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.
Monday, October 02, 2017
Friday, September 29, 2017
Will the real Phidippides Syndrome (if there is one ) please stand up
The legendary Greek courier who ran back and forth in the days surrounding the big battle between the Greek and the Persians in the fifth century BC was named Phidippides. The story goes that he first ran from Athens to Sparta carrying a request of the Athenians to the Spartans for aid and then ran back to Athens with the bad news that Sparta could not help, something about a religious holiday not allowing them to fight,running a total of 280 mile round trip which took about 36 hours each way. That is about 3.8 mph or a 15.7 minute per mile pace- more of a brisk walk but the course was hilly. Then after the Athenians upset the Persians he ran from the site of the battle, the plains of marathon, to Athens to warn the city that the Persians fled Marathon and were hoping to rush to Athens by sea and attack again. This time Phidippdes was in a more of a hurry and ran the 26 miles distance in about 3 hours or about a 7 minute per mile pace and died on arrival.
At least three different clinical presentation have been deemed to be Phidippdes Syndrome (P syndrome)
James O' Keefe commented on the death of a legendary trail runner, Micah True AKA Caballo Blanco, who died on a run and at autopsy was said to have a dilated cardiomyopathy saying that this was an obvious case of P syndrome if there were no other causes of a dilated cardiomyopathy and that P syndrome has some diagnostic,generally agreed upon differentiating features.
Dr. Justin Tivaxx reported a case of a 50 year old half marathon runner who collapsed with and was resuscitated from ventricular fibrillation some 12 hours after a running workout. His MR showed a focal area of late gadolinium enhancement in the basal anterior septal said to not be a coronary artery distribution. This was suggested to be the focus of the previous ventricular fibrillation episode. Dr. Tivaxx presented in his paper an "hypothesis" concerning pathophysiology relevant to endurance exercise cardiac dysfunction and also said "considerable research is needed for to mature into an accepted understanding in clinical practice." Amen, yet some investigators write as if P. Syndrome is an accepted entity and that the general medical audience knows what it is.At the point I don't see how.
A third condition sometimes refers to as P syndrome is the putative clinical entity of exercise induced ARVD.At least two group of researchers have presented some evidence that such an entity exists.
So what is P syndrome, a dilated cardiomyopathy in a endurance athlete, a runner with an area of delayed gadolinium uptake or a person with ARVD who exercises.?
At least three different clinical presentation have been deemed to be Phidippdes Syndrome (P syndrome)
James O' Keefe commented on the death of a legendary trail runner, Micah True AKA Caballo Blanco, who died on a run and at autopsy was said to have a dilated cardiomyopathy saying that this was an obvious case of P syndrome if there were no other causes of a dilated cardiomyopathy and that P syndrome has some diagnostic,generally agreed upon differentiating features.
Dr. Justin Tivaxx reported a case of a 50 year old half marathon runner who collapsed with and was resuscitated from ventricular fibrillation some 12 hours after a running workout. His MR showed a focal area of late gadolinium enhancement in the basal anterior septal said to not be a coronary artery distribution. This was suggested to be the focus of the previous ventricular fibrillation episode. Dr. Tivaxx presented in his paper an "hypothesis" concerning pathophysiology relevant to endurance exercise cardiac dysfunction and also said "considerable research is needed for to mature into an accepted understanding in clinical practice." Amen, yet some investigators write as if P. Syndrome is an accepted entity and that the general medical audience knows what it is.At the point I don't see how.
A third condition sometimes refers to as P syndrome is the putative clinical entity of exercise induced ARVD.At least two group of researchers have presented some evidence that such an entity exists.
So what is P syndrome, a dilated cardiomyopathy in a endurance athlete, a runner with an area of delayed gadolinium uptake or a person with ARVD who exercises.?
Tuesday, September 26, 2017
Does long time aerobic exercise mitigate age related heart stiffness by altering titin isoforms?
Well, with a topic title like that, I expect an overload of hits.
In 1977 Maruyama described a muscle protein that he named connectin, now more commonly referred to as titin.
Titin is responsible for the passive elasticity of muscles and to prevent muscle over stretching. It is the largest protein in nature and is appropriately encoded by the largest human gene, the TTN gene. The titin molecule is the length of the sarcomere stretching from the Z line to the M band in the sarcomere.
Lalande et al (1) describe the link between exercise and titin's properties, specifically passive stiffness.The are a number of titin isoforms, some are long and thin associated with less stiff muscles , while others seem more likely to be related to stiffer muscles.. The authors present animal experiment data that suggest titin stiffness can by modified by such post translational mechanisms such as phosphorylation.
They suggest that "cardiac passive stiffness (k )may be a unifying mechanism "that links the benefits of long time aerobic exercise and the negative cardiovascular effect of sedentary lifestyles.
They review the work of the Dallas group (2) that demonstrated long time endurance athletes have ventricular stiffness similar to that of young sedentary subjects and their meta-analysis (3) that suggested that exercise levels above the US guidelines ( which is 150 minutes of moderate level exercise per week, or 500 Met minutes per week) significantly reduced the risk of diastolic heart failure presumably by mitigating the age and inactivity related increase in cardiac stiffness,
They review animal models that demonstrated exercise induced changes in cardiac passive stiffness that may be related to alterations in titin. To date there are no human data demonstrating that relationship but perhaps post translational alterations in titin offers a mechanism by which endurance exercise maintains cardiac compliance.Anyway it is nice to think so.
1) Lalande, S et al The link between exercise and titin passive stiffness.Exp Physiology 2017 p 1-12
2)Arbab-Zadeh, A Effect of aging and physical activity of left ventricular compliance. Circulation 110,1799
3)Pandey,A Dose-response relationship between physical activity and risk of heart failure: a meta-analysis. Circulation 132 ,1786
In 1977 Maruyama described a muscle protein that he named connectin, now more commonly referred to as titin.
Titin is responsible for the passive elasticity of muscles and to prevent muscle over stretching. It is the largest protein in nature and is appropriately encoded by the largest human gene, the TTN gene. The titin molecule is the length of the sarcomere stretching from the Z line to the M band in the sarcomere.
Lalande et al (1) describe the link between exercise and titin's properties, specifically passive stiffness.The are a number of titin isoforms, some are long and thin associated with less stiff muscles , while others seem more likely to be related to stiffer muscles.. The authors present animal experiment data that suggest titin stiffness can by modified by such post translational mechanisms such as phosphorylation.
They suggest that "cardiac passive stiffness (k )may be a unifying mechanism "that links the benefits of long time aerobic exercise and the negative cardiovascular effect of sedentary lifestyles.
They review the work of the Dallas group (2) that demonstrated long time endurance athletes have ventricular stiffness similar to that of young sedentary subjects and their meta-analysis (3) that suggested that exercise levels above the US guidelines ( which is 150 minutes of moderate level exercise per week, or 500 Met minutes per week) significantly reduced the risk of diastolic heart failure presumably by mitigating the age and inactivity related increase in cardiac stiffness,
They review animal models that demonstrated exercise induced changes in cardiac passive stiffness that may be related to alterations in titin. To date there are no human data demonstrating that relationship but perhaps post translational alterations in titin offers a mechanism by which endurance exercise maintains cardiac compliance.Anyway it is nice to think so.
1) Lalande, S et al The link between exercise and titin passive stiffness.Exp Physiology 2017 p 1-12
2)Arbab-Zadeh, A Effect of aging and physical activity of left ventricular compliance. Circulation 110,1799
3)Pandey,A Dose-response relationship between physical activity and risk of heart failure: a meta-analysis. Circulation 132 ,1786
Will the new war on opioids make patients with pain collateral damage.
Warren Meyer who writes the blog Coyote got it right. He said in part in commenting on Arizona's governor Ducey's announcement of guidelines regarding opioid control:
"Consider that many legitimate users will need more than the legal maximum dosage to control their pain, and thus the issue becomes whether we want to essentially torture innocent sick people by forcing them to remain in excruciating pain in exchange for (possibly) reducing the number of accidental deaths from abusers of these drugs (I say possibly because over the last 40 years the government war on drugs has had such a super stellar track record in reducing narcotic usage)."
CVS Caremark in getting in the act as well with more of their nanny-style pharmacy practices.Their "opioid utilization management" plan includes in part:
This program will include limiting to seven days (the Arizona guidelines mandate 5 days) the supply of opioids dispensed for certain acute prescriptions for patients who are new to therapy; limiting the daily dosage of opioids dispensed based on the strength of the opioid; and requiring the use of immediate-release formulations of opioids before extended-release opioids are dispensed.
Who would know better how much pain pill to prescribe and at what dosage than a large pharmacy-pharmacy management company aided by guidelines from the CDC , an organization in which one is unlikely to find many folks who actually treat patients for pain or anything else for that matter.
If the results of the decades of the war on drugs offer any forecast of the success of this latest surge it may be well be that there will be significant collateral damage to the patients who most need pain control.
never should have made pain which is a symptom into a sign
"Consider that many legitimate users will need more than the legal maximum dosage to control their pain, and thus the issue becomes whether we want to essentially torture innocent sick people by forcing them to remain in excruciating pain in exchange for (possibly) reducing the number of accidental deaths from abusers of these drugs (I say possibly because over the last 40 years the government war on drugs has had such a super stellar track record in reducing narcotic usage)."
CVS Caremark in getting in the act as well with more of their nanny-style pharmacy practices.Their "opioid utilization management" plan includes in part:
This program will include limiting to seven days (the Arizona guidelines mandate 5 days) the supply of opioids dispensed for certain acute prescriptions for patients who are new to therapy; limiting the daily dosage of opioids dispensed based on the strength of the opioid; and requiring the use of immediate-release formulations of opioids before extended-release opioids are dispensed.
Who would know better how much pain pill to prescribe and at what dosage than a large pharmacy-pharmacy management company aided by guidelines from the CDC , an organization in which one is unlikely to find many folks who actually treat patients for pain or anything else for that matter.
If the results of the decades of the war on drugs offer any forecast of the success of this latest surge it may be well be that there will be significant collateral damage to the patients who most need pain control.
never should have made pain which is a symptom into a sign
Monday, September 25, 2017
Sadly we will not get to see how fast Ed Whitlock could run a marathon at age 90.
This year the legendary marathoner Ed Whitlock died at age 86 on March 13 2017 of prostate cancer.
Famous in the running world Whitlock at 72 was the first at age 70 or older to run a marathon is less than 3 hours . He ran a 2:5:10 in 2003. What I find perhaps most amazing was the fact that his running speed in marathons changed so little in the age range when typically a person's O2 max decreases rapidly.See ref 2 below for description of how the decline in aerobic capacity accelerates with age which seems to contradict the literature than has shown a constant linear decline until about age 70 at which time a more rapid descent appears.
At age 70 he ran a 3:00. 23 marathon and at age 76 he ran 3:04.53 and at 80 he ran a 3:35 54.Over a six year period beginning at age 70 his marathon time decreased only about 4 minutes- a time difference easily attributable to varying weather-temperature and wind- and terrain differences over a 26.2 mile course or an extra bath room break.
Physiological testing was done on Whitlock at age 81 and his measured 02 Max was 54. This , as best I can find, is the highest recorded value for a man in his eighties. Earlier, Karlsen (3) reported a value of 50 in an 80 years old Norwegian in 2015.
Trappe et al(1)studied nine 80 years old endurance athletes ( they had exercised regularly for fifty years) and found their O2 max to be from 34-42.
The authors reviewed data from the literature and reported that in a total of 195 non athletic men in their eighties the measured O2 max ranged from 17 to 25.
One can speculate that Whitlock would have been able to run at least a sub 2:15 ( and probably better) marathon in his late 20s or early 30's as his 02 max would have probably been in the 80s which is the range measured in the typical world class marathoner.
While speculation about what some folks who are far out on the normal curve of aerobic capacity are able to do is interesting but perhaps more importantly what can the typical,healthy non-lifetime athlete in his/her eighties do physically. Here we are talking about people whose V02 max ranges from 17 to 25.
They should be able to finish Stage 1 on the Bruce protocol treadmill tests as this is thought to require a 17.5 02 uptake and be roughly comparable to a 15 minute per mile walk. Some would be able to actually finish Stage 2 which corresponds to a 15 minute per mile run. (It requires only 70% as much 02 uptake to walk a fifteen minute mile as it does to fun a mile in fifteen minutes.)According to the data from the CDC and ASM ,walking at less than 5 mph , golfing and ball room dancing would well be in the range of activities easily done by folks in this aerobic capacity range as well as light house work and all activities of daily care.
1)Trappe,S et al New records in aerobic power among octogenarians lifelong athletes. J.A. P 2013, 114 3-10
2) Fleg,Jl Accelerated longitudinal decline of aerobic capacity in healthy older adults. Circ.2005;112;674-682
3) Karlsen T. How to be 80 years old and have a v02 max of a 35 year old.Case reports in Medicine vol. 2015. id no 909561
1/17/18 addendum Several corrections made.
Famous in the running world Whitlock at 72 was the first at age 70 or older to run a marathon is less than 3 hours . He ran a 2:5:10 in 2003. What I find perhaps most amazing was the fact that his running speed in marathons changed so little in the age range when typically a person's O2 max decreases rapidly.See ref 2 below for description of how the decline in aerobic capacity accelerates with age which seems to contradict the literature than has shown a constant linear decline until about age 70 at which time a more rapid descent appears.
At age 70 he ran a 3:00. 23 marathon and at age 76 he ran 3:04.53 and at 80 he ran a 3:35 54.Over a six year period beginning at age 70 his marathon time decreased only about 4 minutes- a time difference easily attributable to varying weather-temperature and wind- and terrain differences over a 26.2 mile course or an extra bath room break.
Physiological testing was done on Whitlock at age 81 and his measured 02 Max was 54. This , as best I can find, is the highest recorded value for a man in his eighties. Earlier, Karlsen (3) reported a value of 50 in an 80 years old Norwegian in 2015.
Trappe et al(1)studied nine 80 years old endurance athletes ( they had exercised regularly for fifty years) and found their O2 max to be from 34-42.
The authors reviewed data from the literature and reported that in a total of 195 non athletic men in their eighties the measured O2 max ranged from 17 to 25.
One can speculate that Whitlock would have been able to run at least a sub 2:15 ( and probably better) marathon in his late 20s or early 30's as his 02 max would have probably been in the 80s which is the range measured in the typical world class marathoner.
While speculation about what some folks who are far out on the normal curve of aerobic capacity are able to do is interesting but perhaps more importantly what can the typical,healthy non-lifetime athlete in his/her eighties do physically. Here we are talking about people whose V02 max ranges from 17 to 25.
They should be able to finish Stage 1 on the Bruce protocol treadmill tests as this is thought to require a 17.5 02 uptake and be roughly comparable to a 15 minute per mile walk. Some would be able to actually finish Stage 2 which corresponds to a 15 minute per mile run. (It requires only 70% as much 02 uptake to walk a fifteen minute mile as it does to fun a mile in fifteen minutes.)According to the data from the CDC and ASM ,walking at less than 5 mph , golfing and ball room dancing would well be in the range of activities easily done by folks in this aerobic capacity range as well as light house work and all activities of daily care.
1)Trappe,S et al New records in aerobic power among octogenarians lifelong athletes. J.A. P 2013, 114 3-10
2) Fleg,Jl Accelerated longitudinal decline of aerobic capacity in healthy older adults. Circ.2005;112;674-682
3) Karlsen T. How to be 80 years old and have a v02 max of a 35 year old.Case reports in Medicine vol. 2015. id no 909561
1/17/18 addendum Several corrections made.
Wednesday, September 20, 2017
Bone Marrow lesions- not "bone marrow edema"
In 1995 in a misguided effort to increase my exercise program I developed severe groin pain that was shown to be hip adductor muscle tears by MR. The MR also demonstrated 2 area interpreted as "bone marrow edema" and the radiologist recommended I see my internist to evaluate with one concern being possible myeloma. A normal protein electrophoresis allayed my concern and I decided to learn what bone marrow edema was all about.
The term "bone marrow edema" (BME) was introduced in 1988 in a radiology journal article which described the MRI findings in a group of patients with severe pain and osteoarthritis (OA) of the hip and knee. Areas of increased signal intensity on T2 weighted images were described in the femoral head and condyles. Followup examinations showed that the lesions were transient and described by the authors as a "bone marrow edema- like" imaging pattern. Since then in spite of histological evidence that the pattern is not really marrow edema,that imaging pattern is often called BME or bone marrow edema
In 2000 a pathological examination of the resected bone in 16 patients with OA who underwent total knee arthroplasy (TKA) demonstrated that the bone in these BME area were in fact not edematous at all but showed varying degrees mainly normal bone and degrees of fibrosis,necrosis,bleeding and abnormal trabeculae. The BE areas demonstrated no more edema than surrounding bone.
The term "bone marrow lesions" ( BML) is now preferable to the pathologically incorrect BME, though BME is still frequently found on MR reports.
It is now recognized that patients with knee osteoarthritis (OA) frequently have these lesions in the femoral condyles and are often but not always associated with exacerbations of pain and that these lesions may be transient and may increase or decrease in size over time and the literature is conflicting regarding how well these BML correlate with the pain. Yet the association with pain is sufficiently strong to apparent warrant various strategies to treat BME. It seems from my sampling of web activity that OA patients regularly are searching for some effective treatment for BME and different operative and non operative approaches have been tried with there being no strong evidence that any approach is very effective.
BML are seen in a variety of settings.
1) Athletes in certain setting have been shown to have BMLs. For example about a third of college basketball players during their active season reported in one paper had lesions in the knee that were asymptomatic and not associated with an other findings on the MRIs. In another study 3/22 marathon runners were shown to have BMLs in the femur after a marathon.
2) trauma
3)Spontaneous osteonecrosis (ON) of the knee (SONK or SPONK)
First described by Ahlbach in 1968 the currently popular etiopathophysiology concept is that the entity is really a subchondral insufficiency fracture (SCIF).The SCIF is thought to sometimes heals in some cases while in others is progressive wherein there is bone necrosis and subsequent impaction of subchondral bone and deleterious change in the contour of the articular surface which facilitates the progression of osteoarthritis.
4) post knee procedure ON. The typical case is a older age female with a medial meniscus tear involving the posterior horn who undergoes an arthroscopy and a partial meniscectomy with or without a chondroplasty on an area of cartilage loss on the medial femoral condyle.
The term "bone marrow edema" (BME) was introduced in 1988 in a radiology journal article which described the MRI findings in a group of patients with severe pain and osteoarthritis (OA) of the hip and knee. Areas of increased signal intensity on T2 weighted images were described in the femoral head and condyles. Followup examinations showed that the lesions were transient and described by the authors as a "bone marrow edema- like" imaging pattern. Since then in spite of histological evidence that the pattern is not really marrow edema,that imaging pattern is often called BME or bone marrow edema
In 2000 a pathological examination of the resected bone in 16 patients with OA who underwent total knee arthroplasy (TKA) demonstrated that the bone in these BME area were in fact not edematous at all but showed varying degrees mainly normal bone and degrees of fibrosis,necrosis,bleeding and abnormal trabeculae. The BE areas demonstrated no more edema than surrounding bone.
The term "bone marrow lesions" ( BML) is now preferable to the pathologically incorrect BME, though BME is still frequently found on MR reports.
It is now recognized that patients with knee osteoarthritis (OA) frequently have these lesions in the femoral condyles and are often but not always associated with exacerbations of pain and that these lesions may be transient and may increase or decrease in size over time and the literature is conflicting regarding how well these BML correlate with the pain. Yet the association with pain is sufficiently strong to apparent warrant various strategies to treat BME. It seems from my sampling of web activity that OA patients regularly are searching for some effective treatment for BME and different operative and non operative approaches have been tried with there being no strong evidence that any approach is very effective.
BML are seen in a variety of settings.
1) Athletes in certain setting have been shown to have BMLs. For example about a third of college basketball players during their active season reported in one paper had lesions in the knee that were asymptomatic and not associated with an other findings on the MRIs. In another study 3/22 marathon runners were shown to have BMLs in the femur after a marathon.
2) trauma
3)Spontaneous osteonecrosis (ON) of the knee (SONK or SPONK)
First described by Ahlbach in 1968 the currently popular etiopathophysiology concept is that the entity is really a subchondral insufficiency fracture (SCIF).The SCIF is thought to sometimes heals in some cases while in others is progressive wherein there is bone necrosis and subsequent impaction of subchondral bone and deleterious change in the contour of the articular surface which facilitates the progression of osteoarthritis.
4) post knee procedure ON. The typical case is a older age female with a medial meniscus tear involving the posterior horn who undergoes an arthroscopy and a partial meniscectomy with or without a chondroplasty on an area of cartilage loss on the medial femoral condyle.
Friday, September 15, 2017
The new "medical professionalism"-the dogs bark and the carvan moves on
Five years ago a push- back to the new medical professionalism was a frequent topic on the medical blogs.Now I hear or read little about it. On several levels it seems to be a fait accompli as least in academic writings and in appropriate politically correct speech. How practicing physicians think about it may be another matter.
I was reminded of one of my earlier blog postings by a letter from CVS CAREMARK who wanted to be sure that I was still taking my BP meds as their records indicated that I had not refilled my prescription on time.
The origin(s) of the phrase " The dogs bark but the caravan moves on " is unclear, but the point is that the barking did not significantly impede the caravan on its journey. I suspect our barking did little.
I repeat a lighted edited version of a posting I offered 5 years ago in the hope that interest may be rekindled and to not let folks forget about the chilling philosophy expressed the book "New Rules". Some of the links may well be broken by now.
"
I was reminded of one of my earlier blog postings by a letter from CVS CAREMARK who wanted to be sure that I was still taking my BP meds as their records indicated that I had not refilled my prescription on time.
The origin(s) of the phrase " The dogs bark but the caravan moves on " is unclear, but the point is that the barking did not significantly impede the caravan on its journey. I suspect our barking did little.
I repeat a lighted edited version of a posting I offered 5 years ago in the hope that interest may be rekindled and to not let folks forget about the chilling philosophy expressed the book "New Rules". Some of the links may well be broken by now.
"
Kudos to Doug Peredina at the blog roadtohellth with this commentary on medical nannies,the activities of CVS Caremark alone those lines and the broader topic of the problems with the new medical professionalism, also known as the "new ethics", a topic of considerable concern to me and one about which I have ranted repeatedly.See here and here.
Dr. Peredina discusses a lawsuit filed against CVS . Dr. Troyen Brennan is the CMO and executive vice-president of CVS Caremark. The following is a quote from the book "New Rules" which was written by Dr. Brennan and the current head of CMS Dr. Donald Berwick. They are discussing the physician patient relationship and say the following:
"Today, this isolated relationship is no longer tenable or possible… Traditional medical ethics, based on the doctor-patient dyad must be reformulated to fit the new mold of the delivery of health care...Regulation must evolve. Regulating for improved medical care involves designing appropriate rules with authority...Health care is being rationalized through critical pathways and guidelines. The primary function of regulation in health care, especially as it affects the quality of medical care, is to constrain decentralized individualized decision making.”
In 2007,Dr. Brennan,then the executive vice president of Aetna cowrote an article in JAMA entitled "Managing Medical Resources. A return to the medical commons" which I blogged about ( see here) and I said in part:
"They speak of an abstract hypothetical " medical commons" and how the current emphasis by the physician on the welfare of the individual patient will spoil the commons much as the farmer who selfishly grazes his cattle on public land without regard for depleting the resource will destroy the resource.Physicians are implored to "reconstitute the medical commons" and think in terms of resource conservation and allocation so at the end the greatest medical good can be done for the greatest number of patients.They admit there is not currently such a commons. There never has been so I am unsure how a return is possible."
With this increasing constraint of decentralized individualized decision ( translation-individual docs advising individual patients about a course of action) someone else must make those decisions. Do you think the folks at insurance companies and pharmacy management companies might enjoy that role? Isn't it interesting that the head of CMS and the vice-president of a pharmacy management company share the same view of the "proper"role of the physician?
Also kudos to DrRich at his blog, which sadly is no longer active, Covert Rationing Blog with this thoughtful and important criticism of the new medical ethics, in which the traditional physician patient relationship with its fiduciary duty of the physician is being replaced with a nebulous duty to society . Also DrRich-in his real life persona of Dr. Richard Fogoros- hosted a discussion on Sermo which from my vantage point was well received and he did an admirable job in fielding a variety of questions. It is instructive and worrisome that a number of the physicians writing in had not even heard about the New Professionalism. If you have not, go here to read about it in the original.
Also kudos to Dr. Beth Haynes at the blog Blackribbonproject for this entry concerning various aspects of the attack on the traditional physician-patient relationship.
This important topic deserves all the attention it can get.
Dr. Peredina discusses a lawsuit filed against CVS . Dr. Troyen Brennan is the CMO and executive vice-president of CVS Caremark. The following is a quote from the book "New Rules" which was written by Dr. Brennan and the current head of CMS Dr. Donald Berwick. They are discussing the physician patient relationship and say the following:
"Today, this isolated relationship is no longer tenable or possible… Traditional medical ethics, based on the doctor-patient dyad must be reformulated to fit the new mold of the delivery of health care...Regulation must evolve. Regulating for improved medical care involves designing appropriate rules with authority...Health care is being rationalized through critical pathways and guidelines. The primary function of regulation in health care, especially as it affects the quality of medical care, is to constrain decentralized individualized decision making.”
In 2007,Dr. Brennan,then the executive vice president of Aetna cowrote an article in JAMA entitled "Managing Medical Resources. A return to the medical commons" which I blogged about ( see here) and I said in part:
"They speak of an abstract hypothetical " medical commons" and how the current emphasis by the physician on the welfare of the individual patient will spoil the commons much as the farmer who selfishly grazes his cattle on public land without regard for depleting the resource will destroy the resource.Physicians are implored to "reconstitute the medical commons" and think in terms of resource conservation and allocation so at the end the greatest medical good can be done for the greatest number of patients.They admit there is not currently such a commons. There never has been so I am unsure how a return is possible."
With this increasing constraint of decentralized individualized decision ( translation-individual docs advising individual patients about a course of action) someone else must make those decisions. Do you think the folks at insurance companies and pharmacy management companies might enjoy that role? Isn't it interesting that the head of CMS and the vice-president of a pharmacy management company share the same view of the "proper"role of the physician?
Also kudos to DrRich at his blog, which sadly is no longer active, Covert Rationing Blog with this thoughtful and important criticism of the new medical ethics, in which the traditional physician patient relationship with its fiduciary duty of the physician is being replaced with a nebulous duty to society . Also DrRich-in his real life persona of Dr. Richard Fogoros- hosted a discussion on Sermo which from my vantage point was well received and he did an admirable job in fielding a variety of questions. It is instructive and worrisome that a number of the physicians writing in had not even heard about the New Professionalism. If you have not, go here to read about it in the original.
Also kudos to Dr. Beth Haynes at the blog Blackribbonproject for this entry concerning various aspects of the attack on the traditional physician-patient relationship.
This important topic deserves all the attention it can get.
Saturday, September 02, 2017
ESPN football commentator quits-Football too dangerous
I have blogged aabout head injury and football several times. What a former player and now former TV football analyst,Ed Cunningham had to say has much more limbic valence.
I refer to what he wanted to say to some football coaches after one of the more meaningless post season Bowl games after watching one the QBs being repeatedly pummeled.
Paraphrased - Dudes, what are you doing- these are just kids.
http://bleacherreport.com/articles/2730459-espn-analyst-ed-cunningham-resigns-due-to-concern-over-head-injuries-in-football?utm_source=cnn.com&utm_medium=referral&utm_campaign=editorial
H/T CNN
addendum 9/4/17 Another quote I had to add. This from a George Will column regarding NFL football. He quotes college football coach Jim Harbaugh who said [football]" is the last bastion in America for toughness in men". Will added ..that thought must amuse Marines patrolling Afghanistan's Helmand province.
I refer to what he wanted to say to some football coaches after one of the more meaningless post season Bowl games after watching one the QBs being repeatedly pummeled.
Paraphrased - Dudes, what are you doing- these are just kids.
http://bleacherreport.com/articles/2730459-espn-analyst-ed-cunningham-resigns-due-to-concern-over-head-injuries-in-football?utm_source=cnn.com&utm_medium=referral&utm_campaign=editorial
H/T CNN
addendum 9/4/17 Another quote I had to add. This from a George Will column regarding NFL football. He quotes college football coach Jim Harbaugh who said [football]" is the last bastion in America for toughness in men". Will added ..that thought must amuse Marines patrolling Afghanistan's Helmand province.
Tuesday, August 22, 2017
Coarse and fine grain distinctions in medicine
Coarse Grain,Fine Grain distinctions in Medicine.
Jacob Bronowski in his "The Origins of Knowledge and Imagination" speaks of what he considers a basic problem in the brain's mechanism namely how to achieve fine discriminations with a coarse apparatus.Further, he says that in many ways "about all" human problems..in science or in literature..center around the same problem.How do you refine the detail with an apparatus which remains at bottom coarse and grainy?"
Consider the randomized clinical trial (RCT) currently thought to be at the apex of the hierarchy of the techniques we use to find medical truth.We are left with aggregate data, groups numbers that are relevant , strictly speaking, to patients having the characteristics of those in the trial but is freqently extrapolated to include many other patients.
Compare this grainy-ness with the progress made in the following example.
Consider the use of MRI in a patient with the clinical picture of optic neuritis.
The finding of white matter abnormalities of a cetain type provide valuable information regarding likelihood of progression to multiple sclerosis. The coarse grain category of optic neuritis has been fine grained a bit by sorting out those patients with a high risk of subsequent development of multiple sclerosis.
The finding of white matter abnormalities of a cetain type provide valuable information regarding likelihood of progression to multiple sclerosis. The coarse grain category of optic neuritis has been fine grained a bit by sorting out those patients with a high risk of subsequent development of multiple sclerosis.
But fine tuning is not a feature the RCT. We can break the aggregate data into sub groups but we loose power to see differences and at the same time we increase the likelihood of Type I errors by cranking out many comparisons. So basically the RCT is a coarse grain apparatus and cannot get any finer, remaining coarse and grainy.
One way to fine tune the aggregate data is to determine the relevant pathophysiology.The example of TPMT deficiency comes to mind. Before the details of this deficiency were mapped out, we could only say that a certain percentage of children treated with a thiopurine type drug developed serious bone marrow failure. Once we learned what the pathophysiology was , testing could be done to see who comprised that percentage and the coarse grain became fine.
Disclosure: This is a lightly edited and revised essay that I originally posted years ago on a now defunct blog.
Monday, August 21, 2017
The perfect country-western song -the perfect medical article
The Perfect Country and Western Song-The perfect Medical article
In the David Allan Coe song, "You never even called me by my name" we are told some of the essential components of the " perfect" country song. Things that should be mentioned are: trains, trucks, mama,prison and getting drunk.
There are also essential components of the perfect medical article and should appear in the introduction and/or the discussion and summary sections. They include: mention of evidence based medicine (this is required even if the article has little if any evidence actually presented), mention of the disease at issue being "a public health problem"(saying it is common is not enough), a word about "quality" and perhaps most importantly stating that "we must be good stewards in this era of scarity of medical resources ". Unlike the essential elements of C&W music, which are timeless, the medical article sine qua nons are of recent vintage.
Non country and Western fans may claim that tired cliches populate some country songs. It could be claimed that "floating abstractions" and politically correct comments are the fluffy fillers of the perfect medical articles.
In the David Allan Coe song, "You never even called me by my name" we are told some of the essential components of the " perfect" country song. Things that should be mentioned are: trains, trucks, mama,prison and getting drunk.
There are also essential components of the perfect medical article and should appear in the introduction and/or the discussion and summary sections. They include: mention of evidence based medicine (this is required even if the article has little if any evidence actually presented), mention of the disease at issue being "a public health problem"(saying it is common is not enough), a word about "quality" and perhaps most importantly stating that "we must be good stewards in this era of scarity of medical resources ". Unlike the essential elements of C&W music, which are timeless, the medical article sine qua nons are of recent vintage.
Non country and Western fans may claim that tired cliches populate some country songs. It could be claimed that "floating abstractions" and politically correct comments are the fluffy fillers of the perfect medical articles.
Sunday, July 30, 2017
In some , is college football enough to cause CTE?
I believe the answer is yes.
202 donated brains from former football players were examined by the Boston University CTE center. Of those who played in the NFL 110/111 had criteria that the center believes to be diagnostic of CTE.
Finding CTE in former NFL players is not breaking news. The data from men who did not participate past the college level is in a way more striking and alarming. 48 out of 53 college players' brains demonstrated pathological finding of CTE and 27 of the 53 were classified as severe. There were 14 brains from men who only played high school football and of those 3 had changes said to be typical of CTE.
This , of course, does not speak to the issue of what is the prevalence of CTE in any group of players. The data here is highly selective The brains were donated typically by family members often in part because of concern that their family member has some mental or behavioral issue.This is numerator based statistics.
Data was not presented but it seems a reasonable assumption that the college players had experienced at least 8 years of football, i.e. high school and college and likely many also took part in Pop Warner of some such youth league .It is an open issue as to whether repetitive subconcussive or concussive head blows are more likely to cause to cause damage to the young brain.It was a reassuring false believe prevalent for many years that young kids just did not hit each other hard enough to cause concussions or brain damage. Data from accelerometer measurements in helmets of youth league players have been shown to reach the range of impact forces seen in high school players so parents should have been disabused of that notion. but I doubt that most are.
The bubble wrapped,helicopted parented generation(s) of kids protected from tri-cycle falls with helmets are for the most part not discouraged from high school football and in many instances cheered on by their parents who seem not to realize why there is often an ambulance parked near the playing field.
202 donated brains from former football players were examined by the Boston University CTE center. Of those who played in the NFL 110/111 had criteria that the center believes to be diagnostic of CTE.
Finding CTE in former NFL players is not breaking news. The data from men who did not participate past the college level is in a way more striking and alarming. 48 out of 53 college players' brains demonstrated pathological finding of CTE and 27 of the 53 were classified as severe. There were 14 brains from men who only played high school football and of those 3 had changes said to be typical of CTE.
This , of course, does not speak to the issue of what is the prevalence of CTE in any group of players. The data here is highly selective The brains were donated typically by family members often in part because of concern that their family member has some mental or behavioral issue.This is numerator based statistics.
Data was not presented but it seems a reasonable assumption that the college players had experienced at least 8 years of football, i.e. high school and college and likely many also took part in Pop Warner of some such youth league .It is an open issue as to whether repetitive subconcussive or concussive head blows are more likely to cause to cause damage to the young brain.It was a reassuring false believe prevalent for many years that young kids just did not hit each other hard enough to cause concussions or brain damage. Data from accelerometer measurements in helmets of youth league players have been shown to reach the range of impact forces seen in high school players so parents should have been disabused of that notion. but I doubt that most are.
The bubble wrapped,helicopted parented generation(s) of kids protected from tri-cycle falls with helmets are for the most part not discouraged from high school football and in many instances cheered on by their parents who seem not to realize why there is often an ambulance parked near the playing field.
Tuesday, June 13, 2017
Is subendocardial fibrosis a reason for the age associated decrease in diastolic function?
It seems to be all about diastole.Simply put- the aging heart has more functional loss in ventricular filling than in ejection of blood ( as least as depicted by the usual measures of systole namely the ejection fraction (EF) at rest and stroke volume at rest). Similarly the largest difference between the exercise capacity of the average jogger and the elite endurance athlete is found in diastole-the elite athlete has markedly superior diastolic function likely on a genetic basis.
Hollingworth and co-workers from Newcastle on Tyne (1) studied left ventricular torsion and diastolic function in presumably healthy adults in various age ranges using cardiac magnetic imaging with tissue tagging.
First some background;
The architecture of the left ventricle has left handed subepicardial fibers and right handed subendocardial fibers which leads to a rotational deformation during cardiac contraction referred to as torsion. The subendocardial fibers are activated first leading to a brief clockwise rotation ( as viewed from the apex of the heart as if you were on the spleen looking up) and then a counterclockwise rotation while the base rotates clockwise. This action has been compared to the two handed movement of wringing out a washrag.
The twisting of the left ventricle during systole is followed by a recoiling or untwisting releasing the energy stored during systole. The untwisting largely occurs mainly in the isovolumic relaxation time . (IVRT). The IVRT is the time after the aortic valve closes and before the mitral valve has not yet opened-a period when no blood is either entering or leaving the ventricle.
The rotation action of the heart can be explained by the orientation of the muscle fibers. The subendocardial fibers are oriented in a right handed direction while the subepicardial fibers run in in a left handed direction and a midlayer is oriented circumferentially .The contraction of all three sets of fibers account for all contractile actions of the heart and the rotational movement.
What at first seem counter-intuitive is the observation that subendocardial disease is associated with hyper-rotations. (2) This is possibly explained by subendocardial fibrosis decreasing the rotational counterbalance to the mechanical advantaged ( longer radius) epicardial rotational direction.
Hollinsworth's study showed the expected decreased early diastolic filling and a " torsion to shortening ratio" that was consistent with lessened subendocardial shortening possibly due to subendocardial fibrosis. So possibly some of the age related diastolic dysfunction may be related to altered and unbalanced untwisting mechanics.
1) Hollingsworth, KG et al Left ventricular torsion energetic and diastolic function in normal human aging. Am j Physiol heart circ physiology 302, H 885-H892,2012 (full text is available on line)
2.Nakatani, S. Left Ventricular rotation and twist:Why should we learn? J. Cardiovas Ultrasound 2011;19 (1): 1-6. Full text is available on line)
Hollingworth and co-workers from Newcastle on Tyne (1) studied left ventricular torsion and diastolic function in presumably healthy adults in various age ranges using cardiac magnetic imaging with tissue tagging.
First some background;
The architecture of the left ventricle has left handed subepicardial fibers and right handed subendocardial fibers which leads to a rotational deformation during cardiac contraction referred to as torsion. The subendocardial fibers are activated first leading to a brief clockwise rotation ( as viewed from the apex of the heart as if you were on the spleen looking up) and then a counterclockwise rotation while the base rotates clockwise. This action has been compared to the two handed movement of wringing out a washrag.
The twisting of the left ventricle during systole is followed by a recoiling or untwisting releasing the energy stored during systole. The untwisting largely occurs mainly in the isovolumic relaxation time . (IVRT). The IVRT is the time after the aortic valve closes and before the mitral valve has not yet opened-a period when no blood is either entering or leaving the ventricle.
The rotation action of the heart can be explained by the orientation of the muscle fibers. The subendocardial fibers are oriented in a right handed direction while the subepicardial fibers run in in a left handed direction and a midlayer is oriented circumferentially .The contraction of all three sets of fibers account for all contractile actions of the heart and the rotational movement.
What at first seem counter-intuitive is the observation that subendocardial disease is associated with hyper-rotations. (2) This is possibly explained by subendocardial fibrosis decreasing the rotational counterbalance to the mechanical advantaged ( longer radius) epicardial rotational direction.
Hollinsworth's study showed the expected decreased early diastolic filling and a " torsion to shortening ratio" that was consistent with lessened subendocardial shortening possibly due to subendocardial fibrosis. So possibly some of the age related diastolic dysfunction may be related to altered and unbalanced untwisting mechanics.
1) Hollingsworth, KG et al Left ventricular torsion energetic and diastolic function in normal human aging. Am j Physiol heart circ physiology 302, H 885-H892,2012 (full text is available on line)
2.Nakatani, S. Left Ventricular rotation and twist:Why should we learn? J. Cardiovas Ultrasound 2011;19 (1): 1-6. Full text is available on line)
Monday, June 12, 2017
After 40 plus years ABIM does audit to see if I have a medical license
What is that all about?
I received a letter from the ABIM informing me that " during a recent audit, ABIM was unable to confirm that you have a valid license to practice medicine." I was requested to send a copy of my license within 30 days and " if ABIM is unable to confirm that you hold a valid license to practice medicine,ABIM will be obliged to suspend your Board Certification and report your certification status as "Not certified".
I replied the same day by Email and send a hard copy of my license by letter . A few days later I received a second letter identical to the first and again I replied by mail with a copy of my license.I have had no reply.
I wondered about their audit procedure. I was able to verify my license in less than 2 minutes by going the website of the state of the medical board in the state in which I have had an uninterrupted license at the same address for over 35 years.If their audit process is as inadequate as it appears to be they will waste more than a little time and effort to confirm licenses and waste time and efforts of diplomats replying to the requests.
Why , after forty years, does ABIM consider it necessary to determine if I have a license?
Is this somehow related to their widely criticized maintenance of certification (MOC) program and the efforts of some organizations to link MOC with state medical license requirements?
Have others received similar letters? Any thoughts about what this is all about?
addendum: It is now more than 2 months and ABIM has still not replied to my email which they had promised in "2-3 weeks" saying they were very busy. 8/19/17
I received a letter from the ABIM informing me that " during a recent audit, ABIM was unable to confirm that you have a valid license to practice medicine." I was requested to send a copy of my license within 30 days and " if ABIM is unable to confirm that you hold a valid license to practice medicine,ABIM will be obliged to suspend your Board Certification and report your certification status as "Not certified".
I replied the same day by Email and send a hard copy of my license by letter . A few days later I received a second letter identical to the first and again I replied by mail with a copy of my license.I have had no reply.
I wondered about their audit procedure. I was able to verify my license in less than 2 minutes by going the website of the state of the medical board in the state in which I have had an uninterrupted license at the same address for over 35 years.If their audit process is as inadequate as it appears to be they will waste more than a little time and effort to confirm licenses and waste time and efforts of diplomats replying to the requests.
Why , after forty years, does ABIM consider it necessary to determine if I have a license?
Is this somehow related to their widely criticized maintenance of certification (MOC) program and the efforts of some organizations to link MOC with state medical license requirements?
Have others received similar letters? Any thoughts about what this is all about?
addendum: It is now more than 2 months and ABIM has still not replied to my email which they had promised in "2-3 weeks" saying they were very busy. 8/19/17
Monday, June 05, 2017
More on subclinical atrial fibrillation (SCAF) and what to do when we find it
A 2014 study-Crystal AF- examined patients with cryptogenic stroke using a implantable cardiac monitor and reported that over a three year period 30% had episodes of atrial fibrillation(AF) lasting 30 seconds on longer. This study likely energized the effort to implant cardiac monitoring devices and to anticoagulate those patients found to have atrial fibrillation (AF).A more recent study might serve to cast some doubt on that practice.
The study,Reveal AF,studied 394 patients using an implantable cardiac monitor with no history of AF but who were considered high risk for stroke based on the CHADS2 score.At the end of 18 months 29.3 % of the patients had episodes of AF of six minutes or more and at 30 months 40% had AF. Further, 12% had AF durations of 6 hours or more.
So we know that AF is common in 1) patients with history of stroke and no obvious cause 2) patients classified as high risk using the CHADS2 scoring system and 3) patients with pacemakers.
Should all patients with cryptogenic stroke shown to have AF by a implantable device receive oral anticoagulation? That seems to be common clinical practice but I am aware of no clinical trials showing the efficacy and safety of that approach. Should all patients with a CHAD2 score similar to that used in the Reveal AF study receive anticoagulation? ( in the trial 56% of the patients were actually prescribed OAC by their private physicians). Should all patients with pacemakers (PMs )with SCAF ( above some level of AF burden) receive OAC?
There are at least 2 randomized clinical trials underway which are designed to determine the effects of OAC on patients with subclinical AF (SCAF) as determined by data collected on patients with pace makers.
In addition a recent study ( see here) and analysis casts more than a little doubt on the validity of the various CHADS risk determination systems.
The prolific EP cardiologist author and blogger John Mandrola puts it this way in his discussion of the Reveal AF " ..if the average high risk older person has the same amount of short-duration AF as a person who just had a stroke how does this ( long term monitoring) help decide on therapy?" Point well taken. Actually at the end of 30 months in Reveal AF trial 40% had SCAF versus 30% with SCAF and 36 months.Taken at face value could nt one claim that AF is protective? I think not but still that just amplifies Mandrola's point.
Dr. H Kamel and associates have published an excellent commentary and review (3) of the mechanisms of stroke and atrial fibrillation which along with the Reveal AF trial results might slow down enthusiasm for implanting devices in all patients with cryptogenic stroke and the increasing call for more screening for the detection of afib.
1)Sanna, T Cryptogenic stroke and Underlying atrial fibrillation NEJM 2014: 370, 2478
2) Reiffel, JA presented at Heart rhythm Society Meeting, May 10-13, 2017.
3)Kamel, H et al Atrial fibrillation and mechanisms of stroke.Time for a new model.Stroke 2016 47 895-900.
Additions made Aug 2,2017 .
The study,Reveal AF,studied 394 patients using an implantable cardiac monitor with no history of AF but who were considered high risk for stroke based on the CHADS2 score.At the end of 18 months 29.3 % of the patients had episodes of AF of six minutes or more and at 30 months 40% had AF. Further, 12% had AF durations of 6 hours or more.
So we know that AF is common in 1) patients with history of stroke and no obvious cause 2) patients classified as high risk using the CHADS2 scoring system and 3) patients with pacemakers.
Should all patients with cryptogenic stroke shown to have AF by a implantable device receive oral anticoagulation? That seems to be common clinical practice but I am aware of no clinical trials showing the efficacy and safety of that approach. Should all patients with a CHAD2 score similar to that used in the Reveal AF study receive anticoagulation? ( in the trial 56% of the patients were actually prescribed OAC by their private physicians). Should all patients with pacemakers (PMs )with SCAF ( above some level of AF burden) receive OAC?
There are at least 2 randomized clinical trials underway which are designed to determine the effects of OAC on patients with subclinical AF (SCAF) as determined by data collected on patients with pace makers.
In addition a recent study ( see here) and analysis casts more than a little doubt on the validity of the various CHADS risk determination systems.
The prolific EP cardiologist author and blogger John Mandrola puts it this way in his discussion of the Reveal AF " ..if the average high risk older person has the same amount of short-duration AF as a person who just had a stroke how does this ( long term monitoring) help decide on therapy?" Point well taken. Actually at the end of 30 months in Reveal AF trial 40% had SCAF versus 30% with SCAF and 36 months.Taken at face value could nt one claim that AF is protective? I think not but still that just amplifies Mandrola's point.
Dr. H Kamel and associates have published an excellent commentary and review (3) of the mechanisms of stroke and atrial fibrillation which along with the Reveal AF trial results might slow down enthusiasm for implanting devices in all patients with cryptogenic stroke and the increasing call for more screening for the detection of afib.
1)Sanna, T Cryptogenic stroke and Underlying atrial fibrillation NEJM 2014: 370, 2478
2) Reiffel, JA presented at Heart rhythm Society Meeting, May 10-13, 2017.
3)Kamel, H et al Atrial fibrillation and mechanisms of stroke.Time for a new model.Stroke 2016 47 895-900.
Additions made Aug 2,2017 .
Friday, May 12, 2017
An increasing cardiac calcium score may not mean increased CVD risk
The coronary calcium score ( for example as done with a EBCT heart scan) is well recognized as a tool to estimate cardiac risk, a higher score meaning a higher risk.
Coronary calcification is by definition coronary artery disease. Calcification may be in the media of arteries or in the intima. Intimal calcification may be dense as is found in fibrous, basically stable plagues which are not prone to rupture and cause an acute coronary event. Spotty calcification can be found in soft, vulnerable plaques that are at risk of rupture.
Serial calcium scans on patients taking statins have shown increase in coronary calcification and yet there is more than abundant evidence that statins ( at least in secondary prevention) can reduce plaques and decrease the risk of coronary events,a situation referred to by some as the "statin paradox" or the "plaque paradox".
A possible explanation to this alleged paradox may be found in a study (1) from Cleveland Clinic in which the authors analyzed intravascular ultrasound images of patients from 8 clinical trials.
Patients with coronary artery disease treated with statins show an increase in coronary calcification.The so-called high intensity statins bring about more increase in calcification while also causing the greatest regression of plaques. The increase in calcification may be one mechanism by which statin therapy stabilizes plagues and makes them less likely to rupture. So serial calcium scans in a patient taking a statin demonstrating increased calcification may not be a warning of increased risk at all.
Quoting Cleveland Clinic's Dr . Steve Nissen:
"This is an important observation that tells us statins work to stabilize plaques by converting softer,cholesterol -laden plaques that are prone to rupture into more stable calcified plaques that are relatively inert.It explains the paradox of why serial measurements of calcium doesn't necessarily work to track the progression of disease and it explains to some extent how statins work.
Internists who like to talk about mechanisms and how things work may find this a compelling story but as an accompanying editorial (3) said this is a hypothesis generating study,causality cannot be inferred and the techniques used have multiple limitations. Human are pattern seeking story telling creatures and this story might catch on-at least until something better comes along.
Shifting gears-there are at least 3 articles that have reported that long time endurance exercisers have higher calcium scores than age matched sedentary controls controls,an observation offered by some authors as more proof that too much exercise is not good. Juxtaposed to that is the epidemiologic evidence that longtime endurance exercise decreases the risk of a coronary event and that elite athletes life longer than sedentary colleagues and yet more calcium in the athletes.Another plaque paradox?
Merghani and co-authors studied 152 maters athletes ( ages 51-63) They found that "most" )( 60%) of the lifelong exercisers has a normal CT coronary angiogram as did a similar number of the controls. However they also reported that the male athletes were more likely to have a CAC score of 300 or more compared to the sedentary controls.The plaques in the athletes were predominately calcific.
Similar results were reported by V.L. Aengevaeren et al (2) who studied 284 lifelong exercisers. In regard to their findings they said:
"The most active group did however had a more benign composition of plaques with fewer mixed plaques and more often only calcified plaques.These observation may explain the increased longevity of endurance athletes despite the presence of more coronary atherosclerotic plaques in the most active participants ".
Eijsvogels and co-workers published an excellent, detailed and extensively referenced review( 4) of the possible harmful effects of acute and chronic exercise . They only briefly mention what was then the preliminary evidence that longtime runners have higher calcium scores as their review preceded Puri's work as well as that of Aengevaren and Merghani
1.Puri, R Impact of statins on serial coronary calcifications during atheroma progression and regression. J Am Coll Cardio 2015;65, 1273-1282
2 Aengevaren VL et al The Relationship between lifelong exercise volume can coronary atherosclerosis in Athletes. Circulation 2017 april 27
3. Shaw LJ The Never Ending story on Coronary Calcium.Is it predictive,punitive or protective? Editorial Comment J of Amer Coll Cardio, 2015 ,65 no 15 1283-1285
4. Eijsvogels,TMN et al Are there deleterious cardiac effects of acute and chronic endurance exercise? Physiol Rev 96 99-125,2015
Coronary calcification is by definition coronary artery disease. Calcification may be in the media of arteries or in the intima. Intimal calcification may be dense as is found in fibrous, basically stable plagues which are not prone to rupture and cause an acute coronary event. Spotty calcification can be found in soft, vulnerable plaques that are at risk of rupture.
Serial calcium scans on patients taking statins have shown increase in coronary calcification and yet there is more than abundant evidence that statins ( at least in secondary prevention) can reduce plaques and decrease the risk of coronary events,a situation referred to by some as the "statin paradox" or the "plaque paradox".
A possible explanation to this alleged paradox may be found in a study (1) from Cleveland Clinic in which the authors analyzed intravascular ultrasound images of patients from 8 clinical trials.
Patients with coronary artery disease treated with statins show an increase in coronary calcification.The so-called high intensity statins bring about more increase in calcification while also causing the greatest regression of plaques. The increase in calcification may be one mechanism by which statin therapy stabilizes plagues and makes them less likely to rupture. So serial calcium scans in a patient taking a statin demonstrating increased calcification may not be a warning of increased risk at all.
Quoting Cleveland Clinic's Dr . Steve Nissen:
"This is an important observation that tells us statins work to stabilize plaques by converting softer,cholesterol -laden plaques that are prone to rupture into more stable calcified plaques that are relatively inert.It explains the paradox of why serial measurements of calcium doesn't necessarily work to track the progression of disease and it explains to some extent how statins work.
Internists who like to talk about mechanisms and how things work may find this a compelling story but as an accompanying editorial (3) said this is a hypothesis generating study,causality cannot be inferred and the techniques used have multiple limitations. Human are pattern seeking story telling creatures and this story might catch on-at least until something better comes along.
Shifting gears-there are at least 3 articles that have reported that long time endurance exercisers have higher calcium scores than age matched sedentary controls controls,an observation offered by some authors as more proof that too much exercise is not good. Juxtaposed to that is the epidemiologic evidence that longtime endurance exercise decreases the risk of a coronary event and that elite athletes life longer than sedentary colleagues and yet more calcium in the athletes.Another plaque paradox?
Merghani and co-authors studied 152 maters athletes ( ages 51-63) They found that "most" )( 60%) of the lifelong exercisers has a normal CT coronary angiogram as did a similar number of the controls. However they also reported that the male athletes were more likely to have a CAC score of 300 or more compared to the sedentary controls.The plaques in the athletes were predominately calcific.
Similar results were reported by V.L. Aengevaeren et al (2) who studied 284 lifelong exercisers. In regard to their findings they said:
"The most active group did however had a more benign composition of plaques with fewer mixed plaques and more often only calcified plaques.These observation may explain the increased longevity of endurance athletes despite the presence of more coronary atherosclerotic plaques in the most active participants ".
Eijsvogels and co-workers published an excellent, detailed and extensively referenced review( 4) of the possible harmful effects of acute and chronic exercise . They only briefly mention what was then the preliminary evidence that longtime runners have higher calcium scores as their review preceded Puri's work as well as that of Aengevaren and Merghani
1.Puri, R Impact of statins on serial coronary calcifications during atheroma progression and regression. J Am Coll Cardio 2015;65, 1273-1282
2 Aengevaren VL et al The Relationship between lifelong exercise volume can coronary atherosclerosis in Athletes. Circulation 2017 april 27
3. Shaw LJ The Never Ending story on Coronary Calcium.Is it predictive,punitive or protective? Editorial Comment J of Amer Coll Cardio, 2015 ,65 no 15 1283-1285
4. Eijsvogels,TMN et al Are there deleterious cardiac effects of acute and chronic endurance exercise? Physiol Rev 96 99-125,2015
Tuesday, May 09, 2017
The annualized decrease in exercise capacity may be even worse than we thought
The longitudinal decline in aerobic capacity is typically said to be 5 -10% per decade from age 40 to about age 70 then a more rapid decline occurs. Data from the Baltimore Longitudinal study of Aging (BLSA) (1) suggests that the decline is not constant across age ranges but rather" accelerates markedly with each successive age decade".
How so?
In cross sectional studies " each succeeding age decade represents a more highly selected group than it predecessor, thus healthy 70 to 90 year-olds may have been physiologically superior to current 20-40 years olds when they were on a similar age. In other words there is inherent selection bias in cross sectional data.
I will not attempt to explain the statistical model used but here are their values for the reduction in men in peak O2 uptake expressed in ml/kilo/min for various decades:
age
30- 39 minus 7
40-49 minus 10
50-59 minus 15
60-69 minus 20
over 70 minus 26
A similar pattern was found in women.
They found that the oxygen pulse (oxygen consumed per heart beat) rate of decline mirrored the rate of decline in peak 02 .Since oxygen pulse is a function of stroke volume and peripheral muscle uptake of oxygen it is not possible to determine if it is cardiac output or muscle uptake that is largely responsible for the decline.
Caveat-The published results are from a mixed-effect prediction model and the median followup was only 7.9 years and prediction is the operative word. Though the study is "longitudinal",numbers in their tables do not represent for example following the same people over a lifetime and noting the per decade change in oxygen uptake. Still their data suggest that the often quoted 5-10 % decrease per decade may be too optimistic and rates of changes likely accelerate with aging.The confidence intervals for each age range are quite large and you have to wonder what are the mechanisms responsible for such wide variation in loss of exercise capacity within an age range. If subendocardial fibrosis is the ( or a) culprit what are the factors that accelerate or retard that process.
1) Fleg, JL Accelerated Longitudinal Decline or Aerobic Capacity in Healthy Older Adults"
Circulation 2005, 112: 674 -682.
How so?
In cross sectional studies " each succeeding age decade represents a more highly selected group than it predecessor, thus healthy 70 to 90 year-olds may have been physiologically superior to current 20-40 years olds when they were on a similar age. In other words there is inherent selection bias in cross sectional data.
I will not attempt to explain the statistical model used but here are their values for the reduction in men in peak O2 uptake expressed in ml/kilo/min for various decades:
age
30- 39 minus 7
40-49 minus 10
50-59 minus 15
60-69 minus 20
over 70 minus 26
A similar pattern was found in women.
They found that the oxygen pulse (oxygen consumed per heart beat) rate of decline mirrored the rate of decline in peak 02 .Since oxygen pulse is a function of stroke volume and peripheral muscle uptake of oxygen it is not possible to determine if it is cardiac output or muscle uptake that is largely responsible for the decline.
Caveat-The published results are from a mixed-effect prediction model and the median followup was only 7.9 years and prediction is the operative word. Though the study is "longitudinal",numbers in their tables do not represent for example following the same people over a lifetime and noting the per decade change in oxygen uptake. Still their data suggest that the often quoted 5-10 % decrease per decade may be too optimistic and rates of changes likely accelerate with aging.The confidence intervals for each age range are quite large and you have to wonder what are the mechanisms responsible for such wide variation in loss of exercise capacity within an age range. If subendocardial fibrosis is the ( or a) culprit what are the factors that accelerate or retard that process.
1) Fleg, JL Accelerated Longitudinal Decline or Aerobic Capacity in Healthy Older Adults"
Circulation 2005, 112: 674 -682.
Sunday, April 23, 2017
"Para Hisian Pacing" as well as selective Bundle of His pacing may bring about a hyper response
I have written before about a sub group of Cardiac resynchronization patients (CRT) who have a hyper response with marked improvement in indices of cardiac function, e.g. ejection fraction and end diastolic volume.
Such responses have been reported with Biventricular pacing (Bi-V) and His Bundle Pacing ( HBP). There are two forms or types of HBP: 1) pure HBP also known as selective and 2) Para Hisian pacing also known as non selective HBP.
The QRS is normalized with selective HBP while in nonselective although the widened QRS duration is significant reduced it may not be restored to the pre bundle branch block configuration. There is both activation of the His Bundle fibers and adjacent ventricular septal muscle giving a fused or fusion ventricular activation pattern and an EKG with a delta wave resembling pre-excitation pattern.
According to Lida et al writing in the December 2016 Journal of Arrhythmia (1) "there seems to be no significant clinical difference between selective HBP and non selective HBP because both do not alter physiological impulse conduction and possibly maintain rapid and synchronous LV ( left ventricular) activation "
A similar case report was published by Ajijola et al from UCLA in 2015 (2)
His Bundle pacing seems to gaining momentum both as an alternative to right ventricular pacing and as a method of cardiac resynchronization.
1)Lida, Y et al Successful resynchronization by permanent His-bundle pacing in patient with pacing -induced cardiomyopathy' J Arrhythmia , 2016 Dec. 32(6), 499-501
2)Ajijola,O et al Hyper-response to cardiac resynchronization with permanent His bundle pacing:Is parahisian pacing sufficient? Heart Rhythm Society, open access article http://dx'doi.org/19.10.hrcr.2015.05.006
Addendum: 5/26/2017 Several papers presented at the May 2017 meeting of the Heart Rhythm Society indicated that His Bundle pacing is ready for prime time. See Dr. John Mandrola's article on Medscape entitled " His Bundle pacing hits the mainstream at HRS 2017".
9/6/2019 On a personal note-It is now almost four years since I was implanted with a Pacemaker with Bundle of His pacing before the practice became more mainstream. I had developed a left bundle branch block and an exercise induced second degree heart block. The LBBB had markedly decreased my exercise tolerance . My LBBB was "fixed" and after getting over a few complications of the procedure my exercise tolerance was back to my pre LBBB level with an EKG pattern that appears to be Parahisian.
Such responses have been reported with Biventricular pacing (Bi-V) and His Bundle Pacing ( HBP). There are two forms or types of HBP: 1) pure HBP also known as selective and 2) Para Hisian pacing also known as non selective HBP.
The QRS is normalized with selective HBP while in nonselective although the widened QRS duration is significant reduced it may not be restored to the pre bundle branch block configuration. There is both activation of the His Bundle fibers and adjacent ventricular septal muscle giving a fused or fusion ventricular activation pattern and an EKG with a delta wave resembling pre-excitation pattern.
According to Lida et al writing in the December 2016 Journal of Arrhythmia (1) "there seems to be no significant clinical difference between selective HBP and non selective HBP because both do not alter physiological impulse conduction and possibly maintain rapid and synchronous LV ( left ventricular) activation "
A similar case report was published by Ajijola et al from UCLA in 2015 (2)
His Bundle pacing seems to gaining momentum both as an alternative to right ventricular pacing and as a method of cardiac resynchronization.
1)Lida, Y et al Successful resynchronization by permanent His-bundle pacing in patient with pacing -induced cardiomyopathy' J Arrhythmia , 2016 Dec. 32(6), 499-501
2)Ajijola,O et al Hyper-response to cardiac resynchronization with permanent His bundle pacing:Is parahisian pacing sufficient? Heart Rhythm Society, open access article http://dx'doi.org/19.10.hrcr.2015.05.006
Addendum: 5/26/2017 Several papers presented at the May 2017 meeting of the Heart Rhythm Society indicated that His Bundle pacing is ready for prime time. See Dr. John Mandrola's article on Medscape entitled " His Bundle pacing hits the mainstream at HRS 2017".
9/6/2019 On a personal note-It is now almost four years since I was implanted with a Pacemaker with Bundle of His pacing before the practice became more mainstream. I had developed a left bundle branch block and an exercise induced second degree heart block. The LBBB had markedly decreased my exercise tolerance . My LBBB was "fixed" and after getting over a few complications of the procedure my exercise tolerance was back to my pre LBBB level with an EKG pattern that appears to be Parahisian.
2/3/21 The term "Parahisian" is no longer used to refer to non-select HBP.In the current terminology "parahisian" is taken to mean close to the His System but not capturing the His Bundle. His capture can either be elective on non selective.
Friday, April 14, 2017
If peak load is the determing parameter runners should have more osteoarthritis
Perhaps it seems counter intuitive that runners do not have a higher incidence of knee osteoarthritis or so the preponderance of epidemiologic data contents.After all the peak load of the articular cartilages in running is much higher than in walking or so the kinesiologists tell us and would not the cumulative higher peak load after many miles of running wear out and maybe chew up the articular cartilages.
Or maybe the explanation does not lie in the peak load.
Ross H Miller from the Department of Kinesiology at the University of Maryland offers an alternative view (1) and an alternative analysis of the relevant forces conspiring to "wear out" the knees.
He suggested that peak load is not the relevant variable but rather it is the "average load per distance traveled" which is said to be surprisingly low and purportedly similar to walking.
Ross also discussed the notion of cartilage conditioning .Knee cartilage glycosaminoglycan content( which affects lubrication and shock absorption ) has been shown in one study to be greater in recreational runners and even greater in high volume runners.
"... a man hears what he wants to hear and disregards the rest" Paul Simon.The Boxer
1) Miller, RH "Joint loading in runners does not initiate knee osteoarthritis" Exerc Sports Sci Rev 45(2), 87-95,4 2017
Or maybe the explanation does not lie in the peak load.
Ross H Miller from the Department of Kinesiology at the University of Maryland offers an alternative view (1) and an alternative analysis of the relevant forces conspiring to "wear out" the knees.
He suggested that peak load is not the relevant variable but rather it is the "average load per distance traveled" which is said to be surprisingly low and purportedly similar to walking.
Ross also discussed the notion of cartilage conditioning .Knee cartilage glycosaminoglycan content( which affects lubrication and shock absorption ) has been shown in one study to be greater in recreational runners and even greater in high volume runners.
"... a man hears what he wants to hear and disregards the rest" Paul Simon.The Boxer
1) Miller, RH "Joint loading in runners does not initiate knee osteoarthritis" Exerc Sports Sci Rev 45(2), 87-95,4 2017
Thursday, March 23, 2017
CRT-non-responders, responders and the rare super responder
About one third of patients with heart failure (HF) do not benefit appreciably or respond to cardiac resynchronization treatment (CRT). Some other have a clinical benefit with physiological confirmation in the form of echocardiographic demonstration of reduction in heart size and increase in the ejection fraction. A relatively small subset show a marked improvement both symptomatically and in terms of impressive improvement in terms of ejection fraction and reduction in left ventricular size.
Neither EKG nor echocardiographic patterns accurately predict who will respond and to what degree. However, patients with a LBBB EKG pattern -particularly using the new criteria suggested by Strauss (1 )- are much more likely to have a favorable response. In fact CRT basically "treats" the electric and associated mechanical dyssynchrony imposed by the left bundle branch block.Some of the variables influencing response include how much myocardial damage may have already occurred in the patient ( e.g. heart attacks) and the location of the left ventricular lead in relationship to left ventricular scar(s).
The most dramatic example of super responders was reported by Vaillent et al in 2013. (2). They described 6 patients with a diagnosis of LBBB without evidence of coronary or other heart disease and an EJ of greater than 50% at the time of diagnosis. Over a period of five to 21 years all developed heart failure severe enough to warrant referral for CRT. Following CRT, ejection fraction improved greatly , five of the six within 3 months .Mean EJ increased from 31 to 56.In one patient , from 26 to 60.Other cardiac functional indices improved as well
The authors suggest that these cases "strongly support the concept of LBBB-induced cardiomyopathy".This idea was apparently suggested earlier by Blanc et al in 2005 (4)
LBBB induced heart failure represents a vary small percentage of patient who are treated with CRT. Ghani et al (3) report on the predictors of long term outcome of "super-responders to CRT which they define as Left ventricular EF (LVEF) greater than 50% ( mean of 54.9%, +/-6) on follow-up echocardiogram.The group whose EF was between 30 and 50% were labelled as "responders"
They describe 56 patients from a group of 347 patients with primary CRT D indication. The predictors were female sex,nonischemic etiology,higher EF at baseline and wider QRS duration.
Vaillant's patients , when compared to Ghani's patient, perhaps could be considered "super super" responders.
1. Strauss DG et al, Defining Left Bundle Branch block in the Era of Cardiac Resynchronization Therapy. American J Cardiology 2011,Vol 107 pg 927-934
2. Vaillant C et al. Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J. Amer College of Cardiology 2013,vol 61, p 1089
3. Ghani, S et al Predictors and long term outcome of super-responders to cardiac resynchronization therapy. Clin Cardiology 2017
4.Blanc J et al. Evaluation of left bundle branch lock as a reversible cause of non-ischemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace 2005;7,604
Neither EKG nor echocardiographic patterns accurately predict who will respond and to what degree. However, patients with a LBBB EKG pattern -particularly using the new criteria suggested by Strauss (1 )- are much more likely to have a favorable response. In fact CRT basically "treats" the electric and associated mechanical dyssynchrony imposed by the left bundle branch block.Some of the variables influencing response include how much myocardial damage may have already occurred in the patient ( e.g. heart attacks) and the location of the left ventricular lead in relationship to left ventricular scar(s).
The most dramatic example of super responders was reported by Vaillent et al in 2013. (2). They described 6 patients with a diagnosis of LBBB without evidence of coronary or other heart disease and an EJ of greater than 50% at the time of diagnosis. Over a period of five to 21 years all developed heart failure severe enough to warrant referral for CRT. Following CRT, ejection fraction improved greatly , five of the six within 3 months .Mean EJ increased from 31 to 56.In one patient , from 26 to 60.Other cardiac functional indices improved as well
The authors suggest that these cases "strongly support the concept of LBBB-induced cardiomyopathy".This idea was apparently suggested earlier by Blanc et al in 2005 (4)
LBBB induced heart failure represents a vary small percentage of patient who are treated with CRT. Ghani et al (3) report on the predictors of long term outcome of "super-responders to CRT which they define as Left ventricular EF (LVEF) greater than 50% ( mean of 54.9%, +/-6) on follow-up echocardiogram.The group whose EF was between 30 and 50% were labelled as "responders"
They describe 56 patients from a group of 347 patients with primary CRT D indication. The predictors were female sex,nonischemic etiology,higher EF at baseline and wider QRS duration.
Vaillant's patients , when compared to Ghani's patient, perhaps could be considered "super super" responders.
1. Strauss DG et al, Defining Left Bundle Branch block in the Era of Cardiac Resynchronization Therapy. American J Cardiology 2011,Vol 107 pg 927-934
2. Vaillant C et al. Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J. Amer College of Cardiology 2013,vol 61, p 1089
3. Ghani, S et al Predictors and long term outcome of super-responders to cardiac resynchronization therapy. Clin Cardiology 2017
4.Blanc J et al. Evaluation of left bundle branch lock as a reversible cause of non-ischemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace 2005;7,604
Sunday, March 19, 2017
Do low levels of cardiovascular fitness predispose to cardiac hypertrophy?
There is evidence that suggests low levels of cardiac fitness predispose to maladaptive cardiac remodeling typically manifest as concentric remodeling and concentric hypertrophy and increased ventricular stiffness and diastolic dysfunction.
Lovic and Kokkinos and co workers correctly point out that the cardiac hypertrophy consequent to high blood pressure differs from the typical physiological cardiac hypertrophy of the endurance athlete realizing that extreme examples of the latter can be difficult to distinguish from the former.
Lovic et al makes the following argument in a 2016 issue of the Journal of Hypertension.
Low fitness level individuals will reach a systolic blood pressure of 150 at low levels of exercise, e.g. 4-5 METS , which are levels commonly encountered in some activities of everyday living.
150 systolic blood pressure is necessary to trigger cardiac remodeling. Individuals, who are more fit, are able to do that level of work without that degree of BP rise. So individuals with low fitness may spend considerable time each day with a BP of sufficient magnitude to trigger hypertrophic changes in the left ventricle, even though their BP as measured in their doctor's office may be normal.
Their data (1) found an inverse relationship between exercise capacity, blood pressure response to exercise and left ventricular mass.Further, they have published data that showed 16 weeks of aerobic training resulted in subjects having a significantly lower blood pressure level when they exercised at the every day activity level of 3-5 METS. A reduction in previously elevated left ventricular mass was also shown.
Other data consistent with this notion comes from a study by Brinker et al ( 2) from Southwestern Medical School in Dallas. They studied subjects aged 42 -67 years of age with stress testing and echocardiography. Those individuals in the lowest fitness category ( they divided the group into 3 fitness levels ) had 40 % concentric hypertrophy as well as a 9% prevalence of diastolic dysfunction ( as defined by the e/a ratio on mitral valve echo flow studies)
Data from the Dallas group and others have outlined the concept of there being two distinct cardiac phenotypes related to the development of both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).They are:
1)Subclinical systolic dysfunction (EF may be normal but abnormalities detectable by measurement of global strain with speckle echocardiography)),with eccentric cardiac hypertrophy with increased LV diameter)-the proposed precursor to HFrEF
2)Subclinical diastolic dysfunction with concentric LV hypertrophy; with increased relative wall thickness (RWT) -the proposed precursor to diastolic heart failure (HFpEF)
Increasing data strongly suggest that low fitness levels predispose to the precursors of HFpEF.
Lovic's work suggesting that exercise induced elevated blood pressure in the unfit during the usual daily activities may be one possible mechanism involved.
1)Lovic, D et al Left ventricular hypertrophy in athletes and hypertensive patients.J Clin Hypertension 2017,
2) Brinker SK et al. An association of Cardiorespiratory Fitness with left ventricular remodeling and diastolic dysfunction. JACC Heart Failure., Vol 2, no 3, 2014, p 238
5/1/17 An embarrassingly large number of typos and misspellings were corrected and again on 5/16/17.
Lovic and Kokkinos and co workers correctly point out that the cardiac hypertrophy consequent to high blood pressure differs from the typical physiological cardiac hypertrophy of the endurance athlete realizing that extreme examples of the latter can be difficult to distinguish from the former.
Lovic et al makes the following argument in a 2016 issue of the Journal of Hypertension.
Low fitness level individuals will reach a systolic blood pressure of 150 at low levels of exercise, e.g. 4-5 METS , which are levels commonly encountered in some activities of everyday living.
150 systolic blood pressure is necessary to trigger cardiac remodeling. Individuals, who are more fit, are able to do that level of work without that degree of BP rise. So individuals with low fitness may spend considerable time each day with a BP of sufficient magnitude to trigger hypertrophic changes in the left ventricle, even though their BP as measured in their doctor's office may be normal.
Their data (1) found an inverse relationship between exercise capacity, blood pressure response to exercise and left ventricular mass.Further, they have published data that showed 16 weeks of aerobic training resulted in subjects having a significantly lower blood pressure level when they exercised at the every day activity level of 3-5 METS. A reduction in previously elevated left ventricular mass was also shown.
Other data consistent with this notion comes from a study by Brinker et al ( 2) from Southwestern Medical School in Dallas. They studied subjects aged 42 -67 years of age with stress testing and echocardiography. Those individuals in the lowest fitness category ( they divided the group into 3 fitness levels ) had 40 % concentric hypertrophy as well as a 9% prevalence of diastolic dysfunction ( as defined by the e/a ratio on mitral valve echo flow studies)
Data from the Dallas group and others have outlined the concept of there being two distinct cardiac phenotypes related to the development of both heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).They are:
1)Subclinical systolic dysfunction (EF may be normal but abnormalities detectable by measurement of global strain with speckle echocardiography)),with eccentric cardiac hypertrophy with increased LV diameter)-the proposed precursor to HFrEF
2)Subclinical diastolic dysfunction with concentric LV hypertrophy; with increased relative wall thickness (RWT) -the proposed precursor to diastolic heart failure (HFpEF)
Increasing data strongly suggest that low fitness levels predispose to the precursors of HFpEF.
Lovic's work suggesting that exercise induced elevated blood pressure in the unfit during the usual daily activities may be one possible mechanism involved.
1)Lovic, D et al Left ventricular hypertrophy in athletes and hypertensive patients.J Clin Hypertension 2017,
2) Brinker SK et al. An association of Cardiorespiratory Fitness with left ventricular remodeling and diastolic dysfunction. JACC Heart Failure., Vol 2, no 3, 2014, p 238
5/1/17 An embarrassingly large number of typos and misspellings were corrected and again on 5/16/17.
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