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Archive for the ‘aortic stenosis’ Category

Syncope is a classical feature of LVOT obstruction especially with valvular aortic stenosis.The mechanism of exertional syncope in Aortic stenosis is traditionally attributable to the fixed obstruction .This fixed obstruction is not able to cope up with increased cardiac output as demanded by the exercising muscles . But exercise  induced reflex as well as local vaso-dilatation mechanism is intact . The consequence is predictable. A critical fall in SVR amidst a obstructed LVOT precipitating a syncope.

However , If the above mechanism is the sole reason for syncope in Aortic stenosis , we have a problem to explain why syncope is  rare even in critical mitral stenosis which is also fixed LV inflow obstruction ?

Is there some thing unique in LVOT obstruction that causes syncope ?

No, it is nothing to do with LVOT .To generate a true pathological syncope, reduction in cardiac output per-se may not be enough . It appears there should be an inappropriate systemic vasodilatation as well to precipitate a syncope.This can happen only if the parasympathetic system gets activated by some means . The trigger is located in the mechano- receptors of left ventricle . Hypertophied left ventricle with high Intra cavitory pressure (Often above 200mmhg) generated due to LVOT obstruction activates the syncope circuit.The same rule may apply for RVOT as well .One could get syncope with critical valvular PS or severe pulmonary hypertension when RV mechanical receptors get a triggered.

What happens in mitral stenosis ?

In mitral stenosis , LV is under- filled ,  wall thickness is normal .There is little likely-hood of LV mechno-receptors to get stimulated as the LV wall stress is normal. This is the reason syncope is less common in mitral stenosis. However , this is not  absolute rule , syncope can still occur in severely narrowed orifice of mitral valve due to low flow state alone or a ball valve thrombus and paroxysms of arrhythmia .

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Aortic stenosis is diagnosed by 2D valve morphology, area ,and pressure gradient across the aortic valve.Though anatomical 2D images and indices are good enough to diagnose severe AS , we are obsessed *  with pressures  which are subjected moment to moment hemodynamic and contractile variables. To record a good gradient we need a normally contracting ventricle and good flow across the narrowed LVOT. If any one of the is critically compromised  gradients can’t be picked up by Doppler.(A new entity of AS was recently included , which fails to generate the gradient in spite of good LV function and the AS being significant.)

So ,whenever one records a “Low gradient AS” there are 4 distinct possibilities.

  1. Truly mild AS
  2. Technical inadequate Doppler alignment , with possible true moderate /severe anatomical  AS .
  3. Low gradient AS due to LV dysfunction, with true moderate /severe anatomical AS
  4. Low gradient AS with Low flow but normal LV function, with true anatomically moderate/severe AS

Echocardiographer should rule out 1 and 2 before going to the complex world of low gradient severe AS.In my personal opinion , the entity of Low flow , Low gradient with Normal LV function appear  redundant ( or is it beyond my understanding ) .One should look at the valve morphology and decide in such situations.

Then , one will shortly bump into this query  is it 2 or 4 ?

How to differentiate a  technically defective  recording  of low gradient AS  from  true low flow due to narrowed LVOT.(Low gradient for me , high gradient for my professor !)

Now, basic readers  may please leave ,

Few inquisitive may ask   ( naturally though)

Does the ” low flow -low gradient AS”  is an exclusive phenomenon  that can occur only with normal LV function  or can it  occur in  dysfunctional left ventricle as well ,  who also have small cavity size and narrow LVOT  ?  (Within the low gradient AS due to LV dysfunction subset ,  How much is attributable  due to anatomial low flow  and how much is related to depressed LV contractile force ?)

Another googly . . .

Why can’t  Doubutamine* stress test  routinely  undertaken in the subset of patients with  with subjects with Low gradient /normal LV function to augment the anatomical low flow and find whether it is true  low flow or not ? *This would mean , a most impractical situation wherein every patient  with even mild AS should need to undergo dobutamine testing to rule out significant AS.

Final message

As of now ,this new concept   “Low flow , Low gradient, with Normal LV function” appears an  intellectual excess with little impact on patient outcome.The proposed new entity ultimately increase the likelyhood of over diagnosing  severe AS.Iam still expecting  more clarity  on the issue. ( or else for the moment forget the pressures and  simply fall back on  a meticulous assessment of 2D valve morphology and take a call , you will be surprised how often we get into man made scientific traps. )

Reference

1.Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction.Pibarot P1, Dumesnil JG.J Am Coll Cardiol. 2012 Nov 6;60(19):1845-53

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