Archive for the ‘Aortic diseases’ 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. )


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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Degenerative Aortic stenosis occur with either normal  or congenitally malformed/ bicuspid valve.This contributes to the major chunk of  aortic valve surgeries and interventions (TAVR) in elderly population  . The optimal  timing of aortic valve replacement in patients with AS is debatable inspite of  well formed guidelines.

Three factors determine it .Symptoms , severity of aortic valve narrowing  and the tactness of LV function .The last parameter is a tricky one .We used to think in the past , severe LV dysfunction is a contraindication to aortic valve surgery. Now we realise ,however severe the LV dysfunction may be , relieving the obstruction will benefit  the patient and  the LV function is  also  likely to improve.

Cardiac physicians  face a dilemma when confronted with a patient  with low gradient and severe LV dysfunction .In this situation they are advised to do doubtamine stress Echo and watch for the gradient .If the gradient  increases that would  imply true fixed stenosis . (In pseudo aortic stenosis increased contractility opens the aortic valve and gradient will fall )

While this concept appears simple .There  are few  important issues that goes unaddressed  as we have not yet fully understood the  mechanism of LV dysfunction in aortic stenosis .(Link to mechansim of LV dysfunction in Aortic stenosis.)

At what degree of aortic stenosis LV goes down fighting and fail to generate the required  gradient ?

Myocardial function  and behaviour at times of hemodynamic stress can be highly  variable and most of us believe it is determined primarily by the genetic switches of myosin and other contractile elements .This is naturally proven at times of hypertensive left ventricular failure (Only in a fraction of the hypertensive population  LV is set to fail  when BP acutely raises.)

Proposed concept

Considering the complexities in cardiac mechanics , hemodynamics (and not to forget the vast control exhibited by genetic imprints over the hemodynamic behavior of LV) , it seems highly plausible even mild degrees of Aortic stenosis can inflict significant myocardial dysfunction in certain patients . Hence the phenomenon of pseudo aortic stenosis needs further critical analysis If this is proven to be true there could be a realistic indication for aortic valve intervention even in patient with low gradient / true Mild AS with LV dysfunction.
A word of caution is required .Relying too much (Which we often do ) on gradients in the assessment of aortic stenosis has skewed our common sense. Its wiser to have a  meaningful look at the valve morphology . A normal appearing  valve in 2D can never cause significant stenosis. Pressure recovery phenomenon also is to be given due respect as it over estimates gradient .This will effectively avoid surprises and guilt on table when we find a relatively good looking valve posted for AVR /TAVI

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The gradient across coarctation  is not  simply (& solely ) determined by degree of obstruction , as one would believe.Understanding the hemodynamics and various factors that can influence the gradient is essential Relieving the  obstruction /gradient by stent or surgery  may not be synonymous with successful treatment as we understand now the entire aorta right from the root to abdomen can influence the gradient ,along with systemic factors.We also know , some of these patients harbor histological abnormalities in the entire stretch of  Aorta , what is  being  referred to as pan aortopathy  , that may influence the long-term outcome.

coarctation gradient collaterals002

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We know aortic regurgitation causes  a deluge of   hugely popular peripheral signs of aortic run off  , which are taught  right from 2nd year medical school.

aortic runoof

When the aorta  leaks it reflects in the entire vascular tree .How is that a  leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?


Is the blood in the finger  trying to follow  the regurgitant  jet  that  go back into left ventricle ? Does the to and fro murmur of  Duroziez over the  femoral artery imply  there is reversal of  blood flow in femoral artery ?

Things are  little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is  dramatically low in chronic  severe AR  by a reflex phenomenon ,  as cardiac out put is increased and vascular tree adopt to it. So, with each  beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of  blood runs off , as if it goes in a free way  making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR  are due to the peripheral mechanisms rather than primary event of aortic run off  into left ventricle.

Why carotid pulse does not show the collapsible nature of  pulse in AR  ?

If aortic leak into LV  is the dominant mechanism ,  carotid  artery should obviously manifest a collapse ,but it doesn’t  ,as carotid has no direct continuity with the  peripheral low resistance circuit

What is the hemo-dynamic  correlates of    descending  aortic flow reversal  in  severe AR ?

The central vascular tree  manifest  some  reversal till the regurgitant  velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise  it is only  the wave form that get reversed  not the actual blood stream.( The momentum gained in systole  continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are  absent in acute AR ?

Acute AR even if it’s  significant does not cause a collapsing  pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.


Answering  the title question ,the mechanism of  Aortic run off  in AR is both central and peripheral.  However  clinical  signs are largely due to high cardiac out put and the resultant   adaptive  response  of the  vascular tree due to low  systemic   vascular  resistance  triggered by  reflex  dilatation of small arterioles of the  peripheral vascular bed.


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Meticulous Aortic imaging is vital for assessing  atherosclerotic plaques in stroke evaluation ,  aneurysms of aorta ( Both dissecting and non dissecting.) and during aortic surgeries. Peri  procedural  aortic imaging has become mandatory in many of the complex aortic endovascular repair as well .

TEE is an extremely useful investigation and has revolutiolised our appraoch to aortic disorders .

However , we have an issue .

blind spot for tee in aortic imaging distal ascending aorta and proximal arch bracho cephalic trunk

How to overcome it ?

During peri-operative TEE a simple but innovative idea is to displace  the tracheal air with saline filled balloon and capture the aortic arch with ultra sound . What a way to un-blind our vision deep inside the thorax  !

A specific catheter is available for this purpose .

a view endo tracheal balloon catheter how to overcome the aortic blind spot in tee

Product catalog

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What happens to diastolic blood pressure in severe Aortic stenosis ?

Traditional answer: The diastolic BP remain unchanged. Only systolic BP falls as it is related to LV  stroke volume .(What we refer to as systolic decapitation of BP  )

Reasoning :Diastolic BP is related to peripheral vascular resistance , hence aortic stenosis has  little impact on diastolic BP .

 Further analysis

If we assume only the systolic blood pressure  is bound to decrease in  AS , at one  critical point of time*  systolic BP  should  approach  the diastolic pressure and pulse pressure should approach zero .This can not happen , hence at that point  diastolic pressure will also fall.

*What is that  point ?

No one really knows !

Correct answer

In severe aortic stenosis  both systolic and diastolic pressure falls , but the fall in systolic BP is more striking .

* Though it is customary for clinicians  to discuss them in isolation both systolic and diastolic  blood pressure are closely coupled parameters..In the absence of peripheral run off one of the  strong determinant of diastolic BP  is . . .  systolic BP !

Complex concepts

1. What happens in combined aortic stenosis and regurgitation ?

In  combined AS and AR   we get  pulsus bisferiens. implying  AR will  elevate the systolic blood pressure in spite of obstruction.

2.What happens in associated systemic Hypertension  and aortic stenosis . (Which is very common combo in elderly )

Since HT will increase the  aortic pressure , the LV-Aorta gradient tend to fall.

However ,this  does not happen always as if the original cause for HT was  dependent  more on the stroke volume rather than peripheral mechanisms .

3. Aortic stenosis with aortic  atherosclerosis .

A stiff aorta augments the percussion wave amplifying the symbolic BP and blunting the  classical anacrotic pulse of AS.

4.What happens to BP  during exercise in  severe AS ?

Exercise demands raise in systolic BP and temporary reduction in diastolic BP due to peripheral  vaso dilatation in exercising muscles.

If a fixed  crtical AS does not allow the systolic BP to raise  as required , diastolic continue to fall pulse pressure should still become wide .

Excercise testing is a tricky business in AS. Some have attempted it to assess the functional capacity.(Read below)



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