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

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

Monday, March 18, 2019

Recent changes in AHA/ACC atrial fibrillation guidelines

One of my favorite EP cardiologists, Dr. John Mandrola,gives his thoughts regarding the 2019 focused update on  atrial fibrillation (AF)  from the AHA/ACC ,Heart Rhythm Society task force.

Here are some of the highlights and the entire article by Mandrola (full text is available) is recommended.

Aspirin is no longer recommended for low risk AF patients. As Mandrola says , just like that, without much of an explanation .

Both the FDA and CMS have approved percutaneous left atrial appendage closure with the Watchman device  and the panel gives it. a class 11b recommendation. Apparently, the panel did not see fit to comment on the 4% risk of device associated thrombosis reported with Watchman.

DOACs now is  officially preferred over warfarin. Not mentioned by Mandrola is the observation that the fewer strokes with DOACs versus warfarin is driven by the fact there  are fewer hemorrhagic strokes with DOAC while there is little if any difference in the number of ischemic strokes.

The task force stated that female sex alone is no longer considered  a risk factor  for stroke in an AF patient per se.

The guideline writers gave a class 11 b (additional studies are need-procedure may be considered) recommendation for AF ablation in heart failure.Mandrola believes the data supporting AF ablation in HF patients is sufficient for the panel to have given a higher recommendation quoting the positive results of the CASTLE-AF trial that showed a 12% absolute risk reduction in death and in heart failure admissions in the ablation cohort.

Mandrola shares my views on the CHA2DS2VASc score . It is "simple to use , but at its core distills a decidedly continuous risk for a future event down to an integer." He references D. R. Quinn's 2017 review of 34 studies of AF ( reference can be found in Mandrola's review) that illustrate the large variation in the baseline risk of stroke in untreated AF patients. Quoting Mandrola " Translation: We have no idea of the risk in untreated patients.",and yet every day cardiologists and other docs crank out the CHA2DS2VASC and mater-of-factly tell their patient that they have x% annual risk of stroke and suggest how much that risk will be reduced by oral anticoagulation.

I have written about Quinn's study before and quoting from Quinn's article "' The majority of cohorts did not observe stroke rates that would indicate a clear expected net clinical benefit for anticoagulating AF patients with a CHA2DS2-VASc score of 1 or 2."

Monday, March 11, 2019

Left anterior fascicular block-comments on epidemiology and ventricular function

Left anterior fascicular block (LAFB) was previously known as left anterior hemiblock (LAH) .The earlier designation can be attributed to the widely accepted   writings of Maurico Rosenbaum whose work ( 1967) seemed to indicate that in humans the left bundle divided into a left  and   a right branch.

This "trifascicular" concept (right bundle branch and the two branches of the left bundle) was widely accepted and persisted  even though  work in 1972 by Demoulin and Kulbertus  make it clear than there was also frequently a septal branch of the left bundle and more importantly that the anatomy of  left bundle is much more complex that simply consisting of two (or three) branchs, i.e. more of a spiderweb or fan.There is great variation in the interconnections and  in few of the 49 careful dissections by Demoulin can a simple pattern of 2 fascicles or even 3 fascicles be seen. (the patterns can be seen on page 283 of reference 1, full text is available)

Realizing that all models are wrong but some are useful ( George Box, circa 1978),it may be that the LAFB model has some value.

LAFB is diagnosed on EKG when the frontal plan axis is between minus 30 and minus 90 with QRS duration les than 120 msec and the patient does not have an inferior wall myocardial infarction,LVH  or WPW syndrome.So, typically LAD equal LAFB in the EKG reading world.

Mandyam et al ( 2) from UCSF studied long term outcomes in patients with LAFB who at the beginning  of the data collection did not have evidence of heart disease. Using data from the Cardiovascular Health Study (CHS), they compared 39 subjects with LAFB with 1625 patients without LAFB over a 19 year period.The average age of the control groups with 71.4 and the age of LAFB group was 74.9

They report LAFB was significantly associated with atrial fibrillation (AF) Heart failure(CHF) and death with the following p values-AF .02,CHF .02, and death .001.

This was a small  ( 39  patients),coarse grain study.The authors point out that although CHS tries to exclude preexisting disease on entry to the program hypertension or asymptomatic coronary artery disease may have been missed. The authors referenced no corroborating studies .

The UCSF article received considerable medical press coverage in part as it offered some suggestion that the previously accepted notion that LAFB was a  "benign" finding might not be correct but within a year their findings were contradicted by research from Copenhagen.

JB Nielsen (4) studied the cardiovascular outcome of 222,227 subjects with a 5.7 year  follow-up period. They did find a statistically significant correction between LAFB and AF, HF and both all cause and cardiovascular mortality. However, after adjusting for age and gender only the all cause risk retains statistical significance.

Quoting the authors: "current EKG definition of LAFB is not always clinically important marker of cardiovascular morbidity and mortality beyond what can be expected by age and sex."

What is the effect of LAFB on left ventricular function?

Leeters and colleagues from The Netherlands studied 28 patients  with RBBB,LAFB and heart failure with 2D speckle tracking regional strain measurements as well as healthy controls and 28 LBBB patients. This is not a study of "lone LAFB" as the patients had RBBB and HF and a number of them had scars detected by CMR. Since the RBBB does not affect Left ventricular activation sequence it is reasonable to assume the delay in activation of the anterior LV is due to the LAFB.The study indicated wall motion abnormalities between the anterior wall and inferior wall of the LV analogous to the classic pattern of septal and lateral LV wall dyssynchrony characteristic of LBBB but apparently less disruptive of cardiac function.

1) Fisher,JH Hemiblocks and the fascicular system:myths and implications. J. Of Interventional cardiac electrophysiology 2018 52: 281-285

2)Mandyam, ML Long-term Outcomes of left anterior fascicular block in the absence of overt cardiovascular disease, JAMA 2014 309 (15)1587

3)Leeters IP, et al Left Ventricular regional contraction abnormalities by echocardiographic speckle tracking in combined right bundle branch block with left anterior fascicular block compared to left bundle branch block.J Electrocardiol 2016 49 (3) 353

4)Nielsen, JB et al Left anterior fascicular block and the risk of cardiovascular outcomes.
JAMA Int Med June 2014, 174(6),1001-1003

Tuesday, February 19, 2019

More data on lifelong exercisers-this time from Ball State

Scott Trappe and colleagues (1) from Ball State Human Performance lab  studied 7 women and 21 men all in their 70's who were lifelong ( fifty years or more) exercisers and compared them to elderly,apparently healthy sedentary  subjects and to heathy young exercisers (average age 25)

The lifelong exercisers exercised 5 days/week with a weekly hourly total of 7 hours. for the past 52 =/- 1 years.

Maximal oxygen uptake was measured on a maximal cycle test and muscles biopsy done to determine a "muscle aerobic profile" (MAP for short). MAP refers to the degree of capillarization and metabolic enzymes eg. Citrate synthase,B-HAD and glycogen phosphorylase  were determined by muscle biopsy in the lateral thigh.

While the MAP was the same as in the young exercising controls the 02 max  of course was not .The set of long time exercising women was small, but rounding up women who have exercisers for fifty years is no small feat.

Comparing the 02 max in young women,exercisers and elderly control women we find: 44,26 and 18 .

The authors conclude : " the data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than the more central aspects of the cardiovascular system."

The authors mention the fragility index and quote that the value for men is 17.5 ml/kilo/ min and make their educated guess about what it is for women giving 14 ml/kilo/min as the value. I am not sure why women would have a lower number since the index is corrected for weight. Folks fortunate to have values well above those numbers are said to have more physiologic reserve to withstand and survive various homeostasis challenges whose frequency is a function of age.

This index should not be confused with another fragility index which gives an indicator of how robust are the results of a clinical trial.See here for more on that.  (A clinical trial would have an FI of 1 if the hypothetical movement of one patient from the success column to the failure column would make the study no longer statistically significant ( at the p of 0.05 level)


1) Gries,J et al Cardiovascular and skeletal muscle health with lifelong exercise
JAP 125: 16736 2018 (full text available on line)

Wednesday, February 13, 2019

In the long run ( or ride) do runners wear out sooner than cyclists?

 Tim Noakes, the MD, PhD exercise physiologist from South Africa has suggested that perhaps many years of running and the gravity assisted  pounding might accelerate the aging process at least as regards muscles and tendons.

If that is the case, might a comparison of the decrement in performance over time between long time runners and long time cyclists be useful  tend to confirm or deny that hypothesis.

Noakes and colleagues made that comparison (see here) and things look better for the cyclists.

Tuesday, February 12, 2019

We knew all along who would be the collateral damage from the "war" on opioids

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."

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 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  did not always 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.

 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 can be 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.

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.