I would like what is the methods you are using to evaluate paradoxical low flow low gradient aortic stenosis
The best parameter, in my opinion, is the Global Longitudinal Strain, which is severely reduced when the EF is still normal.
Integrative approach is recommended (included stress echo Dobutamine).
I'm intrigued by the dobutamine stress suggestion. Principally because I'm only aware of 1 publication (JSACC Imaging recently that examined this. We do use low dose dobutamine in the low flow low LVEF, but have not used it routinely in the low flow normal LVEF group.
Can you explain what you do with the results- do you also use a 'normalized flow' AVA as in the JACC Imaging paper. Seems very cumbersome to do, we've done it a few times.
Thanks
...if the EF is normal .. nor Dobutamine stress neither stroke volume or DVI can discover the initial impairment of myocardial function,... an other good tool to revel it is the dP/dt , if a MR is present. But ...I confirm that GLS can reveal why the assessed severe AS ( low valve area detected by continuity equation with normal EF ) is a real and is one of the most dangerous condition because the LV can fall in a short time leading the patient to death.. that's why in this condition valve replacemet is more urgent than in common LFLG AS. The LGS is the best parameter, in my opinion.
Certainly a difficult group to assess how severe the AS is. We tend to use an integrative approach of remeasuring all the echo values (LVOT diam, LVOT VTI, AV VTI). Agree that stroke volume index is key, but also would look into ZVa (sometimes patient's hypertension causes AV gradients to be reduced) and GLS. There is also data using MAPSE to assess the degree of myocardial fibrosis and differentiating the groups (Hermann JACC 2009). Other imaging modality that we have used selectively is non-contrast CT to assess the AV calcium score (recently shown to be important, Clavel JACC 2013). It's a complex group of patients that tend to have other comorbidities aside from AS. We have only done DSE for PLFLG in few selected cases.
DSE in this patients can be also used also to estimate operative mortality
In my opinion LFLG and normal EF by echo should not be a
final diagnosis. We know that echo might underestimate
LVOT diameter and even more its area leading to overestimation
of severe AS prevalence. This might be a ideal clinical model where
integrate multimidality imaging. AVA by TT echo might be confirmed by
CT valvular calcium score or by AVA measured using MRI or TEE or cath.
Alternatively the low flow state might be' confirmed by 3D or CT or MRI
ventricular volume measurement.
The explanation could be both a systolic or diastolic "subtle" impairement. That is why I think that an integrative approach using both LGS and stroke volume index ( could be reduced also due to diastolic dysfunction) should be used.
It's not easy...but I go for low-dose dobutamine stress echo and/or 3D TEE to calculate the morphological area
... I confirm that only the Logitudinal Global Strain (LGS) is able to reveal that that LV is not able to produce a good gradient despite the preserved EF. In paradoxical AS U find always a very reduced LGS . And the continuity formula is still valid.
Severe AS can produce a low accelerate stoke volume, although the cardiac output keep normal. The fow have a "disacceleration", but the volume is normal. In these cases, the risk of syncope or sudden death increase. I agre with doctors that suggested a integrative approach and very common necessity of immediate surgical treatment.
Dobutamine stress Echo is a useful tool in this situation and is used in our institution as has been alluded to by several others.
DSE can only give the best answer in LGSAS, planimetry on TEE can be misleading in poor LV and low cardiac output situation.
1. First, doublecheck the LVOT diameter on Echo and the aortic gradients (use a stand alone CW probe), to avoid potential source of error. Evaluate energy loss index in case the ascending aorta has a diameter
I recommend the follwing strategy to find out the real degree of AS (and this is the main goal, right?) in any situation of stroke volume (SV) (low, normal, high), echocardiographically:
1. measure the velocities and gradients (mean and peak pressure gradients) and the velocity time integrals
2. measure the subvalv. diameter as exactly as possible
3. calculate the effective valve opening area (AVA) out of these parameters using the continuity equation as AVA is nearly independent from SV!
4. try to evaluate the opening area by planimetry in TTE or even TEE as exactly as possible.
5. make plausibility controls of your measures and calculations:
The interpretation of the degree of the AS now depends on the combination of the subvalv. velocity (low appr. appr. 1.2 m/s), the subvalv. diameter (narrow, normal, wide), the valvular velocity (and corresponding gradients) and most important the effective valve opening areas and the SV.
It is possible to have low gradients in severe AS even in good LV function (small narrow LV with reduced output). So the main parameter is the opening area combined with the estimation of the SV.
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