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Significance of low fractional shortening for pulmonic stenosis?

  • 1yr old FS Bull mastiff
  • Diagnosed with mild pulmonic stenosis at 8 weeks of age. 
  • No clinical signs, LA normal, PA inflow vel ~3m/s, PA regurg vel ~ 1.9m/s, normal EPSS
  • FS is however decreased at 19%, last FS measured at 8 weeks old was 31%
  • I’ve just started learning about echo, am unsure how to interpret the results. 
  • My understanding is: FS is affected by preload, afterload and contractility
  • LVIDs is increased at 1.39 (0.71-1.26)–cornell normalized ref value, is that the reason? 
  • Should I be worried? Dog is asymptomatic.

Thank you!

 

 

lookpris

6 responses to “Significance of low fractional shortening for pulmonic stenosis?”

  1.  
     

    I would check the lv mmode in multiple views as its likely the fs% is artifically low. Im eyeballing about 30-35% on your video. If you measure near the heart base the fs% drops but the closer you get to the papillaries the fs% increases so check in multiple views short and long axis. Also double check the pulm outflow velocity as velocities over 5 m/sec are severe which bring on eventual myocardial failure which drops fs% in that progression so you wont have fs% drop withoout the failure owing to high gradients unless failing for another reason. If velocity is in th e3 m/sec either its mild/moderate or you are offline on your doppler. The ps looks pretty dramatic here so try getting more rvot velocities and see if you get near 5 m/sec first.

    Also typically low grade clinical signs occur when fs% approaches 20%

     

  2. Hi!

    I think the FS is higher than you measured. Always measure from 4-chamber LAX and from SAX views. I don’t think that the PS is severe because the RV is not very hypertrophied but I would still re-check it. The left ventricle looks a bit under-loaded (decreased preload). This can cause a decreased contraction force due to a less activated Frank-Starling mechanism.

    Don’t worry too much about the FS 🙂 

     

    Peter

  3. Hi EL,

    Thanks for the reply. That makes sense about measuring LV at different views. I’ve attached a few more RVOT vel. I tend to take the highest velocity measured assuming the doppler velocity can always be higher than measured?- is that correct?

    But it definitely was not near the 5m/s.

     

    Thanks for the feedback!

  4. Thanks for the feedback Pete! Will be doing both LAX and SAX in future.

    So is it safe to assume that if RV is hypertrophied (in comparison to LV) that PS is severe?

  5. Hmm I see PI  in your last image and only minor elevated pa velocities. Something else must be going on because ps at those views should be much higher like 4-5 m/sec not 2 m/sec. Either simple PI and TR asboth valves are dysplastic. No vsd anywhere right?

  6. Basically, if there is concentric RV hypertrophy present (thickened myocardium without dilation), there must be

    -) either a congenital obstruction to RV outflow (i.e. pulmonic stenosis, congenital pulmonary vascular disease, double chambered right ventricle)#

    -) or a very slowly and chronically progressive increase in pulmonary arterial pressure like in Westies with pulmonary hypertension due to pulmonary fibrosis. Note that other forms of pulmonary hypertension develop more rapidly causing rather dilation than concentric hypertrophy of the right ventricle (e.g. pulmonary hypertension due to pulmonary thrombembolism, overcirculation (e.g. PDA), or heart worms.

    The degree of right ventricular hypertrophy reflects the severity of pulmonic stenosis. A severe stenosis causes severe hypertrophy. A mild stenosis usually does not cause noticable hypertrophy. U can use this to estimate the correctness of your Doppler measurements.

    Best regards

     

    Peter

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