You are only as young as your legs

A high school friend once told me that one of his football coaches told him that wind sprints were important and you were only as young as your legs. I think that this is a physiological insight on the same lofty level as Woody Allens' maxim (1).  The time honored wind sprints have apparently morphed into high intensity interval training which is supposed to be good  for things ranging from improving glucose tolerance to improving 02 uptake and exercise tolerance in heart failure with or without reduced ejection fraction.

The stylized story about muscle loss with aging can be told like this:

From age 40 to age 70 there is 8 % per decade decrease in muscle mass and a 10-15 % decrease in muscle strength. Around age 70 the rate of decline for both increases so that there is a 10-15% decrease in muscle mass per decade and a 25 to 40% decrease in strength.

There is a greater loss in the fast twitch or type 2 fibers with some of the  fast twitch fibers being replaced by type 1.This observation helps explain the greater loss in strength relative to muscle size as type 2 fibers are larger and can generate more force and to some degree they are being replaced by smaller less forceful type 1 fibers.

Decreasing levels of exercise for various reasons accompany aging but not  all  muscle loss can  be blamed on decreased activity. There is to varying degrees loss of the anterior horn cells in the spinal cord which seem to target horn cells that serve type 2 fibers. as well as multiple other changes in muscles that seem refractory to continuing exercise.

 So why should we call the numbers stylized? The estimates of percentage per decade losses are of course averages  which are largely derived from longitudinal studies  and individuals have been noted to vary greatly. Further one study showed that various sample sites from the lateral thigh muscle  which investigators prefer for biopsy studies on muscle fiber type often give rather discrepant fiber distribution counts.




1) As you get older everything that  should be soft gets harder and everything that should be hard get softer. We can all think of examples.

Which master should physicians serve-Dr.Martin Samuels' thoughts

I have written before about what I believe the wrong headed and dangerous views expressed in the Physician Charter.See here.

http://mdredux.blogspot.com/2016/07/is-new-professionalism-and-acps-new.html

Dr.Martin Samuels ,Harvard neurologist, master teacher and lecturer,  expresses his views regarding the issue of who does the physician serve. Which master? See here.

Is the patient or "society" the master? Dr Michel Accad dissects  the related dangerous  notion of population medicine here.


h/t Notes from Dr. RW blog  See here.

Inadequate warfarin dosing may be worse than no warfarin in regard to stroke severity

Sokomoto et al (1) investigated the relationship between adequacy of warfarin dosing and severity of stroke in patients with atrial fibrillation. Inadequate was defined as INR less than 2.0 ( less than 1.6 for patients older than 70 years.)

They studied 477 patients with atrial fibrillation (AF) and acute ischemic stroke,53 of whom were undertreated. Inadequate or insufficient dose of warfarin was present in 53 patients and the odds ratio for a severe stroke was 2.7. The numbers in the study were fairly small but  other research had demonstrated a similar pattern.

The authors suggested that underlying pathophysiology or pharmacologic explanation related to the vitamin K dependent anticoagulant protein,Protein C. Protein C levels decrease earlier and with lower doses of warfarin than do the other vitamin K dependent clotting proteins. So early on in warfarin therapy there may be a procoagulant effect. This was why  in the not-too-long ago-days physicians would treat thromboembolism with a few days of heparin along with the warfarin. Too little warfarin may be more of a pro than an anticoagulant medication.

So we have still another reason why the newer oral  direct acting anticoagulants are better than warfarin.




1) Sakamoto, Y et al, Insufficient warfarin therapy is associated with higher severity of stroke than non anticoagulation in patients with atrial fibrillation and acute anterior-circulation Stroke

Circulation Journal Official Journal of the Japanese Circulation society. 2017 December.

All Left bundle Branch Blocks are not the same

The vast majority of patients with an EKG pattern of LBBB have structural heart disease,that is myocardial disease as opposed to disease only involving the conduction system which  is found in a very small minority-usually estimated to be about 1 % of LBBB cases.

It has been  recognized that some patients with isolated or lone LBBB will over a variable period of time develop a cardiomyopathy.The few clinical reports of  this condition suggests delays of up to over twenty years and often dramatic resolution of heart failure with cardiac resynchronization therapy. ( ref 2)

LBBB is associated with  inter-ventricular and intra-ventricular loss of synchrony, the later being more deleterious to cardiac function. Normally the various areas of segments of the left ventricle contract in sync. In LBBB the typically described or stylized  pattern of abnormal septal motion is : there is early contraction of the septal wall with concomitant bulging of the lateral left ventricular wall followed by late contraction of the lateral wall and bulging of the septum.The delayed ventricular contraction is followed by delayed relaxation of the left ventricle.


Han et al  ( ref 1) using tagged cine cardiac MR described 2 different patterns of abnormal septal movement in patients with LBBB.Interestingly in 2 of the  10 patients there was no septal dyskinesia at all. In some cases ( 50%) of LBBB there was dyskinesia of the entire septum while in others only the anterior septum was dyskinetic.This may at least partially explain why some patients with LLLB have little if any exercise intolerance over many years while other notice a decrease in exercise capacity soon after the onset of LBBB as was the situation in my own case and two others with whom I have had blog level correspondence.


Also animal experiments inducing LBBB have shown a rapid and often significant decrease in left ventricular function soon after the onset of LBBB.Perhaps the key is the presence or absence of the normal left to right activation of the interventricular septum and the degree to which conduction across the septum is delayed.The abnormal septal movement is the basis for the echocardiographic finding of "septal flash"

Of course the real game changer element of LBBB story is the capability of His Bundle pacing to "fix" LBBB  , at least in a significant number of patients with LBBB.


1) Han Y et al Circumferential myocardial strain in cardiomyopathy with and without Left bundle branch block. J. of cardiovascular magnetic resonance .Jan 5 2010, doi:101186/1532-42.9x-12.7
full text available on line.

2) Vaillent C et al  Resolution of left bundle branch block induced cardiomyopathy by cardiac resynchronization therapy. J Am College Cardiology 2013 vol 61 1089