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Archive for the ‘aortic stenosis’ Category

Aortic stenosis evaluation was simple in our days. Gradients across the valve were the key. Now, we have more parameters to bother about. Dynamic AVOs, flow state, resting LV function, contractile reserves, GLS, dobutamine response, etc. MRI assessment will soon overtake echocardiography. 

Hemodynamics of flow across LVOT. MRI 4D volumetric model of normal Aortic stenotic flow in the bicuspid valve (On the left). The more we know, the more we tend to miss! Image courtesy: Northwestern Medicine

The current AS algorithms, though scientific, I am afraid, appear much complicated with some frightening terminologies at least for the beginner. One such category is PLF-LG-AG.

Let us first answer this. What is LG-AS?

We diagnose a case of significant aortic stenosis but desperately miss to pick an adequate gradient across the valve. It is indeed a low gradient AS, still, you are not convinced, since the 2D look of the valve looks severe. Then you find the culprit. It is the dysfunctional ventricle pulling down the gradient. This is called  LG-AS.(one type )

*What is paradoxical -Low flow-Low gradient Aortic stenosis? (PLF-LG AS)

Now, we have another patient. Again it is  LG-AS, but the LV function and EF are normal. Now, you get confused and label it as PLF-LG-AS. 

PLF-LG AS is known to account for approximately one-third of patients with severe AS and preserved LV EF.PLF-LG severe AS is defined by AVA <1.0 cm2, indexed AVA <0.6 cm2/m2, mean gradient <40 mmHg, LV EF ≥50%, and low transvalvular flow (indexed stroke volume <35 mL/m2).

What is the paradox?

AS is severe, but the gradient is not showing at the valve. Wait, don’t think that is the paradox, since this can happen in any category of LG-AS.  So, the real paradox in PLF-LG-AS denotes to the fact that the gradient is low, in spite of normal LV  function (Rather, normal EF %)

Why the paradox? Why gradient is not showing? (In spite of good Ejection fraction ?) 

  • Reduced stroke volume increased afterload due to associated HT are the major hemodynamic mechanisms of PLF-LG AS.
  • The low-flow state can be related to small LV cavity 
  • Significant diastolic dysfunction (Associated Amyloidosis is a new age problem kid on the block. EF is not the only parameter that can compromise the flow you know !)
  • Atrial fibrillation (Ofcourse some cycles will pick up the high gradients, but are they spuriously low or high is the question  ) 
  • Associated mitral valve disease leaks, as well as blocks, will ration the flow to LVOT.

*Finally, every cardiologist should be aware of the following two subsets that could wrongly enter this conundrum of PLF-LG-AS  without much fanfare but with lots of implications.

1. Most importantly, technical issues are the key confounders. Malaligned  LV / LVOT with that of distorted out-of-plane AVO is the commonest cause of failure to pick up the gradient. (Never diagnose PLF-LG-AS  without confirming it is not due to technical ). A tip: Don’t complete AS doppler study without a meticulous search for a good doppler signal from the suprasternal/right parasternal window. 

2. Next one can be named with a provocative term “Paranoid aortic stenosis*”. Once, a  fellow was reporting a shabby-looking calcific valve as low gradient, severe AS with normal LV function. He made this diagnosis solely based on AVO. Later, when it was assessed more scrupulously it turned out to be a true mild aortic stenosis, and none of the decorative echo features he was showing were really pathological. It was an error in the aortic valve area calculation due to LVOT area/VTI measurement errors that got mathematically amplified. An important teaching point emerged from this echo lab fiasco. Mind you, any true mild aortic stenosis (If the area calculation is wrong for some reason) will readily fulfill the criteria of PLF-LG-AS. One simple tip: Never diagnose severe Aortic stenosis without significant LVH.

What is the role of Doubtamine stress echo in PLF-LG-AS ?

It does help in both forms of LG-AS. You need to read about the contractile reserve, the response of dobutamine to flow (Cardiac index), gradient, and the valve area.

How to manage PLF-LG-AS ?

Many of them might be argued to end up in TAVR. So, follow the guidelines carefully but don’t apply them blindly

Final message 

In the evaluation of Aortic stenosis let’s make things simple. Gradients are indeed important. But, realize Doppler gives only pressure data. Converting them to flow and volume data is always error-prone. Instead, let us believe our eyes too.(Need not always depend on o MDCT vision)  Concentrate more on LV morphology, valve pathology, and careful assessment of LV function, finally take a decision to intervene based on true symptomatology and comorbidity.

Reference 

1. For the most authentic knowledge base

2.An excellent review on the topic 

Guzzetti Ezequiel Frontiers in Cardiovascular Medicine 2020

Further thoughts

Is there a “high flow-high gradient”- True mild AS?

High gradients across the AV  generally do not cause much confusion. If the mean gradient is > 40mmhg Aortic stenosis is always severe. Is that right ?. I think so. Exercise-induced paradoxical high flow high gradient AS as an entity is not reported as such. But, what really can happen in high output states, hyper contractile ventricles with high EF? We have observed doppler gradients overestimate the severity of Aortic stenosis. I think there is some dynamic component even in the so-called fixed valvular AS that alters the gradient in response to flow. Do we have proof for this?  OMG, it’s right there in echo lab every day, we are failing to notice it. Look at the AS gradients during AF. It is changing every beat, right.

 

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It was the final case on weekend Echocardiogram review day, I asked my fellow for a brief summary of the patient. 

A 5 -minute conversation

“Yes, sir, he is a 62-year-old male retired govt officer. He has a severely stenosed aortic valve, with a peak gradient of 90 mmHg and a mean gradient that comes to almost 50 mmHg. LV  EF is 58%, GLS is 18, LVH is obvious. LA is not dilated (Didn’t measure volume though), but DT is short. Valve orifice is hovering around 1cm, mild calcium noted in LCC  I am not sure whether it’s bi or tricuspid still. The annulus is 22mm. The mitral valve is perfect, no calcium spill over to the mitral curtain and the rest of the annulus”.

“That is ok, what for he has come”?

“A GP from Tambaram has referred him after he detected a murmur over the chest”.

“Oh Ok. What are his symptoms”?

“He is denying any symptoms”.  

“Are you sure? did you ask him specifically about it during exertion”? 

“Yes, he says he can climb 3 flights of stairs. (In fact, he was sort of amused when I told him to be frank in his expression,since  he has a potentially serious obstruction in the main valve that connects his heart and body.”

“I agree, but his reaction was not inappropriate I thought, after all, he didn’t feel any symptoms right”. “So what shall we do for him?  TAVR? SAVR? or Leave him alone? Shall we put him on the treadmill? to document symptoms? Is it that risky”? 

“But , he says he can walk for a mile or two every day” 

“That’s fine. Can you really predict when his ventricle will fail and he may land up in a semi-emergency surgery?

“I think we can’t,  but why is he is so asymptomatic sir”?

“Wow, that’s more than a million-dollar question. You need to address that query to the vascular Goddess. I don’t know the answer.It is all about the ability of the heart to perfectly balance the ventricle and aorta in spite of severe obstruction. It is something like TIMI 3 flow and good FFR  in a patient with 90% occlusion.) My guess is, the LV does this by modulation of systemic pressure &  resistance in such a way , it neither feels the strain nor does it reduce the stroke volume much. By the way,  have you heard about this ? Z- Va score. I would like you to read about that. It will help you understand the hemodynamic nuances of severe AS and how the ventricle manages to serially couple the afterload of the vascular system”. 

“Make a pardon sir, I haven’t heard about it. What is Zva? 

“Never mind. It is not a new index. Was first introduced 16-years ago by Martin Briand et al from Quebec, heart Institute Canada  J Am Coll Cardiol 2005 Jul 19;46(2):291-8.  Z Va score(Valvulo-Arterial) is the collective flow impedance of the aortic valve and the entire aorta. It is more attractively defined as the cost of blood pressure in mmHg for pushing one ml of blood per body square meter area

Formula for Z va : (Systolic BP × Mean gradient)/ Stroke volume Index

Unit : mmhg /ml/m²

Normal value:  < 3.5 to 4.5 (Actually no normality, rather it must be acceptable value .It is still being defined )  if the cost is more than 5mmhg it suggests significant Aortic stenosis) A high value > 4.5 is a definite index of poor outcome. In a well-compensated heart, Zva is maintained far less than 5 and many such patients are asymptomatic as well. Zva has specific clinical value in all critical AS especially so if they are asymptomatic. It is no longer a research topic, has an important role in the bedside too. Here is an excellent resource on Z Va score from ESC.

 

Final message 

The timing of AVR in aortic stenosis is very critical. All symptomatic severe AS must be immediately intervened. Currently, with surgical risk falling rapidly ( & the option of TAVR looming large) even many of the asymptomatic AS need to be considered for valve intervention at the earliest before or at the onset of LV dysfunction. Zva’s score will definitely add more light to our  limited hemodynamic wisdom in aortic stenosis(Zeineb Hachicha  JACC 2019) 

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Severe aortic stenosis will cut off the systolic BP and hence classical pulsus parvus et tardus occurs. This is what , we have been taught all along.

How for it is true?  

One thing is clear from clinical observation. Systolic BP need not be low, often its normal even in severe Aortic stenosis. The issue becomes curious when  high BP is associated with severe Aortic stenosis. This can happen by a variety of mechanisms.(Aging/Loss of Aortic elasticity /Pressure recovery/Hypertension)  I think, there have been little correlative studies of pulsus parvus with central aortic pressure.

Can Aortic stenosis be a cause for systolic Hypertension?   (This academically murky question rose after I stumbled upon this paper )

This paper from the journal of Human Hypertension which was published many decades ago.It sincerely documented high BP in spite of severe AS . The most crucial aspect of this study , however, was the fact that hypertension was completely corrected after Aortic valve replacement. The authors attributed to this high systolic BP as the transmission of LV chamber pressure. This is a frontal attack on the traditional concept of pulsus parvus and systolic decapitation in LVOT obstruction.

I am not sure, whether knowledge always breeds knowledge. Medical science is equally affected by new-onset Ignorance or not recognizing past knowledge.( Like this paper of 1996.) I think this study is done with a good scientific basis and unable to find any serious flaws. Hats of to the authors. This could lead to a further breakthrough in our understanding of transvalvular gradients in Aortic stenosis and the poorly understood vascular- valvular Interactions. With, catheter-based TAVRs become so common, we can exactly measure the pressure dynamics in the Aortic root pre and post valve replacement. (* My take is , systolic BP in severe Aortic stenosis  is preserved until the onset of LV dysfunction)

Reference

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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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