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Tuesday, June 13, 2017

Is subendocardial fibrosis a reason for the age associated decrease in diastolic function?

It seems to be all about diastole.Simply put- the aging heart has more functional loss in ventricular filling than in  ejection of blood ( as least as depicted by the usual measures of systole namely the ejection fraction (EF) at rest and stroke volume at rest).  Similarly the  largest  difference between the exercise capacity of the average jogger and the elite endurance athlete is found in diastole-the elite athlete has markedly superior diastolic function likely on a genetic basis.

Hollingworth and co-workers from Newcastle on Tyne (1) studied left ventricular torsion and diastolic function in presumably healthy adults in various age ranges using  cardiac magnetic imaging with tissue tagging.

First some background;
The architecture of the left ventricle  has left handed subepicardial fibers and right handed subendocardial fibers which leads to a rotational deformation during cardiac contraction referred to as torsion. The subendocardial fibers are activated first leading to a  brief clockwise rotation ( as viewed from the apex of the heart as if you were on the spleen looking up) and then a counterclockwise rotation  while the base rotates clockwise. This action has been compared  to the two handed movement of wringing out a washrag.

The twisting of the left ventricle during systole is followed by a recoiling  or untwisting releasing the energy stored during systole. The untwisting largely occurs mainly in the isovolumic relaxation time . (IVRT). The IVRT is the  time after the aortic valve closes and before  the mitral valve has not yet opened-a period when no blood is either entering or leaving the ventricle.

 The rotation action of the heart can be explained by the orientation of the muscle fibers. The subendocardial  fibers are oriented in a right handed direction while the subepicardial fibers run in in a left handed direction and a midlayer is oriented circumferentially .The contraction of all three sets of fibers account for all contractile actions  of the heart and the rotational movement.

What at first seem counter-intuitive is the observation that  subendocardial disease is associated with hyper-rotations. (2) This is possibly explained by subendocardial fibrosis decreasing the rotational counterbalance to the mechanical advantaged ( longer radius) epicardial rotational direction.

Hollinsworth's study showed the expected decreased early diastolic filling and a " torsion to shortening ratio" that was consistent with lessened subendocardial shortening possibly  due to subendocardial fibrosis. So possibly some of the age related diastolic dysfunction may be related to altered untwisting mechanics.



1) Hollingsworth, KG et al Left ventricular torsion energetic and diastolic function in normal human aging. Am j Physiol heart circ physiology 302, H 885-H892,2012  (full text is available on line)

2.Nakatani, S. Left Ventricular rotation and twist:Why should we learn? J. Cardiovas Ultrasound 2011;19 (1): 1-6. Full text is available on line)

Monday, June 12, 2017

After 40 plus years ABIM does audit to see if I have a medical license

What is that all about?

 I received a letter from the ABIM informing me that " during a recent audit, ABIM was unable to confirm that you have a valid license to practice medicine." I was requested to send a copy of my license within 30 days and " if ABIM is unable to confirm that you hold a valid license to practice medicine,ABIM will be obliged to suspend your Board Certification and report your certification status as "Not certified".

I replied the same day by Email and send a hard copy of my license by letter . A few days later I received a second letter identical to the first and again I replied by mail with a copy of my license.I have had no reply.

I wondered about their audit procedure. I was able to verify my license in less than 2 minutes by going the website of the state of the medical board in the state in which I have had an uninterrupted license  at the same address for over 35 years.If their audit process is as inadequate as it appears to be they will waste more than a little time and effort to confirm licenses and waste time and efforts of diplomats replying to the requests.

Why , after forty years, does ABIM consider it necessary to determine if I have a license?

Is this somehow related to their widely criticized  maintenance of certification (MOC) program and the efforts of some organizations to link MOC with state medical license requirements?

Have others received similar letters? Any thoughts about what this is all about?

addendum: It is now more than 2 months and ABIM has still not replied to my email which they had promised in "2-3 weeks" saying they were very busy. 8/19/17

Monday, June 05, 2017

More on subclinical atrial fibrillation (SCAF) and what to do when we find it

A 2014 study-Crystal AF- examined patients with cryptogenic stroke using a implantable cardiac monitor and reported that over a three year period 30% had episodes of atrial fibrillation(AF) lasting 30 seconds on longer.

A new study,Reveal AF,studied 394 patients using an implantable cardiac monitor with no history of AF but who  were considered high risk for stroke  based on the CHADS2 score.At the end of 18 months 29.3 % of the patients had episodes of AF of six minutes or more and at 30 months 40% had AF. Further, 12% had AF durations of 6 hours or more.

 So we know that  AF is common in 1) patients with history of stroke and no obvious  cause  2) patients classified as high risk using the CHADS2 scoring system and 3) patients with pacemakers.

Should all patients with cryptogenic stroke shown to have AF by a implantable  device receive oral anticoagulation? That seems to be common clinical practice but I am aware of no clinical trials showing the efficacy and safety of that approach. Should all patients with a CHAD2 score similar to that used in the Reveal AF study receive anticoagulation? ( in the trial 56% of the patients were actually prescribed OAC by their private physicians). Should all patients with pacemakers (PMs )with SCAF ( above some level of AF burden) receive OAC?

There are at least 2 randomized clinical trials underway which are designed to determine the effects of OAC on patients  with subclinical AF (SCAF) as determined by data collected on patients with pace makers.

In addition a recent study ( see here) and analysis casts more than a little doubt on the validity of the various CHADS risk determination systems.

The prolific EP cardiologist author and blogger John Mandrola  puts it this way in his discussion of the Reveal AF  " ..if the average high risk older person has the same amount of short-duration AF as a person who just had a stroke how does this ( long term monitoring) help decide on therapy?"  Point well taken. Actually at the end of 30 months in Reveal AF trial 40% had SCAF versus 30% with SCAF and 36 months.Taken at face value could nt  one claim that AF is protective? I think not but still that just amplifies Mandrola's point.

Dr. H Kamel and associates have published an excellent commentary and review (3) of the mechanisms of stroke and atrial fibrillation which along with the Reveal AF trial results might slow down enthusiasm  for implanting devices in all patients with cryptogenic stroke and the increasing call for more screening for the detection of afib.

1)Sanna, T Cryptogenic stroke and Underlying atrial fibrillation NEJM 2014: 370, 2478


2) Reiffel, JA presented at Heart rhythm Society Meeting, May 10-13, 2017.

3)Kamel, H et al Atrial fibrillation and mechanisms of stroke.Time for a new model.Stroke 2016 47 895-900.


Additions made Aug 2,2017 .