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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?


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.

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.

Friday, May 12, 2017

An increasing cardiac calcium score may not mean increased CVD risk

The coronary calcium score (  for example as done with a EBCT heart scan) is well recognized as a tool to estimate  cardiac risk, a higher score meaning a higher risk.

Coronary calcification is by definition coronary artery disease. Calcification may be in the media of arteries or in the intima. Intimal calcification may be dense as is  found in fibrous, basically stable plagues which are not prone to rupture and cause an acute coronary event. Spotty calcification can be found in soft, vulnerable plaques that are at risk of rupture.

Serial calcium scans on patients taking statins have shown increase in coronary calcification and yet there is more than abundant  evidence that statins ( at least in secondary prevention) can reduce plaques and  decrease the risk of coronary events,a situation referred to by some as the "statin paradox" or the "plaque paradox".

A possible explanation  to this alleged paradox may be found in a study (1) from Cleveland Clinic in which the authors analyzed intravascular ultrasound images of patients from 8 clinical trials.

Patients with coronary artery disease treated with statins show an increase in coronary calcification.The so-called high intensity statins bring about more increase in calcification while also causing the greatest regression of plaques. The increase in calcification may be one mechanism by which statin therapy stabilizes plagues and makes them less likely to rupture. So serial calcium scans in a patient taking a statin demonstrating increased calcification may not be a warning of increased risk at all.

Quoting Cleveland Clinic's  Dr . Steve Nissen:

"This is an important observation that tells us statins work to stabilize plaques by converting softer,cholesterol -laden plaques that are prone to rupture into more stable calcified plaques that are relatively inert.It explains the paradox of why serial measurements of calcium doesn't necessarily work to track the progression of disease and it explains to some extent how statins work.

Internists who like to talk about mechanisms and how things work may find this a compelling story but as an accompanying editorial (3) said this is a hypothesis generating study,causality cannot be inferred and the techniques used have multiple limitations. Human are pattern seeking story telling creatures and this story might catch on-at least until something better comes along.


Shifting gears-there are at least 3 articles that have reported that long time endurance exercisers have higher calcium scores than age matched  sedentary controls controls,an observation offered by some authors as  more proof that too much exercise is not good. Juxtaposed to that is the epidemiologic evidence that longtime endurance exercise decreases the risk of a coronary event and that elite athletes life longer than sedentary colleagues and yet more calcium in the athletes.Another plaque paradox?

Merghani and co-authors studied 152 maters athletes ( ages 51-63) They found that "most" )( 60%)  of the lifelong exercisers  has a normal CT coronary angiogram as did a similar number of the controls. However they also reported that the male athletes were more likely to have a CAC score of 300 or more compared to the sedentary controls.The plaques in  the athletes were predominately calcific.

Similar results were reported by V.L. Aengevaeren et al (2) who studied 284 lifelong exercisers. In regard to their findings they said:

"The most active group did however had a more benign composition of plaques with fewer mixed plaques and more often only calcified plaques.These observation may explain the increased longevity of endurance athletes  despite the presence of more coronary atherosclerotic plaques in the most active participants ".

Eijsvogels and co-workers published an excellent, detailed and extensively referenced  review( 4) of the possible harmful effects of acute and chronic exercise .  They only briefly mention what was then the preliminary evidence that longtime runners have higher calcium scores as their review preceded Puri's work as well as that of Aengevaren and Merghani

1.Puri, R Impact of statins on serial coronary calcifications during atheroma progression  and regression. J Am Coll Cardio 2015;65, 1273-1282


2 Aengevaren VL et al The Relationship between lifelong exercise volume can coronary atherosclerosis in Athletes. Circulation 2017 april 27

3. Shaw LJ The Never Ending story on Coronary Calcium.Is it predictive,punitive or protective? Editorial Comment J of Amer Coll Cardio, 2015 ,65 no 15 1283-1285

4. Eijsvogels,TMN et al Are there deleterious cardiac effects of acute and chronic endurance exercise? Physiol Rev 96 99-125,2015

Tuesday, May 09, 2017

The annualized decrease in exercise capacity may be even worse than we thought

The longitudinal decline in aerobic capacity is typically said to be 5 -10% per decade from age 40 to about age 70  then a more rapid decline occurs. Data from the Baltimore Longitudinal study of Aging (BLSA) (1) suggests that the decline is not constant across age ranges  but rather" accelerates markedly   with each successive age decade".

 How so?

In cross sectional studies " each succeeding age decade  represents a more highly selected group than it predecessor, thus healthy 70 to 90 year-olds may have been physiologically superior to current 20-40 years olds when they were on a similar age. In other words there is inherent selection bias in cross sectional data.

I will not attempt to explain the statistical model used but here are their values for the reduction  in men in peak O2 uptake expressed in ml/kil0/min for various decades:

age
30- 39 minus 7
40-49  minus 10
50-59  minus 15
60-69 minus 20
over 70 minus 26
                    
 A similar pattern was found in women.

They found that the oxygen pulse (oxygen consumed per heart beat) rate of decline mirrored the rate of decline in peak 02 .Since oxygen pulse is a function of stroke volume and peripheral muscle uptake of oxygen it is not possible to determine if it is cardiac output or muscle uptake that is largely responsible for the decline.

Caveat-The published results are from a mixed-effect prediction model and the median followup was only 7.9 years and prediction is the operative word. Though the study is "longitudinal" numbers in their tables do not represent for example following the same people over a lifetime and noting the per decade change in oxygen uptake. Still their data suggest that the often quoted 5-10 % decrease per decade may be too optimistic and rates of changes likely accelerate with aging.The confidence intervals for each age range are quite large and you have to wonder what are the mechanisms responsible for such wide variation in loss of exercise capacity within a age range. If subendocardial  fibrosis is the ( or a) culprit what are the actors that accelerate or retard that process.



1) Fleg, JL Accelerated Longitudinal Decline or Aerobic Capacity in Healthy Older Adults"
Circulation 2005, 112: 674 -682.

Sunday, April 23, 2017

"Para Hisian Pacing" as well as selective Bundle of His pacing may bring about a hyper response

I have written before about a sub group of Cardiac resynchronization patients (CRT)   who have a hyper response with marked improvement in indices of cardiac   function, e.g. ejection fraction and end diastolic volume.

Such responses have been reported with Biventricular pacing  (Bi-V) and  His Bundle Pacing ( HBP). There are two forms or types of HBP: 1) pure HBP also known as selective and 2) Para Hisian pacing also known as non  selective HBP.

The QRS is normalized with selective HBP while in nonselective although the widened QRS duration is significant reduced it may not be restored to the pre  bundle branch block  configuration. There is both activation of the His Bundle fibers and adjacent ventricular septal muscle giving a fused or fusion ventricular activation pattern. 

According to Lida et al writing in the December 2016 Journal of Arrhythmia (1) "there seems to be no significant clinical difference between selective HBP and non selective HBP because both do not alter physiological impulse conduction and possibly maintain rapid and synchronous LV ( left ventricular) activation "

A similar case report was published by Ajijola et al  from UCLA in 2015 (2)

His Bundle pacing seems to gaining momentum both as an alternative to right ventricular pacing and as a method of cardiac resynchronization.

1)Lida, Y et al Successful resynchronization by permanent His-bundle pacing in patient with pacing -induced cardiomyopathy' J Arrhythmia , 2016 Dec. 32(6), 499-501

2)Ajijola,O et al Hyper-response to cardiac resynchronization with permanent His bundle pacing:Is parahisian pacing sufficient? Heart Rhythm Society, open access article http://dx'doi.org/19.10.hrcr.2015.05.006

Addendum:  5/26/2017  Several papers presented at the May 2017 meeting of the Heart Rhythm Society indicated that His Bundle pacing is ready for prime time.  See Dr. John Mandrola's  article on Medscape entitled " His Bundle pacing hits the mainstream at HRS 2017".
On a personal note-It is now almost two years since I was implanted with a Pacemaker with Bundle of His pacing before the practice became more mainstream. I had developed a left bundle branch block and an exercise induced second degree heart block. The LBBB had  markedly decreased my exercise tolerance . My LBBB was "fixed" and after getting over a few complications of the procedure my exercise tolerance was back to my pre LBBB level .


Friday, April 14, 2017

If peak load is the determing parameter runners should have more osteoarthritis

Perhaps it seems counter intuitive that runners do not have a higher incidence of knee osteoarthritis or so the preponderance of epidemiologic data contents.After all the peak load of the articular cartilages in running is much higher than in walking or so the kinesiologists tell us and would not the cumulative higher peak load after many miles of running wear out and maybe chew up the articular cartilages.

Or maybe the explanation does not lie in the peak load.

 Ross H Miller from the Department of Kinesiology at the University of Maryland offers an alternative view (1) and an alternative analysis of the relevant forces conspiring to "wear out" the knees.

He suggested that peak load is not the relevant variable but rather it is the "average load per distance traveled"  which is said to be surprisingly low and purportedly similar to walking.

Ross also discussed the notion of cartilage conditioning .Knee cartilage glycosaminoglycan content( which affects lubrication and shock absorption ) has been  shown in one study to be greater in recreational runners and even greater in high volume runners.

"... a man hears what he wants to hear and disregards the rest" Paul Simon.The Boxer



1) Miller, RH "Joint loading in runners does not initiate knee osteoarthritis" Exerc Sports Sci  Rev 45(2), 87-95,4 2017