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.
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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

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 wondered if the estimate of battery life was disproportionately shorter than what may have  been expected on the basis of the settings .She forwarded the data to the home office and the engineers found nothing to do to improve the settings.Her concern and interest was appreciated but ..

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. 

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

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.

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 ?

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.

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

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.