This NYT article puts faces on those who bear the collateral damage. No satisfaction from "I told you so" here
Anyone remember "Cure sometimes,treat often,comfort always."
Tuesday, February 12, 2019
Sunday, February 10, 2019
All cases of LBBB do not have the same ventricular contraction pattern or same response to CRT
The block in left bundle branch block (LBBB)-and this can apply to right bundle as well-may not be actually in the left bundle branch, as least as it has been traditionally described.And the "block" may not mean complete disruption of the electrical cardiac system perhaps just a delay.Further amazingly, at least sometimes,electrical stimulation of the His Bundle can "fix" LBBB obtaining a normal QRS complex.
The traditional text book electrical anatomical pathway is from sa node to av node to His bundle and then a division into left and right bundle branches and then to branching purkinje fibers out to the myocardium.
Anatomical work at least as early as 1971 and physiological studies in 1977-1978 demonstrated in both the canine and human heart that the right and left bundles were actually anatomically distinct within the bundle of His.This was described as longitudinal dissociation.
It has been known at least as early as 1978 that stimulation of the his bundle can normalize the ekg pattern of LBBB and RBBB,Presumably-according to the longitudinal dissociation model - in these situations the lesion or block in the bundle branch was in the His bundle and that stimulation distal to the lesions resulted in a normal ekg.
In other words the left and right bundles are organized longitudinally and separate within the His Bundle.So a lesion in the His bundle could cause LBBB and could be corrected by stimulation distal to the block.
The work done in the 1970s did not really apply to clinical situations until cardiac resynchronization (CRT) was proven effective in the treatment of heart failure in the 1990s. About 30% of patients did not seem to respond to CRT and it was soon realized that the presence of LBBB was a favorable prognostic factor and that , in a sense it was the impaired electrical conduction system which was the culprit that caused mechanical dyssynchrony that could markedly impair cardiac function and in some after a variable lag period lead to disadvantageous cardiac hypertrophy, chamber enlargement and remodeling and heart failure
Further it has been suggested ( Strauss et al ) that the traditional ekg criteria for LBBB need to be replaced with critieria that make the diagnosis much more specific and therefore useful in predicting response from CRT.The QRS duration should be 0.14 seconds for men and 0.13 for women and there should be a double humped QRS either in lead i and AVL or V5 and V6 ( i.e. 2 contiguous leads) .Using the old criteria,according to Strauss, lead to overdiagnosis of true LBBB and included patients who actually had LVH ( left ventricular hypertrophy) and left anterior hemiblock). It was suggested that patients with "true "LBBB" by EKG are the ones who are likely to benefit from cardiac resynchronization therapy (CRT).
However, results from Denmark and Pittsburgh by Dr. Niels Risum (2) indicated that the sine qua non of "true" LBBB is not necessarily the EKG pattern but rather the mechanical activation pattern ( basically delayed left ventricular activation )which they described in terms of 2D strain echocardiography and that neither the supposedly specific Strauss criteria nor the traditional criteria always would indicate which patients would have that contraction pattern and would therefore be more likely respond to CRT.See end note # 1for Risum criteria:
Risum and colleagues content that all patients with LBBB diagnosed on EKG do not have delayed left ventricular activation which correspond to their criteria for "classic" LBBB activation pattern.
Risum's work offers an explanation for at least some of the widely quoted 30% CRT poor response rate .Interestingly, as early as 1979 several different patterns of septal movement were described on echocardiogram in LBBB.( Fujii et al )
Their data demonstrated that during a 4 year follow-up 40% of patients without the classic pattern had an adverse event (combined end point of death,need for LVAD,or heart transplant) versus 14 % in the group with the classic pattern.So since it is not 100% versus 0 % the presence or absence of Risum's classic pattern does not explain all cases of CRT failure.
It would not be expected, on mechanistic grounds, for Bi-Ventricular pacing to improve cardiac output in patients with right bundle branch block since in RBBB the electrical activation and the contraction pattern of the left ventricle would not be abnormal.There is considerable clinical data that CRT results in RBBB are definitely worse than in LBBB; However, there may be an exception.
Rosenbaum described an RBBB pattern in which there is left axis deviation and broad slurred r waves in I and Avl which was termed LBBB masquerading as RBBB in which an argument has been made that Bi-V pacing might be on benefit.(1)
1)Auriccho, A Does Cardiac Resynchronization therapy have a role in patients with right bundle branch block.irc. Arrhymia Electrophysiol 2014 pg 532
2)Risum,N et al, Identification of typical left bundle branch block contraction by strain echocardiography is additive to electrocardiography in prediction of long term outcomes after cardiac resynchronization therapy. Journal American College of Cardioogy 2015 vol 66 no 6 pg 632
3)Fujii, J K, et al mode and cross sectional echocardiographic study of left ventricular wall motions in complete left bundle branch block. Brit Heart Journal 1979 42 (3) 255
end note 1
Risum 2d strain echo criteria:
1)early shortening of at least one segment of the septal wall atnd early stretching of at least one segment of the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure
The traditional text book electrical anatomical pathway is from sa node to av node to His bundle and then a division into left and right bundle branches and then to branching purkinje fibers out to the myocardium.
Anatomical work at least as early as 1971 and physiological studies in 1977-1978 demonstrated in both the canine and human heart that the right and left bundles were actually anatomically distinct within the bundle of His.This was described as longitudinal dissociation.
It has been known at least as early as 1978 that stimulation of the his bundle can normalize the ekg pattern of LBBB and RBBB,Presumably-according to the longitudinal dissociation model - in these situations the lesion or block in the bundle branch was in the His bundle and that stimulation distal to the lesions resulted in a normal ekg.
In other words the left and right bundles are organized longitudinally and separate within the His Bundle.So a lesion in the His bundle could cause LBBB and could be corrected by stimulation distal to the block.
The work done in the 1970s did not really apply to clinical situations until cardiac resynchronization (CRT) was proven effective in the treatment of heart failure in the 1990s. About 30% of patients did not seem to respond to CRT and it was soon realized that the presence of LBBB was a favorable prognostic factor and that , in a sense it was the impaired electrical conduction system which was the culprit that caused mechanical dyssynchrony that could markedly impair cardiac function and in some after a variable lag period lead to disadvantageous cardiac hypertrophy, chamber enlargement and remodeling and heart failure
Further it has been suggested ( Strauss et al ) that the traditional ekg criteria for LBBB need to be replaced with critieria that make the diagnosis much more specific and therefore useful in predicting response from CRT.The QRS duration should be 0.14 seconds for men and 0.13 for women and there should be a double humped QRS either in lead i and AVL or V5 and V6 ( i.e. 2 contiguous leads) .Using the old criteria,according to Strauss, lead to overdiagnosis of true LBBB and included patients who actually had LVH ( left ventricular hypertrophy) and left anterior hemiblock). It was suggested that patients with "true "LBBB" by EKG are the ones who are likely to benefit from cardiac resynchronization therapy (CRT).
However, results from Denmark and Pittsburgh by Dr. Niels Risum (2) indicated that the sine qua non of "true" LBBB is not necessarily the EKG pattern but rather the mechanical activation pattern ( basically delayed left ventricular activation )which they described in terms of 2D strain echocardiography and that neither the supposedly specific Strauss criteria nor the traditional criteria always would indicate which patients would have that contraction pattern and would therefore be more likely respond to CRT.See end note # 1for Risum criteria:
Risum and colleagues content that all patients with LBBB diagnosed on EKG do not have delayed left ventricular activation which correspond to their criteria for "classic" LBBB activation pattern.
Risum's work offers an explanation for at least some of the widely quoted 30% CRT poor response rate .Interestingly, as early as 1979 several different patterns of septal movement were described on echocardiogram in LBBB.( Fujii et al )
Their data demonstrated that during a 4 year follow-up 40% of patients without the classic pattern had an adverse event (combined end point of death,need for LVAD,or heart transplant) versus 14 % in the group with the classic pattern.So since it is not 100% versus 0 % the presence or absence of Risum's classic pattern does not explain all cases of CRT failure.
It would not be expected, on mechanistic grounds, for Bi-Ventricular pacing to improve cardiac output in patients with right bundle branch block since in RBBB the electrical activation and the contraction pattern of the left ventricle would not be abnormal.There is considerable clinical data that CRT results in RBBB are definitely worse than in LBBB; However, there may be an exception.
Rosenbaum described an RBBB pattern in which there is left axis deviation and broad slurred r waves in I and Avl which was termed LBBB masquerading as RBBB in which an argument has been made that Bi-V pacing might be on benefit.(1)
1)Auriccho, A Does Cardiac Resynchronization therapy have a role in patients with right bundle branch block.irc. Arrhymia Electrophysiol 2014 pg 532
2)Risum,N et al, Identification of typical left bundle branch block contraction by strain echocardiography is additive to electrocardiography in prediction of long term outcomes after cardiac resynchronization therapy. Journal American College of Cardioogy 2015 vol 66 no 6 pg 632
3)Fujii, J K, et al mode and cross sectional echocardiographic study of left ventricular wall motions in complete left bundle branch block. Brit Heart Journal 1979 42 (3) 255
end note 1
Risum 2d strain echo criteria:
1)early shortening of at least one segment of the septal wall atnd early stretching of at least one segment of the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure
Thursday, February 07, 2019
Lone Left bundle branch block and increased afterload -bad combination
I have commented before on functional impairment associated with LBBB. See here.
J Aalen and colleagues (1) see here demonstrated that cardiac output in asymptomatic patients with isolated LBBB is very sensitive to afterload as in elevated arterial pressure as would also occur with strenuous exercise. (Full text is available on line,)
Dr Aalan studied the effect of increasing afterload on left ventricular ejection fraction (LVEF) in 11 asymptomatic patients with isolated ( or lone) LBBB. Afterload was increased not by exercise by increasing blood pressure (increase of 38 +/-12 mm Hg) by pneumatic extremity constrictors and handgrip exercise .
The controls subjects decreased their LVEF from 60 to 54 while the LBBB patients decreased their LVEF from 56 to 42. The increased heart rate and after load accentuated the effect of the left ventricular dyssynchronous contraction which consists of early septal contraction with bulging of the lateral left ventricular wall and delayed lateral wall contraction and bulging of the septum. In LBBB both the IVCT and the IVRT are increased, i.e slowed contraction and prolonged relaxation.
The severity of cardiac functional impairment is not reflected by the resting LVEF. Most studies have indicated at most a mild decrease. On a personal note, when I developed a LBBB my decrease in running speed was by about 20% -close to the 25% decrease in LVEF note in Aalan's paper. (decrease from a fairly comfortable 12 minute mile run to a difficult 15 minute mile with unusual calf discomfort)
I received 2 comments on the blog post mentioned in the first paragraph from readers indicating their exercise history after LBBB onset was similar to mine.
Lone LBBB is often considered asymptomatic and often is at rest. A person not doing strenuous exercise would likely not notice any problem and probably for that reason many texts describe LBBB as asymptomatic. For example, Mayo Clinic Patient website -" in most people BBB does not cause symptoms " and Up to Date "LBBB can also be seen in asymptomatic patients with structurally normal hearts."(Both accessed on 2/6/19) The key here is "with structurally normal hearts". Patients with already reduced EFs may experience significant worsening of exercise ability with onset of LBBB.
1) Aalen J et al Afterload hypersensitivity in patients with left bundle branch block . Jan, 2018 JACC Cardiovas imaging.
J Aalen and colleagues (1) see here demonstrated that cardiac output in asymptomatic patients with isolated LBBB is very sensitive to afterload as in elevated arterial pressure as would also occur with strenuous exercise. (Full text is available on line,)
Dr Aalan studied the effect of increasing afterload on left ventricular ejection fraction (LVEF) in 11 asymptomatic patients with isolated ( or lone) LBBB. Afterload was increased not by exercise by increasing blood pressure (increase of 38 +/-12 mm Hg) by pneumatic extremity constrictors and handgrip exercise .
The controls subjects decreased their LVEF from 60 to 54 while the LBBB patients decreased their LVEF from 56 to 42. The increased heart rate and after load accentuated the effect of the left ventricular dyssynchronous contraction which consists of early septal contraction with bulging of the lateral left ventricular wall and delayed lateral wall contraction and bulging of the septum. In LBBB both the IVCT and the IVRT are increased, i.e slowed contraction and prolonged relaxation.
The severity of cardiac functional impairment is not reflected by the resting LVEF. Most studies have indicated at most a mild decrease. On a personal note, when I developed a LBBB my decrease in running speed was by about 20% -close to the 25% decrease in LVEF note in Aalan's paper. (decrease from a fairly comfortable 12 minute mile run to a difficult 15 minute mile with unusual calf discomfort)
I received 2 comments on the blog post mentioned in the first paragraph from readers indicating their exercise history after LBBB onset was similar to mine.
Lone LBBB is often considered asymptomatic and often is at rest. A person not doing strenuous exercise would likely not notice any problem and probably for that reason many texts describe LBBB as asymptomatic. For example, Mayo Clinic Patient website -" in most people BBB does not cause symptoms " and Up to Date "LBBB can also be seen in asymptomatic patients with structurally normal hearts."(Both accessed on 2/6/19) The key here is "with structurally normal hearts". Patients with already reduced EFs may experience significant worsening of exercise ability with onset of LBBB.
1) Aalen J et al Afterload hypersensitivity in patients with left bundle branch block . Jan, 2018 JACC Cardiovas imaging.
Thursday, January 31, 2019
Is the link between atrial fibrillation and obesity epicardial fat?
The epicardial fat pad image on chest x-rays was long regarded as nothing more than a barely interesting incidental finding of no clinical importance. That no longer appears to be the case.
The epidemiologic data having established a sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes, and more recently detailed scrutiny of the role or roles of epicardial fat to which has been assigned the ironic designation, of EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.
At least as early as 2003 cardiac fat acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.
Now EAT is accused of playing a role in the genesis of AF.
Dr, Mahajan and co-workers from Australia studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left atrium adjacent to EAT.
Author quotes:
" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "
"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"
1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.
2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128
The epidemiologic data having established a sound correlation between obesity and risk of atrial fibrillation , the electrophysiologic (EP) cardiologists began to speculate on possible mechanistic explanations. These so far have included activation of pro-fibrotic pathways,atrial fibrosis, abnormal connexin, ( gap junction proteins necessary for heart cell action potential propagation) diastolic dysfunction , paracrine effect due to proximity of epicardial fat to myocytes, and more recently detailed scrutiny of the role or roles of epicardial fat to which has been assigned the ironic designation, of EAT (epicardial adipose tissue) in deleterious remodeling of the left atrium.
At least as early as 2003 cardiac fat acting like an endocrine organ was identified as a source of inflammatory cytokines ( Il-6,TNF-alpha, etc) that could possibly promote coronary artery disease. Mazurek et al (2) found higher levels of inflammatory cytokines in patients with significant CAD.
Now EAT is accused of playing a role in the genesis of AF.
Dr, Mahajan and co-workers from Australia studied 27 obese patients and 27 non obese patients who underwent AF ablation for AF. The obese groups demonstrated evidence of electroanatomical remodeling (global reduction in conduction velocity and increased electrogram fractionation) .The obese group had increased EAT and low atrial voltage in the posterior aspect of the left atrium adjacent to EAT.
Author quotes:
" obesity related conduction abnormalities were most prominent in the posterior left atrium which was in close contact with the epicardial fat. "
"Obesity results in expansion of EAT and marked electroanatomical remodeling of the left atrium,creating a substrate for AF"
1)Mahajan, R etl al Electroanatomical Remodeling of the atria in Obesity. Impact of adjacent epicardial Fat.JACC, clinical electrophysiology vol 4, no 12, 2018 ,p 1531.
2)Mazurk, T et al Human Epicardial adipose tissue is a source of inflammatory mediators.
Circulation 2003, 108 r122-128
Monday, January 28, 2019
Did a third randomized trial for PSA screening reconcile the conflict betwen the first two?
Did the third RCT settle the issue of the efficacy of PSA screening for prostate disease? The short answer is no - that settling purportedly was achieved by another statistical analysis. ( see reference # 2 for that) at least for a while .
There are now three large RCTs (1) that have addressed the subject.
1) the PLCO
2) The ERSPC
3) the Cluster Randomized Trial of PSA testing for Prostate Cancer.
Only the ERSPC demonstrated reduction in cancer in an "invitation to screening" with PSA setting.
So did the two out three being negative settle the issue? Not even close.
In 2012, faced with two conflicting RCTs the USPSTF decided to recommend against screening with PSA.Then a third RCT was completed showing no difference in mortality in the PSA screened group.
So if the score was 2 to 1 showing no benefit for PSA screening why did the USPSTF recant and return to their recommendation of "shared decision making" in 2018?
The answer seems to be that Tsodikov from the University of Michigan ( and 21 other authors from various institutions) did some adroit statistical footwork (2) in an effort to reconcile the disparate findings. Their work appears successful with the conclusion
being that when the proper type analysis is done (taking into account mean lead time) both the PLCO and the ERSPC both demonstrated approximately the same decrease in mortality with PSA screening.
Note the original analysis did not show a benefit to screening .
So now the score is two RCTs in favor of screening with one against and the current USPSTF recommendation is for shared decision making.
1)A blueprint for cancer screening and early detection :Advanced screening's contribution to cancer control. Wender RC et al . Ca,A Cancer Journal for Clinicians, Vol 49, no 1 Jan/Feb 2019 ( This is an excellent review of screening for cancer detection in average risk, asymptomatic adults including breast,cervix,colorectal,endometrial,lung and prostate.}
2)Tsodikov, A Reconciling the effects of screening on prostate cancer mortrality in the ERSPC and PLCO trials, An Intern Med. 2018, 168 608
"Life is short,art long,opportunity fleeting, experience treacherous,judgment difficult."Hippocrates.
There are now three large RCTs (1) that have addressed the subject.
1) the PLCO
2) The ERSPC
3) the Cluster Randomized Trial of PSA testing for Prostate Cancer.
Only the ERSPC demonstrated reduction in cancer in an "invitation to screening" with PSA setting.
So did the two out three being negative settle the issue? Not even close.
In 2012, faced with two conflicting RCTs the USPSTF decided to recommend against screening with PSA.Then a third RCT was completed showing no difference in mortality in the PSA screened group.
So if the score was 2 to 1 showing no benefit for PSA screening why did the USPSTF recant and return to their recommendation of "shared decision making" in 2018?
The answer seems to be that Tsodikov from the University of Michigan ( and 21 other authors from various institutions) did some adroit statistical footwork (2) in an effort to reconcile the disparate findings. Their work appears successful with the conclusion
being that when the proper type analysis is done (taking into account mean lead time) both the PLCO and the ERSPC both demonstrated approximately the same decrease in mortality with PSA screening.
Note the original analysis did not show a benefit to screening .
So now the score is two RCTs in favor of screening with one against and the current USPSTF recommendation is for shared decision making.
1)A blueprint for cancer screening and early detection :Advanced screening's contribution to cancer control. Wender RC et al . Ca,A Cancer Journal for Clinicians, Vol 49, no 1 Jan/Feb 2019 ( This is an excellent review of screening for cancer detection in average risk, asymptomatic adults including breast,cervix,colorectal,endometrial,lung and prostate.}
2)Tsodikov, A Reconciling the effects of screening on prostate cancer mortrality in the ERSPC and PLCO trials, An Intern Med. 2018, 168 608
"Life is short,art long,opportunity fleeting, experience treacherous,judgment difficult."Hippocrates.
Sunday, January 27, 2019
Left bundle branch block -a really big deal part 2
Left bundle branch block (LBBB) is associated with a contraction pattern(s), that are dyssynchronous in regard to the pattern of left venricular (LV) relaxation and contraction.
The first "big deal " I commented on was the observation that the ventricular dyssynchrony associated with LBBB per se can lead to heart failure. See here.
The next big deal is that the pattern of ventricular dyssynchrony typical of "true" LBBB is determinative of a favorable clinical response to CRT and the presence of a LBBB EKG pattern does not necessary indicate a underlying LBBB dyssynchronous pattern.
Risum et al (1) list 3 criteria for the typical contraction pattern of a "true"LBBB
(these apply to description of a longitudinal stain curve in a 4 chamber 2-D strain echocardiogram)
1)early shortening of one or more segment in the ventricular septal wall and early stretching in one or more segments in the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure
The early shortening of the septum is recognizable on standard echocardiography and referred to as "septal flash". "Apical rocking" is another echo finding in which there is a rocking motion of the LV apical myocardium perpendicular to the long axis. These two findings seem to be the findings on routine echo exams that correspond at least to some degree (possibly large degree) to the Risum's criteria from strain echocardiography and perhaps share to some degree the predictive power as regards outcomes of cardiac resynchronization therapy (CRT).
Those patients with a ekg pattern of LBBB and these findings on strain echo are much more likely to have a favorable clinical response to CRT.
Not all patients with a typical LBBB EkG pattern have what Risum refers to as the typical LBBB contraction pattern which is predictive of likelihood of favorable response. to CRT.This seems to hold true in regard to both the standard criteria for LBBB and the newer Strauss criteria .
Quoting Risum : "It seems reasonable to believe that the main mechanism underlying the differential effect from CRT according to QRS morphology is whether a significant activation delay is present in the LV". ( my underlining)
Question: Does the presence of septal flash and apical rocking predict likelihood of success with CRT as good or better than Risum's criteria? Have the two set of criteria been directly compared? While I could find no direct comparison ,Stankovic et al (2) published data that indicated apical rock and septal flash could predict reverse remodeling with a sensitivity of 84 % and 79% and the absence of both was associated with unfavorable long term survival.
Bottom line from Risum's work is that a patient may have EKG criteria for LBBB (either the standard criteria or the new criteria proposed by Strauss) and not have the mechanical dyssynchrony pattern described by Risum and not respond well to RCT.
So is the evidence strong enough to recommend pre-implantation 2d strain echo and not proceed with Bi-V pacing if the Risum criteria are not met? Is the absence of apical rock and septal flash reason to not proceed with Bi-v (or His Bundle) implantation?
1) Risum , N Identification of typical left bundle branch block contraction by strain echocardiography is additive electrocariography in prediction of long-term outcome after cardiac resynchronization
J Amer Coll of cardiology, 2015, vol 66, no. 631-641
2)Stankovic, I Relationship of visually assessed apical rocking and septal flah and long term survival following cardiac resynchronization therapy (PREDICT-CRT) Eur Heart J Cardiovasc Imaging. 2016,Mar 17 (3)262-9
addendum 1/30/19 reference to the Stankovic paper added
The first "big deal " I commented on was the observation that the ventricular dyssynchrony associated with LBBB per se can lead to heart failure. See here.
The next big deal is that the pattern of ventricular dyssynchrony typical of "true" LBBB is determinative of a favorable clinical response to CRT and the presence of a LBBB EKG pattern does not necessary indicate a underlying LBBB dyssynchronous pattern.
Risum et al (1) list 3 criteria for the typical contraction pattern of a "true"LBBB
(these apply to description of a longitudinal stain curve in a 4 chamber 2-D strain echocardiogram)
1)early shortening of one or more segment in the ventricular septal wall and early stretching in one or more segments in the lateral wall
2)early septal peak shortening
3)lateral wall peak shortening after aortic valve closure
The early shortening of the septum is recognizable on standard echocardiography and referred to as "septal flash". "Apical rocking" is another echo finding in which there is a rocking motion of the LV apical myocardium perpendicular to the long axis. These two findings seem to be the findings on routine echo exams that correspond at least to some degree (possibly large degree) to the Risum's criteria from strain echocardiography and perhaps share to some degree the predictive power as regards outcomes of cardiac resynchronization therapy (CRT).
Those patients with a ekg pattern of LBBB and these findings on strain echo are much more likely to have a favorable clinical response to CRT.
Not all patients with a typical LBBB EkG pattern have what Risum refers to as the typical LBBB contraction pattern which is predictive of likelihood of favorable response. to CRT.This seems to hold true in regard to both the standard criteria for LBBB and the newer Strauss criteria .
Quoting Risum : "It seems reasonable to believe that the main mechanism underlying the differential effect from CRT according to QRS morphology is whether a significant activation delay is present in the LV". ( my underlining)
Question: Does the presence of septal flash and apical rocking predict likelihood of success with CRT as good or better than Risum's criteria? Have the two set of criteria been directly compared? While I could find no direct comparison ,Stankovic et al (2) published data that indicated apical rock and septal flash could predict reverse remodeling with a sensitivity of 84 % and 79% and the absence of both was associated with unfavorable long term survival.
Bottom line from Risum's work is that a patient may have EKG criteria for LBBB (either the standard criteria or the new criteria proposed by Strauss) and not have the mechanical dyssynchrony pattern described by Risum and not respond well to RCT.
So is the evidence strong enough to recommend pre-implantation 2d strain echo and not proceed with Bi-V pacing if the Risum criteria are not met? Is the absence of apical rock and septal flash reason to not proceed with Bi-v (or His Bundle) implantation?
1) Risum , N Identification of typical left bundle branch block contraction by strain echocardiography is additive electrocariography in prediction of long-term outcome after cardiac resynchronization
J Amer Coll of cardiology, 2015, vol 66, no. 631-641
2)Stankovic, I Relationship of visually assessed apical rocking and septal flah and long term survival following cardiac resynchronization therapy (PREDICT-CRT) Eur Heart J Cardiovasc Imaging. 2016,Mar 17 (3)262-9
addendum 1/30/19 reference to the Stankovic paper added
Thursday, January 24, 2019
Once I thought I knew how to advise people how to eat to reduce heart disease risk , Now....
Read this recent brief overview of diet and fats and carbs and and cholesterol levels and heart disease risk and see if you would presume to advise patients on how to eat. I am glad that I am out of that business.
I have written several times on medical hubris . In light of what we think we "know" now and what I advised ten years ago,I think "who is without sin....." I believed I had the answer while having answers was little more than parroting the recommendations of boards and organizations.
You have to remember the lawyer's classic query "Doctor, where you wrong then or are you wrong now/"
Neither the pre-operative beta blocker debacle nor the post menopausal use of estrogen and progesterone missteps seem to be a teaching moment for the population medicine devotees. The pop med folks , as explicated here would presume to take funds away from the treatment of some to fund preventive program to others which would "after a few generations" bring about a utilitarian gain by some metric even as some might suffer now.
At the time of this writing serious doubt has been cast on the previously widely disseminated advice about how to eat to avoid heart disease and who should take aspirin for primary prevention of coronary artery disease and who , if anyone, shovel be screened to detect low vitamin D levels, just to name a few of the ever changing array of medical recommendation to prevent disease and death.
The internist who once upon a time was thought to be the physician trained to diagnose and treat complex complicated medical conditions has to extent that she is now a ambulist ( at least those who are not now hospitalists) sends her time in part giving advice about how to prevent disease. How to eat,how often to get a cervical cancer screening test or a colonoscopy , who should take statins of aspirin or vitamins and how much to exercise. For this you did not need to study four years in medical school and then three of more years of internal medicine training.You just need to subscribe to a service ( an app on your IPAD) to keep you up to date on the latest, and every changing, recommendation of various panels.
I have written several times on medical hubris . In light of what we think we "know" now and what I advised ten years ago,I think "who is without sin....." I believed I had the answer while having answers was little more than parroting the recommendations of boards and organizations.
You have to remember the lawyer's classic query "Doctor, where you wrong then or are you wrong now/"
Neither the pre-operative beta blocker debacle nor the post menopausal use of estrogen and progesterone missteps seem to be a teaching moment for the population medicine devotees. The pop med folks , as explicated here would presume to take funds away from the treatment of some to fund preventive program to others which would "after a few generations" bring about a utilitarian gain by some metric even as some might suffer now.
At the time of this writing serious doubt has been cast on the previously widely disseminated advice about how to eat to avoid heart disease and who should take aspirin for primary prevention of coronary artery disease and who , if anyone, shovel be screened to detect low vitamin D levels, just to name a few of the ever changing array of medical recommendation to prevent disease and death.
The internist who once upon a time was thought to be the physician trained to diagnose and treat complex complicated medical conditions has to extent that she is now a ambulist ( at least those who are not now hospitalists) sends her time in part giving advice about how to prevent disease. How to eat,how often to get a cervical cancer screening test or a colonoscopy , who should take statins of aspirin or vitamins and how much to exercise. For this you did not need to study four years in medical school and then three of more years of internal medicine training.You just need to subscribe to a service ( an app on your IPAD) to keep you up to date on the latest, and every changing, recommendation of various panels.
Friday, January 18, 2019
"Some people do not deserve health care reform?what would Maimonides have said?
The notion of someone "not deserving medical care reform" has appeared at least twice in writings by physicians. KevinMD taked about it here as he called attention to a commentary by Dr Edwin Leap. Dr.Leap is a long time medical blogger and ER physician and submitted this essay to an online version of a newspaper.
My first cursory reading of the essay and KevinMD's comments I erroneously read it to say " "Do some people not deserve medical care"
Sometime ago I wrote about a wonderful essay by Dr. Lawrence J. Hergoff published in JAMA which seems to address this line of thought.
Near the end of his current manuscript he quotes part of the Oath of Maimonides:
"May I never see in the patients anything but a fellow creature in pain."
I added:
Not as someone who deserves his dyspnea because of cigarette use defying years of advice to quit, not as someone whose ascites is his just due from profligate use of alcohol, not as someone who should not be in this country at all, not as someone who would not be having the myocardial infarction at all if he had done what his doctors told him to do and not as someone who is taking "scarce medical resources" from someone who deserves them more or for whom the treatment could be more cost effective but as a fellow human whose is in need of what physicians spent so many years of their lives preparing themselves to be able to offer.
The oath ( Maimonides) should remind us that being face to face with a fellow human in need
..makes judgment beyond the biomedical not only unnecessary but inappropriate.
My first cursory reading of the essay and KevinMD's comments I erroneously read it to say " "Do some people not deserve medical care"
Sometime ago I wrote about a wonderful essay by Dr. Lawrence J. Hergoff published in JAMA which seems to address this line of thought.
Near the end of his current manuscript he quotes part of the Oath of Maimonides:
"May I never see in the patients anything but a fellow creature in pain."
I added:
Not as someone who deserves his dyspnea because of cigarette use defying years of advice to quit, not as someone whose ascites is his just due from profligate use of alcohol, not as someone who should not be in this country at all, not as someone who would not be having the myocardial infarction at all if he had done what his doctors told him to do and not as someone who is taking "scarce medical resources" from someone who deserves them more or for whom the treatment could be more cost effective but as a fellow human whose is in need of what physicians spent so many years of their lives preparing themselves to be able to offer.
The oath ( Maimonides) should remind us that being face to face with a fellow human in need
..makes judgment beyond the biomedical not only unnecessary but inappropriate.
Tuesday, January 15, 2019
Comments on the "Extreme Exercise Hypothesis"
Dr. THM Eijsvogels from the Netherlands has written extensively about the relationship between endurance exercise levels and various cardiovascular outcomes and findings.
His recent (1) review with an annotated references list is available in full text on line.
Maybe the first question should be "what do you mean "extreme'?
U.S. National and WHO guidelines recommend 250 minutes of moderate exercise per week or 125 minutes of vigorous ( greater than 7 METS) per week based on in part a well established reduction in cardiovascular mortality and morbidity as well as numerous other health benefits. However ,US guidelines also state that exercise above that levels is associated with added benefits. But how far "above" should one go. Can you go too far?
Is there a U-shaped curve when you plot health risk of the Y axis and exercise training volume on the x axis? If so, can the inflection point be defined?
Arem (2015) combined data from six prospective population based cohorts ( 661,137 individuals).Maximal all-cause mortality risk reduction was noted at exercise level of 3-5 times current recommendations and even those exercising at 10 times current recommendation had a lower mortality risk ( HR 0.69, 95% CI 0.59-0.78). But at the highest level the degree of risk reduction was less than that achieved by lower exercise levels,
Ten times would be 25 hours ( one full day) of moderate exercise per week,I suggest very few exercise at that level while many preparing for a marathon would likely exercise as much as 7 or 8 hours a week (3-5 the recommend levels). Olympic rowers might exercise as much as 17-18 hours a week .The relatively few exercisers at the highest volume make the confidence intervals for HR estimation at that exercise level so large as to not be reliable or useful.
Eijsvogels summarizes the quest for "what do mean by extreme" with this understatement:
" Based on limited current evidence and numerous potential confounders, it is difficult to delineate an upper limit for the for the benefits of physical activity at this time."
So there is no epidemiologic support for a U shaped relationship between exercise volume and health risk at least as measuring all-cause mortality. But what about certain medical conditions that have been reported to be increased in long time endurance athletes at levels said to be higher than those who exercise less.
The usual suspects include 1) atrial fibrillation 2)cardiac fibrosis 3)coronary artery calcifications.
I have commented on atrial fibrillation before ( see here) and will likely have more to say later and have blogged about the coronary calcification paradox before( see here).
Cardiac or myocardial fibrosis (MF) is detected by cardiac MRI imaging with injection of gadolinium and is referred to as late gadolinium enhancement (LGE).There is a recognized pattern of LGE designating the localized fibrosis following a heart attack. The LGE pattern at issue in endurance athletes is something different-, i.e. a non-ischemic pattern. .
Van de Schoor et al did a systematic Pub Med search (2) and identified 65 athletes with MR imaging. A subgroup (30 subjects) were identified in an MRI study of 509 athletes.
The most frequent pattern was that located near the interventricular septum and right ventricular insertion points. The significance of this type of myocardial fibrosis is unclear.
Levine (3) et al have suggested that LGE in endurance athletes may not represent irreversible fibrosis and note that a similar pattern of LGE at the insertion points is seen in hypertrophic cardiomyopathy and also pulmonary hypertension.
Chan et al (4) described the histopathology in patients with hypertrophic cardiomyopathy (HCM). In a multi institutional study of 1293 HCM 10% demonstrated small areas of LGE in the area of ventricular insertion into the ventricular septum. Biopsies showed " greatly expanded extracellular space" with intestinal fibrosis and disorganized myocyte patterns." The authors emphasized the pattern was not that of myocyte death and replacement fibrosis.
Perhaps a similar histologic pattern would be found in the endurance athletes but to my knowledge that information is not available.
LGE has been reported in participants in various sports , the first case was a soccer player. Its significance and underlying mechanism ( repetitive microtrauma, transient pulmonary artery pressure over load ??) are not known.
I have to agree with Eijsvogels' summary statement : )"There is limited evidence that supports the "extreme exercise hypothesis",the most compelling relating to the increased risk of atrial fibrillation at high volume of exercise. 2) cardiac abnormalities may be present in a small proportion of the most active veteran athletes …"
1)Eijsvogels, TMH, er al The "Extreme Exercise Hypothesis:Recent findings and cardiovascular
health Implications. C"urr Teat Options Cardio Med 2018 20:84
2)Van de Schoor, F ,et all Myocardial Fibrosis in athletes . Mayo Clin Proc 2016,2016
3)Abdullah, Sm Lifelong Physical Activity regardless of does is not associated with myocardial
fibrosis. Circ Cardiovas Imaging. 2016 9,:e005511 (ful text)
4)Chan R, et al Significance of late gadolinium enhancement at right ventricular attachment to ventricular septum in patients with hypertrophic cardiomyopathy. Am J cardiol. 2015:116 436
His recent (1) review with an annotated references list is available in full text on line.
Maybe the first question should be "what do you mean "extreme'?
U.S. National and WHO guidelines recommend 250 minutes of moderate exercise per week or 125 minutes of vigorous ( greater than 7 METS) per week based on in part a well established reduction in cardiovascular mortality and morbidity as well as numerous other health benefits. However ,US guidelines also state that exercise above that levels is associated with added benefits. But how far "above" should one go. Can you go too far?
Is there a U-shaped curve when you plot health risk of the Y axis and exercise training volume on the x axis? If so, can the inflection point be defined?
Arem (2015) combined data from six prospective population based cohorts ( 661,137 individuals).Maximal all-cause mortality risk reduction was noted at exercise level of 3-5 times current recommendations and even those exercising at 10 times current recommendation had a lower mortality risk ( HR 0.69, 95% CI 0.59-0.78). But at the highest level the degree of risk reduction was less than that achieved by lower exercise levels,
Ten times would be 25 hours ( one full day) of moderate exercise per week,I suggest very few exercise at that level while many preparing for a marathon would likely exercise as much as 7 or 8 hours a week (3-5 the recommend levels). Olympic rowers might exercise as much as 17-18 hours a week .The relatively few exercisers at the highest volume make the confidence intervals for HR estimation at that exercise level so large as to not be reliable or useful.
Eijsvogels summarizes the quest for "what do mean by extreme" with this understatement:
" Based on limited current evidence and numerous potential confounders, it is difficult to delineate an upper limit for the for the benefits of physical activity at this time."
So there is no epidemiologic support for a U shaped relationship between exercise volume and health risk at least as measuring all-cause mortality. But what about certain medical conditions that have been reported to be increased in long time endurance athletes at levels said to be higher than those who exercise less.
The usual suspects include 1) atrial fibrillation 2)cardiac fibrosis 3)coronary artery calcifications.
I have commented on atrial fibrillation before ( see here) and will likely have more to say later and have blogged about the coronary calcification paradox before( see here).
Cardiac or myocardial fibrosis (MF) is detected by cardiac MRI imaging with injection of gadolinium and is referred to as late gadolinium enhancement (LGE).There is a recognized pattern of LGE designating the localized fibrosis following a heart attack. The LGE pattern at issue in endurance athletes is something different-, i.e. a non-ischemic pattern. .
Van de Schoor et al did a systematic Pub Med search (2) and identified 65 athletes with MR imaging. A subgroup (30 subjects) were identified in an MRI study of 509 athletes.
The most frequent pattern was that located near the interventricular septum and right ventricular insertion points. The significance of this type of myocardial fibrosis is unclear.
Levine (3) et al have suggested that LGE in endurance athletes may not represent irreversible fibrosis and note that a similar pattern of LGE at the insertion points is seen in hypertrophic cardiomyopathy and also pulmonary hypertension.
Chan et al (4) described the histopathology in patients with hypertrophic cardiomyopathy (HCM). In a multi institutional study of 1293 HCM 10% demonstrated small areas of LGE in the area of ventricular insertion into the ventricular septum. Biopsies showed " greatly expanded extracellular space" with intestinal fibrosis and disorganized myocyte patterns." The authors emphasized the pattern was not that of myocyte death and replacement fibrosis.
Perhaps a similar histologic pattern would be found in the endurance athletes but to my knowledge that information is not available.
LGE has been reported in participants in various sports , the first case was a soccer player. Its significance and underlying mechanism ( repetitive microtrauma, transient pulmonary artery pressure over load ??) are not known.
I have to agree with Eijsvogels' summary statement : )"There is limited evidence that supports the "extreme exercise hypothesis",the most compelling relating to the increased risk of atrial fibrillation at high volume of exercise. 2) cardiac abnormalities may be present in a small proportion of the most active veteran athletes …"
1)Eijsvogels, TMH, er al The "Extreme Exercise Hypothesis:Recent findings and cardiovascular
health Implications. C"urr Teat Options Cardio Med 2018 20:84
2)Van de Schoor, F ,et all Myocardial Fibrosis in athletes . Mayo Clin Proc 2016,2016
3)Abdullah, Sm Lifelong Physical Activity regardless of does is not associated with myocardial
fibrosis. Circ Cardiovas Imaging. 2016 9,:e005511 (ful text)
4)Chan R, et al Significance of late gadolinium enhancement at right ventricular attachment to ventricular septum in patients with hypertrophic cardiomyopathy. Am J cardiol. 2015:116 436
Monday, January 07, 2019
The concept of medical commons is a bogus and dangerous concept
A fundamental concept of the various types of egalitarianism is. neither coherent,correct and operationally meaningful. .. That concept is : Individually possessed resources or assets should be considered as part of a collective pool owned by everyone and that all have an equal right to some share of the pool.
In regard to a private property system the rights of the owner in general terms are clear. The owner has the right to use his property,exclude others from us of the property and dispose of the property through sale,gift or inheritance.
In contrast , the rights are in a common ownership system are vague and indeterminate. Feser said it is not clear how one can be said to "own" something if no one in principle is excluded from making a claim on that something.
Even a cursory survey of the twentieth century reveals how tragic and unsuccessful were attempts to build a society based on the notion of common ownership and the abolition of private property. The Bolshevik revolution promised peace,freedom ,equality and prosperity and delivered mass murder and starvation.Communist China's attempt in that regard were no better .The dramatic nighttime photograph of the Korean peninsula showing darkness in the north and countless points of light in the south tells the story of the difference between the two systems of ownership..
Yet the movement to consider medical or health care resources as a central pool or a medical commons has had surprisingly wide acceptance in certain medical organizations and medical academia and among health care planners and policy wonks.
Even though the concept of a collective pool of individually possessed resources is basically void of meaningful operational content a derivative metaphor-that of the physician as a steward of the mythical medical resources-has been promulgated and to some a surprising degree accepted and has become part of a major and growing effort to control medical care and has become part of the discourse about health care policy.
The rules by which a collective of healthcare resources would be allocated are not defined, but those who advocate the physician as steward of these resources have several things in mind to make the metaphor operationally meaningful, the most important of which is the purported ethical requirement of physicians to adhere to guidelines which in their most at least superficially justifiable analytical form are based on a cost benefit analysis and in their least evidence based form , expert opinion.
Cost effective analysis has been smuggled into the professionalism package in the trojan horse of social justice. This is bogus as well. The utilitarian mantra of the greatest good for the greatest number is not necessarily a part of the concept of social justice.The basis of social justice is equal respect for all humans while utilitarians would favor policies that benefit the aggregate though some individual may loose. The prominent egalitarian John Rawls rejected utilitarian allocations because they ignored the separateness of individuals and in his mythical behind- the- veil contract he believed that individuals would not sign up for a society that would sacrifice them for some aggregate benefit.
In regard to a private property system the rights of the owner in general terms are clear. The owner has the right to use his property,exclude others from us of the property and dispose of the property through sale,gift or inheritance.
In contrast , the rights are in a common ownership system are vague and indeterminate. Feser said it is not clear how one can be said to "own" something if no one in principle is excluded from making a claim on that something.
Even a cursory survey of the twentieth century reveals how tragic and unsuccessful were attempts to build a society based on the notion of common ownership and the abolition of private property. The Bolshevik revolution promised peace,freedom ,equality and prosperity and delivered mass murder and starvation.Communist China's attempt in that regard were no better .The dramatic nighttime photograph of the Korean peninsula showing darkness in the north and countless points of light in the south tells the story of the difference between the two systems of ownership..
Yet the movement to consider medical or health care resources as a central pool or a medical commons has had surprisingly wide acceptance in certain medical organizations and medical academia and among health care planners and policy wonks.
Even though the concept of a collective pool of individually possessed resources is basically void of meaningful operational content a derivative metaphor-that of the physician as a steward of the mythical medical resources-has been promulgated and to some a surprising degree accepted and has become part of a major and growing effort to control medical care and has become part of the discourse about health care policy.
The rules by which a collective of healthcare resources would be allocated are not defined, but those who advocate the physician as steward of these resources have several things in mind to make the metaphor operationally meaningful, the most important of which is the purported ethical requirement of physicians to adhere to guidelines which in their most at least superficially justifiable analytical form are based on a cost benefit analysis and in their least evidence based form , expert opinion.
Cost effective analysis has been smuggled into the professionalism package in the trojan horse of social justice. This is bogus as well. The utilitarian mantra of the greatest good for the greatest number is not necessarily a part of the concept of social justice.The basis of social justice is equal respect for all humans while utilitarians would favor policies that benefit the aggregate though some individual may loose. The prominent egalitarian John Rawls rejected utilitarian allocations because they ignored the separateness of individuals and in his mythical behind- the- veil contract he believed that individuals would not sign up for a society that would sacrifice them for some aggregate benefit.
High value? Fuzzy concept? who gets to decide?
"Some measures are golden, but mostly those that we have tested. We have
a responsibility as a profession to challenge this concept without
seeing clear evidence that patients benefit from labeling some measures
as value. Value and quality are fuzzy concepts. How can one oppose
using value and quality? No one opposes the concept, but we all should
demand that the implementation of measures does improve patient
outcomes. We should all worry." From a blog commentary by Dr. Robert Centor. Yes, we should all worry.
Value and quality have be become buzz words- to be blended into "value statements" and purported goals .
Classical economists ' notion of value as something imparted into a good by the labor expended in its production was overturned by economists in the late 1800s when Menger and others introduced the idea of marginal subjective value. The value of a good or service was subjective,that is in the eye of the beholder, and was made "at the margin".The value of the tenth piece of apple pie is less to a person than is the value of the first piece. Great effort and artistic skill might be expended in the production of an artistically beautiful pogo stick but labeling it a high value product would not bring about large sales of such a product. Few potential consumers would value such a product.
Marx 's labor theory of value is resurrected in the payment system for medicare "The doc fix" carried that archaic misconception further. The Medicare payment scheme contains elements likely to be admired by the old time Soviet Union central planners.
Third party payers embrace the notion of high value medical care . The words quality and high value are loose, vague and indeterminate but seem to have considerable rhetorical value . They are found to a degree making them worthless in myriads of value and missions statements of various organizations whose actual activities and goals have nothing to do with those statements.
Value and quality have be become buzz words- to be blended into "value statements" and purported goals .
Classical economists ' notion of value as something imparted into a good by the labor expended in its production was overturned by economists in the late 1800s when Menger and others introduced the idea of marginal subjective value. The value of a good or service was subjective,that is in the eye of the beholder, and was made "at the margin".The value of the tenth piece of apple pie is less to a person than is the value of the first piece. Great effort and artistic skill might be expended in the production of an artistically beautiful pogo stick but labeling it a high value product would not bring about large sales of such a product. Few potential consumers would value such a product.
Marx 's labor theory of value is resurrected in the payment system for medicare "The doc fix" carried that archaic misconception further. The Medicare payment scheme contains elements likely to be admired by the old time Soviet Union central planners.
Third party payers embrace the notion of high value medical care . The words quality and high value are loose, vague and indeterminate but seem to have considerable rhetorical value . They are found to a degree making them worthless in myriads of value and missions statements of various organizations whose actual activities and goals have nothing to do with those statements.
Some
measures are golden, but mostly those that we have tested. We have a
responsibility as a profession to challenge this concept without seeing
clear evidence that patients benefit from labeling some measures as
value. Value and quality are fuzzy concepts. How can one oppose using
value and quality? No one opposes the concept, but we all should demand
that the implementation of measures does improve patient outcomes. We
should all worry.
- See more at: http://www.medrants.com/archives/8118#comments
- See more at: http://www.medrants.com/archives/8118#comments
Some
measures are golden, but mostly those that we have tested. We have a
responsibility as a profession to challenge this concept without seeing
clear evidence that patients benefit from labeling some measures as
value. Value and quality are fuzzy concepts. How can one oppose using
value and quality? No one opposes the concept, but we all should demand
that the implementation of measures does improve patient outcomes. We
should all worry.
- See more at: http://www.medrants.com/archives/8118#comments
- See more at: http://www.medrants.com/archives/8118#comments
Some
measures are golden, but mostly those that we have tested. We have a
responsibility as a profession to challenge this concept without seeing
clear evidence that patients benefit from labeling some measures as
value. Value and quality are fuzzy concepts. How can one oppose using
value and quality? No one opposes the concept, but we all should demand
that the implementation of measures does improve patient outcomes. We
should all worry.
- See more at: http://www.medrants.com/archives/8118#comments
- See more at: http://www.medrants.com/archives/8118#comments
Thursday, January 03, 2019
What happens to your heart in you train really hard for a year or two may depend on your age
First -what happened to the hearts of young men and women who trained intensively for one year in preparation for a marathon.See below for changes noted in older subjects.
Dr.Benjamin Levine (1) and colleagues at the Institute for Exercise and the Environment performed extensive physiologic studies on 12 subjects ( aged 29 +/- 6 years) and provided valuable insight into the functional and structural change in their hearts over one year.
The training program was intensive and progressive and was divided into four 3 months periods or segments. The third quarter included 2 hour long runs and 4 th quarter involved 7 -9 hours per week with 3 hour long runs and interval training.
What distinguishes the elite endurance athlete's heart from other equally well trained athletes is the very large stroke volume which in turn depend on a very large end diastolic left ventricular volume (LVEDV). A very compliant left ventricle is the key (.It may be more accurate to state "compliant heart" as that would include a more easily stretched pericardium facilitating diastolic filling.)
The maximal 0xygen uptake increased from 40.3 =/-1.6 to 48.7 =/-2.5. (The 02 max for elite marathoners is typically 70 to 80 plus). Maximal stroke volume increased from 98 to 113 ml.
A key finding was that both right and left ventricular mass increased to levels similar to those seen in elite athletes but the LV volume did not change until six months of training. In the first 6 months of training when training did not include significant high intensity training the left ventricle remodeling was concentric and eccentric remodeling ( i.e. increased LV volume) did not occur more intense exercise was part of the regimen.The right ventricle began "eccentric" hypertrophy early on. Question -is the eccentric pattern dependent on the addition of some HIT or interval training in addition to the moderate intensity exercise.
Cardiac catherization data derived measures of LV compliance improved but did not approach those typically observed in elite athletes. The "Starling Curves" which plot pulmonary capillary wedge pressure (PCWP) which is an index of left ventricular filling pressure on the x axis versus stroke volume on the y axis shifted up and to the left suggesting an improvement in left ventricular compliance, i.e a ventricle more easily filled.
Their morphology measurements which were done by cardiac MR ( generally thought to be more accurate than echocardiographic measurements) did not conform with the Morganroth hypothesis (1975) which stated that endurance exercise lead to eccentric hypertrophy which is a balanced increase in wall thickenss and ventricular volume while strength training leads to concentric hypertrophy with an increase in wall thickness with no significant change in cavity size.
Levine's subjects first had a LV concentric pattern and only after more intense ( volume and intensity) exercise was part of the program did the classic endurance athletes eccentric pattern become evident. A certain level of intensity of exercise seemed to be necessary for aerobic exercise to cause eccentric hypertrophy. This seems to run contrary to the notion that endurance exercise is simply a "volume overload event".
Levine's group has also reported on a similar project (2) involving older ( age 68-74) subjects and although their training program was vigorous it was less intense than the young subjects.The 02 max increased on average by 19%,arterial elastance decreased, LV mass increased with no change in the mass volume ratio ( i.e physiologic remodeling) but the Staring curves did not indicate a more compliant left ventricle.So good things happened but improved LV compliance was not one of them.
The third publication (3) in Levine's hat trick involves similar measurements of heart function and structure in middle age subjects over a two year period.The details are complex and interested readers can find details in ref 3 which has entire text without firewall.
The two year training program involved at least 30 minute session of moderate exercise 4-5 times per week with at least one high intensity exercise session ( the Norwegian 4x4).
The authors were able to show an improvement in compliance using the techniques ( The Starling curves) mentioned above .The data offer the hope that "middle age" is not too late to start .
Levine suggests that sedentary aging effect of the heart has 3 stages; 1) loss of relaxation 2)loss of compliance or stiffening of the myocardium and 3) remodeling.This sedentary aging may predispose to heart failure with preserved ejection fraction (HFpEF) perhaps when confronted by another "hit" such as hypertension,obesity,and diabetes. Levine's data suggests that some doable amount of endurance exercise might retard or mitigate the process . (Whether high intensity exercise is a necessary component is still an open question)
t
1) Arbab-Zadeh, A "cardiac remodeling in response to 1 year of intensive endurance training.
Circulation 2014, 130 (24) 2152
2)Fujimoto,N Cardiovascular effects of 1 year of progressive and vigorous exercise training in previously sedentary individuals older than 65 years of age. Circ. 2010, 122 (18), 1797
3) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized
trial.Circulation,2018 137; (full text available on line without firewall)
addendum 2/17/19 Comment about pericardium added.
Dr.Benjamin Levine (1) and colleagues at the Institute for Exercise and the Environment performed extensive physiologic studies on 12 subjects ( aged 29 +/- 6 years) and provided valuable insight into the functional and structural change in their hearts over one year.
The training program was intensive and progressive and was divided into four 3 months periods or segments. The third quarter included 2 hour long runs and 4 th quarter involved 7 -9 hours per week with 3 hour long runs and interval training.
The cardiovascular system of the trained endurance athlete differs in a number of ways from the untrained person.These include:
1.increased red blood cell mass and blood volume
2.increased numbers of mitochondria and capillaries in leg muscles.
3.lower peripheral arterial resistance
4.lower systolic and diastolic blood pressure during exercise.
What distinguishes the elite endurance athlete's heart from other equally well trained athletes is the very large stroke volume which in turn depend on a very large end diastolic left ventricular volume (LVEDV). A very compliant left ventricle is the key (.It may be more accurate to state "compliant heart" as that would include a more easily stretched pericardium facilitating diastolic filling.)
The maximal 0xygen uptake increased from 40.3 =/-1.6 to 48.7 =/-2.5. (The 02 max for elite marathoners is typically 70 to 80 plus). Maximal stroke volume increased from 98 to 113 ml.
A key finding was that both right and left ventricular mass increased to levels similar to those seen in elite athletes but the LV volume did not change until six months of training. In the first 6 months of training when training did not include significant high intensity training the left ventricle remodeling was concentric and eccentric remodeling ( i.e. increased LV volume) did not occur more intense exercise was part of the regimen.The right ventricle began "eccentric" hypertrophy early on. Question -is the eccentric pattern dependent on the addition of some HIT or interval training in addition to the moderate intensity exercise.
Cardiac catherization data derived measures of LV compliance improved but did not approach those typically observed in elite athletes. The "Starling Curves" which plot pulmonary capillary wedge pressure (PCWP) which is an index of left ventricular filling pressure on the x axis versus stroke volume on the y axis shifted up and to the left suggesting an improvement in left ventricular compliance, i.e a ventricle more easily filled.
Their morphology measurements which were done by cardiac MR ( generally thought to be more accurate than echocardiographic measurements) did not conform with the Morganroth hypothesis (1975) which stated that endurance exercise lead to eccentric hypertrophy which is a balanced increase in wall thickenss and ventricular volume while strength training leads to concentric hypertrophy with an increase in wall thickness with no significant change in cavity size.
Levine's subjects first had a LV concentric pattern and only after more intense ( volume and intensity) exercise was part of the program did the classic endurance athletes eccentric pattern become evident. A certain level of intensity of exercise seemed to be necessary for aerobic exercise to cause eccentric hypertrophy. This seems to run contrary to the notion that endurance exercise is simply a "volume overload event".
Levine's group has also reported on a similar project (2) involving older ( age 68-74) subjects and although their training program was vigorous it was less intense than the young subjects.The 02 max increased on average by 19%,arterial elastance decreased, LV mass increased with no change in the mass volume ratio ( i.e physiologic remodeling) but the Staring curves did not indicate a more compliant left ventricle.So good things happened but improved LV compliance was not one of them.
The third publication (3) in Levine's hat trick involves similar measurements of heart function and structure in middle age subjects over a two year period.The details are complex and interested readers can find details in ref 3 which has entire text without firewall.
The two year training program involved at least 30 minute session of moderate exercise 4-5 times per week with at least one high intensity exercise session ( the Norwegian 4x4).
The authors were able to show an improvement in compliance using the techniques ( The Starling curves) mentioned above .The data offer the hope that "middle age" is not too late to start .
Levine suggests that sedentary aging effect of the heart has 3 stages; 1) loss of relaxation 2)loss of compliance or stiffening of the myocardium and 3) remodeling.This sedentary aging may predispose to heart failure with preserved ejection fraction (HFpEF) perhaps when confronted by another "hit" such as hypertension,obesity,and diabetes. Levine's data suggests that some doable amount of endurance exercise might retard or mitigate the process . (Whether high intensity exercise is a necessary component is still an open question)
t
1) Arbab-Zadeh, A "cardiac remodeling in response to 1 year of intensive endurance training.
Circulation 2014, 130 (24) 2152
2)Fujimoto,N Cardiovascular effects of 1 year of progressive and vigorous exercise training in previously sedentary individuals older than 65 years of age. Circ. 2010, 122 (18), 1797
3) Howden EJ et al Reversing the cardiac effects of sedentary aging.A randomized
trial.Circulation,2018 137; (full text available on line without firewall)
addendum 2/17/19 Comment about pericardium added.
Monday, December 31, 2018
Left Bundle Branch block cardiomyopathy-incidence
Altered cardiac function has been recognized in Left Bundle Branch Block (LBBB) as early as 1989 (1).
In 2005,Blanc et al (2)described five patients with dilated cardiomyopathy whose cardiac function was "normalized" by cardiac resynchronization therapy (CRT) suggesting that longstanding LBBB could cause a cardiomyopathy that was potentially reversible by CRT.Prior to Blanc's paper, animal studies had demonstrated that LBBB could cause progressive cardiac structural and functional loss that could be to some degree reversible with CRT.Blanc suggested that his paper introduced "a new concept of left ventricular dyssynchrony-induced cardiomyopathy"
In 2013 Vaillant (4) et al published data with similar cases that tended to support Blanc's thesis.
.
The topic of concern here is so called isolated LBBB as a cause of cardiomyopathy. i.e LBBB not associated with ischemic heart disease or other recognized causes of a cardiomyopathy , LBBB as a cause of a dyssynchronopathy.
HV Barot et al (3) from Lahey clinic identified patients with LBBB ,without evidence of coronary artery disease or other recognized cause of cardiomyopathy and an LVEF greater than 45% and followed them for 40 +/- 24 months. Of a total of 94 patients meeting the entry criteria, 13 developed a significant decrease in EF to 31+/-7 % .
All lone LBBB instances are not created equal.The degree of dyssynchrony and the patterns of altered depolarizations vary as does the resultant degree of loss of LV function and the likelihood and rate of progression of a cardiomyopathy.
From a clinical point of view several questions are important. What factors indicate that a asymptomatic patient with LBBB will develop heart failure? What should the clinical management be when a patient with LBBB develops a significant decrease in ejection fraction?
The experience reported by Wang et al (5) strongly suggests that the usual heart failure package of medications is not very effective in LBBB induced heart failure.At what point should CRT ( either BI-V or His Bundle pacing) be considered ?
1) Grines,CL et al Functional abnormalities in isolated left bundle branch block.The effect of interventricular asynchrony.Circulation 1989:79, 845
2) Blanc,JJ et al Evaluation of left bundle branch block as a reversible cause of non-ischemic dilated cardiomyopathy with serve heart failure. A new concept of left ventricular dyssynchroncy-induced cardiomyopathy. Europace. 2005,7 604-610
3)Barot, HV Incidence of Left bundle branch block-associated cardiomyopathy. Journal of Cardiac Failure August 2017, vol 23, issue 8, supplement, p S55
4) Vaillant, C. et al Resolution of left bndle branch block-induced cardiomyopathy by cardiac resynchronization therapy. J Am Coll. Cardiol. 2013:61, 1089
In 2005,Blanc et al (2)described five patients with dilated cardiomyopathy whose cardiac function was "normalized" by cardiac resynchronization therapy (CRT) suggesting that longstanding LBBB could cause a cardiomyopathy that was potentially reversible by CRT.Prior to Blanc's paper, animal studies had demonstrated that LBBB could cause progressive cardiac structural and functional loss that could be to some degree reversible with CRT.Blanc suggested that his paper introduced "a new concept of left ventricular dyssynchrony-induced cardiomyopathy"
In 2013 Vaillant (4) et al published data with similar cases that tended to support Blanc's thesis.
.
The topic of concern here is so called isolated LBBB as a cause of cardiomyopathy. i.e LBBB not associated with ischemic heart disease or other recognized causes of a cardiomyopathy , LBBB as a cause of a dyssynchronopathy.
HV Barot et al (3) from Lahey clinic identified patients with LBBB ,without evidence of coronary artery disease or other recognized cause of cardiomyopathy and an LVEF greater than 45% and followed them for 40 +/- 24 months. Of a total of 94 patients meeting the entry criteria, 13 developed a significant decrease in EF to 31+/-7 % .
All lone LBBB instances are not created equal.The degree of dyssynchrony and the patterns of altered depolarizations vary as does the resultant degree of loss of LV function and the likelihood and rate of progression of a cardiomyopathy.
From a clinical point of view several questions are important. What factors indicate that a asymptomatic patient with LBBB will develop heart failure? What should the clinical management be when a patient with LBBB develops a significant decrease in ejection fraction?
The experience reported by Wang et al (5) strongly suggests that the usual heart failure package of medications is not very effective in LBBB induced heart failure.At what point should CRT ( either BI-V or His Bundle pacing) be considered ?
1) Grines,CL et al Functional abnormalities in isolated left bundle branch block.The effect of interventricular asynchrony.Circulation 1989:79, 845
2) Blanc,JJ et al Evaluation of left bundle branch block as a reversible cause of non-ischemic dilated cardiomyopathy with serve heart failure. A new concept of left ventricular dyssynchroncy-induced cardiomyopathy. Europace. 2005,7 604-610
3)Barot, HV Incidence of Left bundle branch block-associated cardiomyopathy. Journal of Cardiac Failure August 2017, vol 23, issue 8, supplement, p S55
4) Vaillant, C. et al Resolution of left bndle branch block-induced cardiomyopathy by cardiac resynchronization therapy. J Am Coll. Cardiol. 2013:61, 1089
5)Wang,NC et al New onset left bundle branch block-associated idiopathic nonischemic cardiomyopathy and time from diagnosis to cardiac resynchronization therapy. The NEOLITH II study PACE 2018 Jan 4
Friday, December 21, 2018
Variably unreliable information form Pacemaker technicians
In the first three years of of having a pacemaker (PM) implanted, the following instances of misinformation,lack of proper oversight or misdiagnosis occurred.I did not need that having a titanium foreign body crammed under my left chest wall muscle attached to wires coursing to various parts of my heart was quite enough to ramp up my anxiety level to at least sub-panic attack levels.
1)In October 2015 I had a pacemaker implanted- one which is designed for bi-ventricular pacing the most common form of CRT (cardiac resynchronization therapy).
2)The technician who assisted and provided technical advice to the EP cardiologist at the time of the implantation told me on the following day that my home -bedside PM communication device would send a recording every night to the manufacturer's web site and then to the hospital PM center.
Only 6 months later was I informed by him , in reply to a question from me, that no -that was not true and that arrangement was only for devices with a defibrillator which I did not have. So for six months I made a effort to be near near by communication device device each night.
2.In October of 2016 my device recorded several episodes designed as AF/AT (atrial fibrillation/atrial tachycardia) Episodes of AF are thought to be common ( at least 30% by three years in patients with a PM- according to one data base).This lead to to my fairly extensive literature review of the issue of AHRE ( atria high rate episode). I learned that the topic is controversial and opinion varies as to what if any threshold there is for "signficiant volume of AF" to justify anticoagulation. (There are 2 randomized clinical trials underway that are designed to try and answer that question)
Also, All AHREs so designated by the PM's algorithms are not in fact AF. The phenomenon of far field r wave sensing and and a less common and more obscure PM rhythm disturbance known as recurrent, non reentrant ventricular atrial synchrony (RNRVAS) are capable of mimicking AF.The technician at the hospital PM center who is tasked with screening the remote interrogation report had not recognized that the rhythm was FFA and apparently did not feel that the issue required calling the matter to the attention of the EP cardiologist.
I send an email to my EP cardiologist and I was told the issue of short episodes of possible AF are very controversial and I did not need to come any sooner or consider taking anticoagulants. He apparently did not address the possible issue of FFS or RNRVAS) or actually review my interrogation report until months later even though I has asked in my email if the data really indicated AF.
However three months later, at routine office followup a Medtronic technician said that the earlier interrogation did not actually show AF but rather FFS the reoccurrence of which he intended to prevent by increasing the sensitivity threshold(i.e making detection less sensitive) on the atrial lead. The EP cardiologist agreed, and I later leaned that FFS is not an uncommon cause of AHREs particularly so in the type of lead placement that I have. (Placement in the Bundle of His which in my case is higher up in the ventricle than the standard apical placement of the RV lead-sometimes the His Bundle Lead is in the atrium)
3)At an August 2018 in office PM interrogation, the technician and I entered into a conversation about battery life estimation and she
In talking to her I quoted the section of the device manual in regard to the device powering down a bit with several settings once three months has passed after the recommended replacement time ( RRT date). She said no that was not the case with my particular model However, I contacted the pacemaker company technical support and they confirmed the manual's description was correct.
4)Issue of high left ventricular (LV) threshold occurring on multiple of the every three month reports.It was not until October 2017 (2 years after implantation ) that the left ventricular management system was switched to "monitor". I can only speculate as to the degree to which battery life was shortened by what seems to be the less than prompt attention to that issue.
The interrogation report is fairly long and reviewing it requires considerable technical knowledge about cardiology, PMs in general as well as certain details regarding the specific brand,various programmable setting and particular model and various lead placement configurations .Being a retired physician I have had the time and interest to spend a fairly large amount of time and effort into learning about PM lore and in particular the interrogation reports. The somewhat shaken confidence in the folks monitoring the wires in my heart has certainly provided incentive to learn how to read the reports.
1)In October 2015 I had a pacemaker implanted- one which is designed for bi-ventricular pacing the most common form of CRT (cardiac resynchronization therapy).
2)The technician who assisted and provided technical advice to the EP cardiologist at the time of the implantation told me on the following day that my home -bedside PM communication device would send a recording every night to the manufacturer's web site and then to the hospital PM center.
Only 6 months later was I informed by him , in reply to a question from me, that no -that was not true and that arrangement was only for devices with a defibrillator which I did not have. So for six months I made a effort to be near near by communication device device each night.
2.In October of 2016 my device recorded several episodes designed as AF/AT (atrial fibrillation/atrial tachycardia) Episodes of AF are thought to be common ( at least 30% by three years in patients with a PM- according to one data base).This lead to to my fairly extensive literature review of the issue of AHRE ( atria high rate episode). I learned that the topic is controversial and opinion varies as to what if any threshold there is for "signficiant volume of AF" to justify anticoagulation. (There are 2 randomized clinical trials underway that are designed to try and answer that question)
Also, All AHREs so designated by the PM's algorithms are not in fact AF. The phenomenon of far field r wave sensing and and a less common and more obscure PM rhythm disturbance known as recurrent, non reentrant ventricular atrial synchrony (RNRVAS) are capable of mimicking AF.The technician at the hospital PM center who is tasked with screening the remote interrogation report had not recognized that the rhythm was FFA and apparently did not feel that the issue required calling the matter to the attention of the EP cardiologist.
Tuesday, December 18, 2018
Cardiovascular function and muscle studies on "lifelong" exercisers
Gries et al from Ball State Human Performance Lab have published the results of a study of cardiovascular function and muscle enzyme levels on long term aerobic exercisers who did aerobic exercise for fifty (50 !) years and compared them to non exercisers of comparable age and to young exercisers.
The life time exercisers were divided into 2 groups based on the intensity of lifelong exercise with the "performance" group consisting on competitive runners and the others called the "fitness" group which I take to mean they exercised to be fit and were not competitive athletes.Both subgroups of the
lifelong exercisers exercised 5 days per week with an impressive 7 hours of exercise per week.
The maximal oxygen consumptions values were , (expressed as ml/kilo/min):
performance group 38.1 +/-1
fitness group 27.1 +/- 2
young exercisers 53 +/- 3
Not surprising that the competitive group would have a significantly higher 02 max.In regard to muscle enzyme levels there were no differences between the competitive and fitness groups and levels were similar to the values seen in the young group.
Similar values for 02 max in longterm exercisers were reported (1) by Benjamin Levine's group from Southwestern. They also reported a significant higher 02 max in the competitive subgroup versus the non-competitive subgroup ( 39.5+/- 5.3 versus 32.5+/-5)
These two studies present data on two subgroups of long time or "lifelong" exercisers with the competitive groups having significantly higher maximal oxygen uptakes. Both subgroups exercised for many hours a week but presumably the competitive group in each study exercised at a higher intensity. Is the difference in measured maximal oxygen uptake due to the intensity of training or is the difference due to the competitive group having the genetic endowments that bestow a super compliant left ventricle capable of rapidly filling and allowing a higher exercise stroke volume.
1) Bhella PS , Impact of lifelong exercise "dose"on left ventricular compliance and distensibility
JACC vol 64 2014
The life time exercisers were divided into 2 groups based on the intensity of lifelong exercise with the "performance" group consisting on competitive runners and the others called the "fitness" group which I take to mean they exercised to be fit and were not competitive athletes.Both subgroups of the
lifelong exercisers exercised 5 days per week with an impressive 7 hours of exercise per week.
The maximal oxygen consumptions values were , (expressed as ml/kilo/min):
performance group 38.1 +/-1
fitness group 27.1 +/- 2
young exercisers 53 +/- 3
Not surprising that the competitive group would have a significantly higher 02 max.In regard to muscle enzyme levels there were no differences between the competitive and fitness groups and levels were similar to the values seen in the young group.
Similar values for 02 max in longterm exercisers were reported (1) by Benjamin Levine's group from Southwestern. They also reported a significant higher 02 max in the competitive subgroup versus the non-competitive subgroup ( 39.5+/- 5.3 versus 32.5+/-5)
These two studies present data on two subgroups of long time or "lifelong" exercisers with the competitive groups having significantly higher maximal oxygen uptakes. Both subgroups exercised for many hours a week but presumably the competitive group in each study exercised at a higher intensity. Is the difference in measured maximal oxygen uptake due to the intensity of training or is the difference due to the competitive group having the genetic endowments that bestow a super compliant left ventricle capable of rapidly filling and allowing a higher exercise stroke volume.
1) Bhella PS , Impact of lifelong exercise "dose"on left ventricular compliance and distensibility
JACC vol 64 2014
Monday, December 17, 2018
More use restriction for fluroquinolones from FDA
FDA recommends against use of fluroquinolones for 1) acute bacterial sinusitis, 2) acute exacerbations of chronic bronchitis.and 3) uncomplicated urinary tract infection because of increasing concerns about adverse effects.
The warning emphasized the adverse effects of hypoglycemia and various psychiatric symptoms.
For possible mechanisms regarding fluroquinolone related hypoglycemia see this detailed review.
The warning emphasized the adverse effects of hypoglycemia and various psychiatric symptoms.
For possible mechanisms regarding fluroquinolone related hypoglycemia see this detailed review.
Sunday, December 16, 2018
Milton Friedman's " 4 ways to spend money" and health care spending
Milton Friedman spoke of the four ways people could spend money based on the funding source and the recipient of the goods or services and the associated mind sets,incentives and constraints that each arrangement supports. In his book "Free to Choose" he presented a four quadrant diagram, a version of which can be found here.
The left upper quadrant represents the situation in which you spend your own money on yourself, a situation where one typically exerts some degree of prudence a thought not found to same degree in the other arrangements.
In the RUQ you spend someone else's money on yourself.
Much (most ?) health care spending seems to be in the RUQ which is clearly the case with Medicare and Medicaid spending and from one view point employees spending their employer based health insurance money.Although you could consider that type of insurance basically part of the employee's compensation so maybe that should be in the LUQ ,folks tend to act as if they are spending someone else's money so I'll leave that in the RUQ.
The LLQ denotes your spending their money on someone else, such as Aunt Hattie buying a birthday gift for her niece in which getting what the niece really wants may not be the determining factor.
The RLQ represents you spending some one else's money on someone else.Think of a welfare program dispensing money .
The concern over high and rising health care costs is sometimes (and in my view correctly) focused on the governmental spending on health care. However, increasingly pundits and health care policy wonks and "thought leaders" frame the issue as one in which total health spending is a threat to nation's fiscal solvency. .
The argument that government spending is out of control, relies on foreign funding and the national debt is growing to a dangerous level resonates across the political spectrum of views. Regardless of the validity of various elements of that sentiment how would spending in the LUQ relate those concerns?
Would not individual spending their own money on things (even medical care)for themselves increase the C part of the GDP formula? Would not increase in spending be exactly what economists of the Keynesian view prescribe to bolster a economy lacking in the right type of "animal spirits"? Why would policy wonks want to limit personal spending? Are they really basing their proposal for more control over individual actions on legitimate concerns for the future economic safety on the country? Or is it the progressive view ( as well the NeoCons view) that society is best managed by wise leaders ?
The left upper quadrant represents the situation in which you spend your own money on yourself, a situation where one typically exerts some degree of prudence a thought not found to same degree in the other arrangements.
In the RUQ you spend someone else's money on yourself.
Much (most ?) health care spending seems to be in the RUQ which is clearly the case with Medicare and Medicaid spending and from one view point employees spending their employer based health insurance money.Although you could consider that type of insurance basically part of the employee's compensation so maybe that should be in the LUQ ,folks tend to act as if they are spending someone else's money so I'll leave that in the RUQ.
The LLQ denotes your spending their money on someone else, such as Aunt Hattie buying a birthday gift for her niece in which getting what the niece really wants may not be the determining factor.
The RLQ represents you spending some one else's money on someone else.Think of a welfare program dispensing money .
The concern over high and rising health care costs is sometimes (and in my view correctly) focused on the governmental spending on health care. However, increasingly pundits and health care policy wonks and "thought leaders" frame the issue as one in which total health spending is a threat to nation's fiscal solvency. .
The argument that government spending is out of control, relies on foreign funding and the national debt is growing to a dangerous level resonates across the political spectrum of views. Regardless of the validity of various elements of that sentiment how would spending in the LUQ relate those concerns?
Would not individual spending their own money on things (even medical care)for themselves increase the C part of the GDP formula? Would not increase in spending be exactly what economists of the Keynesian view prescribe to bolster a economy lacking in the right type of "animal spirits"? Why would policy wonks want to limit personal spending? Are they really basing their proposal for more control over individual actions on legitimate concerns for the future economic safety on the country? Or is it the progressive view ( as well the NeoCons view) that society is best managed by wise leaders ?
Wednesday, December 05, 2018
If there is increased coronary calcification in some long time endurance atheletes,is that a good or bad thing?
If there is increased coronary calcification in long time endurance athletes,is that a good thing or a bad thing? Also if true is it true only in white males? The Cardia Study (1) found an increased risk of coronary calcification in white men ( depending on what statistical model was used) but not black men.
Funnily enough a similar question can be asked in regard to the use of statins with more calcification reported in users of the more potent ( in terms of LDL lowering power) statins.(I am aware of no racial differences reported in that regard)
So is the absolute worse thing you, as a white male could do would be to run excessively for 30 years and take the most potent statin ever?
1) Laddu DR 25-year physical activity trajectories and development of coronary artery disease as measured by coronary artery calcification.
Funnily enough a similar question can be asked in regard to the use of statins with more calcification reported in users of the more potent ( in terms of LDL lowering power) statins.(I am aware of no racial differences reported in that regard)
So is the absolute worse thing you, as a white male could do would be to run excessively for 30 years and take the most potent statin ever?
1) Laddu DR 25-year physical activity trajectories and development of coronary artery disease as measured by coronary artery calcification.
Tuesday, December 04, 2018
Is the key to prevention of post ablation atrial fibrillation risk factor modification?
Dr. Rajeen Pathar (1) and co researchers from Adelaide Australia seem to think so.
Hypertension,diabetes,obesity, sleep apnea and smoking are recognized risk factors for the development of atrial fibrillation (AF).The authors reasoned that the same risk factors might predispose to recurrence of AF after a successful atrial fibrillation ablation and that aggressive risk factor reduction just might decrease the recurrence rate. Their published data (1) tends to support that hypothesis.
A excellent discussion of risk factor importance in AF by Dr. John Mandrola on Medscape can be found here.
1) Pathak,RK Aggressive risk factor reduction study for atrial fibrillation and implications for the outcome of ablation.The Arrest-AF study. JACC2014 Dec 2;64 (2) 2222
Hypertension,diabetes,obesity, sleep apnea and smoking are recognized risk factors for the development of atrial fibrillation (AF).The authors reasoned that the same risk factors might predispose to recurrence of AF after a successful atrial fibrillation ablation and that aggressive risk factor reduction just might decrease the recurrence rate. Their published data (1) tends to support that hypothesis.
A excellent discussion of risk factor importance in AF by Dr. John Mandrola on Medscape can be found here.
1) Pathak,RK Aggressive risk factor reduction study for atrial fibrillation and implications for the outcome of ablation.The Arrest-AF study. JACC2014 Dec 2;64 (2) 2222
Monday, December 03, 2018
kids fredquently getting hit the head is not a good idea
More data accumulate indicating MR changes in the brain are associated with sub concussive blows in youth football in a single season.
Functional MR studies (fMr) have shown changes in both gray and white matter correlated with the number of blows to the head as measured by impact detecting systems placed inside football helmet's.
The immediate and long term effect on the young brain is not known and the relationship to CTE is speculative.
Maybe the developing brain is more vulnerable to harm from multiple mini traumas or maybe it is more adaptive .
Meanwhile the experiments continue in youth football leagues and under Friday Night Lights.
Murugeson from Southwestern Medical School in Dallas presented data at recent RSNA meeting demonstrating functional MR changes in a single season of high school football correlated with sub concussive head blows.So these are kids who had no reported concussion. Data from a Wake Forrest study indicated majority of sub concussive blows occurring during practice.
Functional MR studies (fMr) have shown changes in both gray and white matter correlated with the number of blows to the head as measured by impact detecting systems placed inside football helmet's.
The immediate and long term effect on the young brain is not known and the relationship to CTE is speculative.
Maybe the developing brain is more vulnerable to harm from multiple mini traumas or maybe it is more adaptive .
Meanwhile the experiments continue in youth football leagues and under Friday Night Lights.
Murugeson from Southwestern Medical School in Dallas presented data at recent RSNA meeting demonstrating functional MR changes in a single season of high school football correlated with sub concussive head blows.So these are kids who had no reported concussion. Data from a Wake Forrest study indicated majority of sub concussive blows occurring during practice.
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