter described by the Dallas group as a small heart, with concentric remodeling or hypertrophy and impaired filling or impaired diastolic function.
Heart size in this context refers to the volume of ventricle at the end of diastole (end diastolic ventricular volume). Concentric remodeling means no chamber enlargement with ventricular wall thickening. The terms concentric and eccentric dates back at least to the Morganroth hypothesis in 1975 from his cardiac echo study of endurance athletes and resistance training athletes.
As more data was generated it appeared that there is more to it that what Dr. Morganroth suggested. Some data from the Dallas group suggested that in the first year of aerobic training at least some folks develop concentric type changes and only later ( or perhaps with more intense training-long runs and/or high intensity interval training) does the classical runners heart pattern appear. Another study failed to show any concentric hypertrophy after a six month period of weight training.Studies involving rowers and cyclists show a mixed pattern.
Basically,the athlete's heart (at least the endurance athlete's heart) is big (but not in a bad way) muscular and very compliant and can relax quickly so that it can pump large volume of blood rapidly for prolonged periods of time. How much of that picture is genetic and how much is due to long time training is not known Whether levels of exercise equal to or slightly greater than the 2008 party line recommendations will mitigate the current "epidemic" of diastolic heart failure is an attractive hypothesis and one that I would like to believe.
"A man hears what he wants to hears and disregards the rest" - Paul Simon,song "The Boxer",1969
addendum 11/7/17- Several typos corrected along with minor editorial tweaks.
Echocardiography and other imaging techniques have provided detailed information emphasizing the importance of diastole, the filling process of the ventricle priming the heart pump for systole or ventricular contraction.Indeed a key distinguishing feature of the endurance athlete's heart is its superior filling or diastolic function. The better diastolic function or ventricular filling the better is one's fitness or exercise level.
Knowledge of diastole has lead to a new concept of heart failure, one if which systolic function is said to be normal- at least at rest.Actually less than that is claimed as the systolic function is represented by one test of that function namely the ejection fraction done at rest. This has lead to the notion of "HFpEF" or heart failure with preserved ejection fraction and HFrEF, or heart failure with reduced ejection fraction. HFpEF is said to represent at least half of HF cases and other than exercise training there seems to be little evidence of an effective therapeutic approach. There are several echocardiographic tests used to assess diastolic function: EA ratio. E/E prime ratio,left atrial volume, etc .
Woody Allen's basic axiom of physiology can be paraphrased : as we get older everything that should be soft gets stiff and everything should be stiff gets soft. Aging certainly makes the left ventricle get stiff and the aorta as well.
The group from Dallas having the wealth of patient data available from the Cooper Longevity institute has published several articles claiming that long time endurance athletes are able to maintain a much more compliant left ventricle than matched persons with little on no regular aerobic exercise. Further their data suggest that a group with exercise levels lower than that of the competitive runner group ( about 2-3 hours per week of aerobic exercise) fare almost as well in regard to left ventricular compliance.This suggest that training or exercise far short of running marathon every year or doing the full Iron man type triathlon will suffice.
Ventricular compliance is one factor to consider in regard to diastolic function- another is the relaxation capability and in that regard long term endurance exercise does not mitigate the age related loss of optimal relaxation function. One way to measure relaxation is with the isovolumic relaxation time or.IVRT. This is the time interval after aortic valve closure and mitral valve opening. It is prolonged as humans age and the IVRT was no shorter in the fit group or the super fit group versus the sedentary group in the Dallas articles. .
The heart remodels itself. The remodeling pattern is different in the fit person from that in the sedentary person, the latter described by the Dallas group as a small heart, with concentric remodeling or hypertrophy and impaired filling or impaired diastolic function.
Heart size in this context refers to the volume of ventricle at the end of diastole (end diastolic ventricular volume). Concentric remodeling means no chamber enlargement with ventricular wall thickening. The terms concentric and eccentric dates back at least to the Morganroth hypothesis in 1975 from his cardiac echo study of endurance athletes and resistance training athletes.
As more data was generated it appeared that there is more to it that what Dr. Morganroth suggested. Some data from the Dallas group suggested that in the first year of aerobic training at least some folks develop concentric type changes and only later ( or perhaps with more intense training-long runs and/or high intensity interval training) does the classical runners heart pattern appear. Another study failed to show any concentric hypertrophy after a six month period of weight training.Studies involving rowers and cyclists show a mixed pattern.
Basically,the athlete's heart (at least the endurance athlete's heart) is big (but not in a bad way) muscular and very compliant and can relax quickly so that it can pump large volume of blood rapidly for prolonged periods of time. How much of that picture is genetic and how much is due to long time training is not known Whether levels of exercise equal to or slightly greater than the 2008 party line recommendations will mitigate the current "epidemic" of diastolic heart failure is an attractive hypothesis and one that I would like to believe.
"A man hears what he wants to hears and disregards the rest" - Paul Simon,song "The Boxer",1969
addendum 11/7/17- Several typos corrected along with minor editorial tweaks.
Thursday, October 05, 2017
Review of deaths occuring during triathlons
Most deaths that occur in a triathlon happen in the swimming phase.
A detailed report on triathlon deaths can be found in a recent issue of the Annals of Internal Medicine.
See here.
There were 135 sudden deaths,resuscitated cardiac arrests and trauma related deaths recorded in the period 1985 to 2016.
90 occurred in the swimming phase,7 in the bike phase,15 in the running phase and 8 in the post race period.
85% of the events occurred in males and the average age of death was 46.7 plus.minus 12.4 and the risk of death was greatest in participants over age 60.Almost 40% of the events occurred in first time participants.
One of the co-authors, Dr Larry Creswall,who writes the blog " Athlete's Heart Blog" discusses the results and offers suggestions for way to improve safety and response to incidents. See here
A detailed report on triathlon deaths can be found in a recent issue of the Annals of Internal Medicine.
See here.
There were 135 sudden deaths,resuscitated cardiac arrests and trauma related deaths recorded in the period 1985 to 2016.
90 occurred in the swimming phase,7 in the bike phase,15 in the running phase and 8 in the post race period.
85% of the events occurred in males and the average age of death was 46.7 plus.minus 12.4 and the risk of death was greatest in participants over age 60.Almost 40% of the events occurred in first time participants.
One of the co-authors, Dr Larry Creswall,who writes the blog " Athlete's Heart Blog" discusses the results and offers suggestions for way to improve safety and response to incidents. See here
Tuesday, October 03, 2017
What is the signficance of "myocardial fibrosis" in endurance athletes?
The quote around myocardial fibrosis is to make the point that the discussion is not about large areas of fibrosis or athletes with extensive fibrosis resulting in heart failure. The fibrosis refers here to small areas of uncertain significance detected by Cardiac MR studies with gadolinium. These areas are referred to as areas of delayed gadolinium enhancement (DGE) and are presumed ( probably correctly ) to be focal areas of fibrosis and are typically found at the insertion points of the right ventricle to the left ventricle. There is no question that DGE may indicate myocardial fibrosis-what has been questioned is whether DGE necessarily indicates fibrosis in endurance athletes and whether there is any clinical significance to those DGEs which do not fit a pattern consistent with a coronary artery distribution.
A recent article by Eijsvogel (1) et al described extensive cardiac function studies including MR and 2D speckle tracking imaging in 4 long term endurance athletes in whom DGE was demonstrated and compared the results to 5 other long term athletes without DGE . Both group had normal echo studies and normal and normal global function (longitudinal strain and strain rate) . However the DGE group had larger cardiac volumes and some ( remember there were only 4) showed some attenuation of strain in the regions of DGE or fibrosis. Both group has a long history of endurance training ( around 42-42 years) and both group were in their late fifties.
So as sophisticated as this extensive physiologic testing was in this project is my take is all we have learned is that some endurance athletes have more exercise induced remodeling and have bigger hearts and some-but not all- of those who had DGE have subtle regional decrease in strain but normal global function.
Another conjecture regarding the significance of DGE was offered by Trivax (3) who postulated that a demonstrated DGE in a runner was the cause of an episode of ventricular fibrillation. To his credit Dr. Trivax emphasized this was only an hypothesis , one I think that has not been further substantiated by subsequent case reports.
Levine (2) has offered commentary challenging the claim there is an increase in fibrosis in endurance athletes and also has suggested that the DGE-at least in some cases- might actually represent edema from acute prolonged strain in the right ventricular insertion points.
1)Eijsvogel TM et al Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis. Eur J. of sport Science 2017,
2)Levine BD Can Intensive exercise Harm the heart? Circulation 2014:130, 987-991
3)Trivax JE, Phidippides cardiomyopathy: a review and case illustration. Clin Cardiol.2012 #% 69-73
A recent article by Eijsvogel (1) et al described extensive cardiac function studies including MR and 2D speckle tracking imaging in 4 long term endurance athletes in whom DGE was demonstrated and compared the results to 5 other long term athletes without DGE . Both group had normal echo studies and normal and normal global function (longitudinal strain and strain rate) . However the DGE group had larger cardiac volumes and some ( remember there were only 4) showed some attenuation of strain in the regions of DGE or fibrosis. Both group has a long history of endurance training ( around 42-42 years) and both group were in their late fifties.
So as sophisticated as this extensive physiologic testing was in this project is my take is all we have learned is that some endurance athletes have more exercise induced remodeling and have bigger hearts and some-but not all- of those who had DGE have subtle regional decrease in strain but normal global function.
Another conjecture regarding the significance of DGE was offered by Trivax (3) who postulated that a demonstrated DGE in a runner was the cause of an episode of ventricular fibrillation. To his credit Dr. Trivax emphasized this was only an hypothesis , one I think that has not been further substantiated by subsequent case reports.
Levine (2) has offered commentary challenging the claim there is an increase in fibrosis in endurance athletes and also has suggested that the DGE-at least in some cases- might actually represent edema from acute prolonged strain in the right ventricular insertion points.
1)Eijsvogel TM et al Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis. Eur J. of sport Science 2017,
2)Levine BD Can Intensive exercise Harm the heart? Circulation 2014:130, 987-991
3)Trivax JE, Phidippides cardiomyopathy: a review and case illustration. Clin Cardiol.2012 #% 69-73
Monday, October 02, 2017
Annother observatonal epidemiolgic study wiill not settle the issue of the exercise cardiovascular mortality relationship.
There is no debate about the general nature of the relationship between regular exercise and cardiovascular risk and even over-all mortality. As exercise levels ( duration,or frequency or intensity ) increases the CVD risk decreases i.e there is an inverse relationship.
Controversy exists,however, about 1) whether there is a point beyond which CVD risk is no longer reduced ( does the curve slope up?) and 2) is there a point beyond which there is actual harm
The general point that exercise is inversely related to decreased CVD risk is more than generally accepted even though all the data as regards primary prevention is observational There have been and never will be any randomized clinical trials ( However, there is RCT evidence that a cardiac rehab exercise program will decrease CVD mortality).
In recent years concern has been expressed concerning cardiac problems in endurance athletes including increased risk of atrial fibrillation, and the development of areas of cardiac fibrosis ( detected on gadolinium scans) which have been reputed to predispose to rhythm disturbance and abnormalities of the right ventricle resembling an genetic condition known as ARVD (arrhythmogenic right ventricular dysplasia). These and possibly other heart conditions might provide a possible mechanism(s) responsible for a purported U shaped curve describing cardiovascular mortality and exercise level.It should be noted that there is conflicting evidence as to the shape of this curve, i.e. inverse or u shaped and it is easy to reference a number of studies that support either proposition.The strongest evidence- in regard to the claim that "too much" exercise is harmful- is for the relationship between endurance exercise and atrial fibrillation but even in this regard data also conflict.
Dr. James Okeefe along with Dr. Carl Lavie and others have written extensively and often spoken about the hazards of too much exercise and have recommend that relatively low levels of aerobic exercise are adequate to decrease cardiovascular risk.Low levels of exercise have been associated with significance reduction in CVD In fact, simply standing for greater than 2 hours per day is said to be associated with a 10% decrease in all cause mortality - a claim that strains credulity.
Dr. BD Levine from Southwestern Medical school has provided evidence that higher levels of exercise than the currently recommended levels not only protect against coronary artery disease but can also provide some protection of the age associated loss of ventricular compliance which arguably predisposes to heart failure with preserved ejection fraction. (HFpEF) also known as diastolic heart failure. Other workers at the same institution have recently provided some epidemiological proof of that concept. Levin has argued that levels of exercise higher than the current recommendation but significantly lower that that practiced, for example by iron man triathletes,will importantly help maintain good left ventricular function and perhaps ultimately favorably impact the current "epidemic" of HFpEF.
Eijsvogel et al have provided evidence that the current recommendation regarding exercise to prevent cardiovascular risk may be too low as far as prevention of heart failure (HF) The current (2008) recommendation are for 2 1/2 hours of moderate or one hour and 15 minutes of vigorous exercise per week. (I am reminded of John Von Neumann 's quote " There's no sense in being precise when you don't even know what you're talking about")
Eijsvogel's article defines moderate as 3- 5.9 METS of energy expenditure and vigorous as greater than 6 METS.
For point of reference, running a fifteen minute mile requires about 7 METS ( 24.4 02 uptake) which is equivalent to the 02 requirement for completing Stage 2 of the Bruce protocol. About 5 METs are needed to finish stage 1 ( 1.7 mph at 10% grade) . Running at 5 MPH or a 12 minute mile requires 8.6 METS. Running 4 MPH require a 02 uptake of about 25 ( 7 METS)
A sometimes used prediction equation that approximates a person's maximal 02 uptake is 3.8 times how long in minutes the person could preserver on the Bruce treadmill protocol.
Eijsvogel and co-workers used the data from the work of Wen and Tsai and of Arem to construct a cardiovascular disease mortality -physical activity curve . and found the "sweet spot" of 41 MET hours per week or 2460 METS hours per week The sweet spot ( not their term) means the level of exercise at which the maximal benefit in terms of reduction of CVD risk is reached.
This corresponds to 9 hours of walking or 4.8 hours of running at a 12 minute mile.
This is 3 to 4 times higher than the widely quoted 2008 recommendations of 2.5 hours of moderate or 75 minutes of vigorous exercise per week.
Another study by Lee et al also derived a activity CD risk relationship curve and found a lower sweet spot.
So the sweet spot from Lee's data is run for 3.5 hours per week versus 4.8 in Eijsvogel's article. O'Keefe seems to rely on Lee's data when he recommends for one to "limit one's vigorous exercise to 30-50 minutes a day. Not every one would consider running 3 1/2 hours per week at a 12 minute per mile pace a small amount of exercise and this would represent about 2- 3 times the 2008 recommendations and accepting Levine's thesis would be sufficient (if done for many years) be enough to decrease not only te risk of CVD is general but also the risk of developing heart failure with preserved ejection fraction (HFpEF).
But what will happen in terms of cardiovascular harm if you exceed the fifty minutes per day recommended by Okeefe and Lavie.From reading Eijsvogel's analysis- my sense of is , not much. His group was unable to show an increased CV risk at any level though using some parameters of exercise intensity or duration the curve sloped up slightly at the far right but was not statistically significant.
Another study demonstrating more coronary calcifications and myocardial fibrosis in Older endurance athletes
The article by Merghani et al (1) at least at first glance seems to be more bad news for long time endurance athletes in regard to the development of coronary artery disease.
The study subjects were 152 men who had logged an average of 31 years of endurance exercise type activities. All had echocardiograms,24 hour Holter, stress ECG,CT coronary angiograms (CAC) and cardiac MRs with gadolinium as did 92 age matched controls with similar Framingham Risk scores.
15 athletes and none of the controls had delayed gadolinium enhancement (DGE) on the MRs, 7 of which had a coronary artery pattern.(The DGE issue will need to be written about at a later date-for now the focus is on the calcification.)
60% of the athletes and 63% of controls had a normal CAC score but only athletes (11.3%) has a CAC score of 300 or greater. So the incidence of any calcification was about the same in athletes and controls but the athletes had more calcium and more demonstrable luminal stenosis ( greater than 50%) in 7.5% of the athletes and in none of the controls.
So does this mean that long time endurance exercise increased the risk of coronary artery disease?
Maybe an answer to that is related to another question-does the increase in calcium scores noted in patients taking statins mean that statins increase the risk of coronary artery disease which is , of course, a conclusion contrary to realms of clinical trial results demonstrating the value of statins, at least in secondary prevention.
In regard to the second question there is a great deal of data regarding what could be called the statin plaque paradox-statins increase coronary artery calcium even as they shrike the plaques. A calcium score could increase even as the plaques regress because of the increased density of calcification bought about by the statins.However not only did Merghani's runners have higher Calcium scores a few did have luminal stenosis related to the calcification.
A review of serial coronary intravascular ultrasound (IVUS) data gathered up from 8 large clinical studies may shed some on light on that issue.
The bottom line is that statins may increase the calcium scores (Agatson score) by increasing the calcification of plaques while decreasing the volume of the plaques, the effect being greater with the more potent ( as measured by magnitude of cholesterol lowering) statins having a greater plaque shrinkage effect.My sense of the literature is that other than the more fringy group of "statin deniers" there is no abundance of data suggesting that statins increase the risk of coronary heart disease.
More possible good news for long term exercisers who have already made up their minds that what they do is good, can be found in a 2016 article (2)Shuaib Abdullah and Benjamin Levine reviewing their data of healthy exercisers stratified by exercise levels and previous articles that made the association between myocardial fibrosis ( as indicated by late gadolinium enhancement (LGE) on cardiac MRs) concluded "that increasing levels of lifelong physical activity were not associated with focal myocardial fibrosis ".Although some athletes may demonstrated LGE the authors suggest that they may not represent fibrosis but rather possibly "exaggeration of the normal local myocardial architecture or edema caused by exercise-induced right ventricular overload and paradoxical septal motion".The more commonly expressed view is that LGE is more common in endurance athletes and does represent fibrosis typically at the insertion points of the right ventricle to the left but their significance is not known.
No one since a pathologist decades ago (Tom Bassler) ( footnote 1) would now claim that endurance exercise is completely effective immunization against coronary artery disease but there will be a major paradigm shift if and when it is more conclusively shown that long term endurance exercise increases the risk of coronary artery disease.
Quoting from Levine ( ref 3):
"Although it would be foolish to argue that extraordinary endurance exercise can never be harmful, it is equally inappropriate to frighten individuals who wish to undertake competitive endurance training, including marathons,triathlons, or even ultra endurance events, based on fear of accelerating coronary artery disease or initiating a cardiomyopathic process." [ Levine does not however, deny the epidemiologic evidence that there is a increase risk of atrial fibrillation though there are conflicting data and the magnitude of the putative risk is a open question]
Sorting out cause and effect is no easy matter and may not be possible in cross sectional, observational studies in conditions in which there is a high "causal density".The relationship between exercise levels, intensity of statin therapy and the list of recognized coronary artery disease risk factors is by no means unraveled.
1)Merghani, A et al Prevalence of subclinical coronary artery disease in Master Endurance Athletes. Circ. 2017, May 2, 2017 Vol 135, issue no 12
2) Abdullah, SM et al Lifelong physical activity regardless of dose is not associated with myocardial fibrosis. Circulation Cardiovascular Imaging, 2016;9 e
3) Levine BD Can Intensive exercise harm the heart? Circulation 2014: 130, 97-99L
Footnote 1 Dr.Thomas J Bassler actually was slightly more circumspect saying that if one could finish a marathon in under 4 hours he would not die of a heart attack in the next 6 years. He wrote and spoke often in the 1970s about the value of long distance running. He died Dec 2011 at the age of 79 . Maybe his best quote is (paraphrased):
If you decide to lead a sedentary life style better see your doctor first.
Footnote 2 and disclosure
Paul Simon's lines ( a man believes what he wants to believe and disregards the rest )
is a modern musical echo of Hume's comment that reason is the servant of passion .
My history of marathon running over 40 plus years may well reveal
my biases.
11/13/17 Footnote 2 added as well as adding a new final paragraph.
Addendum: 1/31/18. Further thought.More statin and maybe more running may increase the calcium score ( it seems to) but both may make a coronary event less likely.At least I like to think so.
The study subjects were 152 men who had logged an average of 31 years of endurance exercise type activities. All had echocardiograms,24 hour Holter, stress ECG,CT coronary angiograms (CAC) and cardiac MRs with gadolinium as did 92 age matched controls with similar Framingham Risk scores.
15 athletes and none of the controls had delayed gadolinium enhancement (DGE) on the MRs, 7 of which had a coronary artery pattern.(The DGE issue will need to be written about at a later date-for now the focus is on the calcification.)
60% of the athletes and 63% of controls had a normal CAC score but only athletes (11.3%) has a CAC score of 300 or greater. So the incidence of any calcification was about the same in athletes and controls but the athletes had more calcium and more demonstrable luminal stenosis ( greater than 50%) in 7.5% of the athletes and in none of the controls.
So does this mean that long time endurance exercise increased the risk of coronary artery disease?
Maybe an answer to that is related to another question-does the increase in calcium scores noted in patients taking statins mean that statins increase the risk of coronary artery disease which is , of course, a conclusion contrary to realms of clinical trial results demonstrating the value of statins, at least in secondary prevention.
In regard to the second question there is a great deal of data regarding what could be called the statin plaque paradox-statins increase coronary artery calcium even as they shrike the plaques. A calcium score could increase even as the plaques regress because of the increased density of calcification bought about by the statins.However not only did Merghani's runners have higher Calcium scores a few did have luminal stenosis related to the calcification.
A review of serial coronary intravascular ultrasound (IVUS) data gathered up from 8 large clinical studies may shed some on light on that issue.
The bottom line is that statins may increase the calcium scores (Agatson score) by increasing the calcification of plaques while decreasing the volume of the plaques, the effect being greater with the more potent ( as measured by magnitude of cholesterol lowering) statins having a greater plaque shrinkage effect.My sense of the literature is that other than the more fringy group of "statin deniers" there is no abundance of data suggesting that statins increase the risk of coronary heart disease.
More possible good news for long term exercisers who have already made up their minds that what they do is good, can be found in a 2016 article (2)Shuaib Abdullah and Benjamin Levine reviewing their data of healthy exercisers stratified by exercise levels and previous articles that made the association between myocardial fibrosis ( as indicated by late gadolinium enhancement (LGE) on cardiac MRs) concluded "that increasing levels of lifelong physical activity were not associated with focal myocardial fibrosis ".Although some athletes may demonstrated LGE the authors suggest that they may not represent fibrosis but rather possibly "exaggeration of the normal local myocardial architecture or edema caused by exercise-induced right ventricular overload and paradoxical septal motion".The more commonly expressed view is that LGE is more common in endurance athletes and does represent fibrosis typically at the insertion points of the right ventricle to the left but their significance is not known.
No one since a pathologist decades ago (Tom Bassler) ( footnote 1) would now claim that endurance exercise is completely effective immunization against coronary artery disease but there will be a major paradigm shift if and when it is more conclusively shown that long term endurance exercise increases the risk of coronary artery disease.
Quoting from Levine ( ref 3):
"Although it would be foolish to argue that extraordinary endurance exercise can never be harmful, it is equally inappropriate to frighten individuals who wish to undertake competitive endurance training, including marathons,triathlons, or even ultra endurance events, based on fear of accelerating coronary artery disease or initiating a cardiomyopathic process." [ Levine does not however, deny the epidemiologic evidence that there is a increase risk of atrial fibrillation though there are conflicting data and the magnitude of the putative risk is a open question]
Sorting out cause and effect is no easy matter and may not be possible in cross sectional, observational studies in conditions in which there is a high "causal density".The relationship between exercise levels, intensity of statin therapy and the list of recognized coronary artery disease risk factors is by no means unraveled.
1)Merghani, A et al Prevalence of subclinical coronary artery disease in Master Endurance Athletes. Circ. 2017, May 2, 2017 Vol 135, issue no 12
2) Abdullah, SM et al Lifelong physical activity regardless of dose is not associated with myocardial fibrosis. Circulation Cardiovascular Imaging, 2016;9 e
3) Levine BD Can Intensive exercise harm the heart? Circulation 2014: 130, 97-99L
Footnote 1 Dr.Thomas J Bassler actually was slightly more circumspect saying that if one could finish a marathon in under 4 hours he would not die of a heart attack in the next 6 years. He wrote and spoke often in the 1970s about the value of long distance running. He died Dec 2011 at the age of 79 . Maybe his best quote is (paraphrased):
If you decide to lead a sedentary life style better see your doctor first.
Footnote 2 and disclosure
Paul Simon's lines ( a man believes what he wants to believe and disregards the rest )
is a modern musical echo of Hume's comment that reason is the servant of passion .
My history of marathon running over 40 plus years may well reveal
my biases.
11/13/17 Footnote 2 added as well as adding a new final paragraph.
Addendum: 1/31/18. Further thought.More statin and maybe more running may increase the calcium score ( it seems to) but both may make a coronary event less likely.At least I like to think so.
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