– 1 year, 3 month old Dutch Shephard presented with a grade 3-4 systolic murmur, not clinical for heart disease and just spayed with no anesthetic concerns
– echo shows SAS with a fibrous ridge at the entrance of the LVOT, aortic widening, AI and MR
– the LV walls and chamber normal in diastole, no LAE (so compensated) – mitral valves look normal
– Aortic Max Velocity 3.6 m/s (PG 52.1 mmHG) (could not get a subcostal view due to patient’s tensing)
Some questions:
– 1 year, 3 month old Dutch Shephard presented with a grade 3-4 systolic murmur, not clinical for heart disease and just spayed with no anesthetic concerns
– echo shows SAS with a fibrous ridge at the entrance of the LVOT, aortic widening, AI and MR
– the LV walls and chamber normal in diastole, no LAE (so compensated) – mitral valves look normal
– Aortic Max Velocity 3.6 m/s (PG 52.1 mmHG) (could not get a subcostal view due to patient’s tensing)
Some questions:
1. I can not find a consistent reference on how to grade this SAS (all over the map!) – mild? mild-moderate? moderate?
2. When should a repeat echo, if any, be recommended?
3. Are antibiotics currently in vogue to be given before dental procedures due to increased risk of endocarditis?
Comments
I did some research in the
I did some research in the second edition of June Boons Veterinary Echocardiogrphy.
It appears that there are multiple ways to judge the severity of a SAS. I will list a few.
2D:
Cross-Secrional Area of Stenosis:
Area at transverse obstruction
Area at sinus of Valsalva
Normal LOT: AO= 0.509-.737
0.3-0.5= modrate severity, < 0.3= severe stenosis, > 0.5= mild stenosisi
Useful in low or high stroke volume settings with overlap betwen normal and mild
Note: Degree of Left Ventricular Hypertrophy in SAS does not correlate well with severity.
Doppler:
AO flow profile in SAS:
-Severe SAS rounded profile- no longer rapid accleration
-Dynamic componnt- late peaking flow
SAS severity based on Pressure Gradient:
– < 50 mm Hg= mild
-> 50 mm Hg but < 80-90= moderate
->80-90 mm Hg = severe
Pressure gradients will be affected by:
1. Aortic insufficiency
2. Mitral regurgitation
3. Placement of the continuous wave cursor. L apical aortic measurements tend to underestimate velocity by 26%. Sub Xyphoid meaurements are usually higher.
In your dog there is no sign of concentric hyprtrophy at this time. Your CW profile is still peaking an not rounded. The pressure gradient that you measured would be a bit over 50 which would make the stenosis moderate (but this may be underestimated). I would also guess the cross sectional area ratio would indicate moderate SAS.
Now we can weigh in with the experts.
Thanks Randy – I used those
Thanks Randy – I used those cut-off pressure gradients you listed in this case and called it mild-moderate myself. I didn’t do all those other fancy measurements : )
For those that don’t have the
For those that don’t have the Curbside guide https://sonopath.com/products/book
here is the section on SAS and should answer your question JP
Subvalvular Aortic Stenosis
http://www.sonopath.com/SAS
http://www.sonopath.com/EchoModler
Description: Subvalvular aortic stenosis (SAS) is the second most common heart defect in dogs and is more common in larger breeds, such as the Newfoundland, Golden Retriever, Boxer, and Rottweiler.
Clinical Signs: Primary clinical signs include an ejection character heart-based murmur, syncope, and occasionally congestive heart failure (CHF). Hypokinetic pulses may be present in more advanced cases. Primary differentials include pulmonic stenosis, ventricular septal defect, mitral regurgitation, patent ductus arteriosus, and an idiopathic flow murmur. SAS patients are predisposed to bacterial endocarditis and necessitate prolonged antibiotic therapy during surgical and dental procedures as well as under circumstances where an infection, such as pyoderma, pyometra, or a UTI, may be present.
Diagnostics: Radiographs may present as completely normal or they can reveal an aortic bulge as well as left atrial and ventricular enlargement. Pulmonary venous congestion and CHF are also sometimes detected.
Ascertaining NT-proBNP levels may be useful in young puppies with murmurs as a means of screening for congenital anomalies. One study showed that median NT-proBNP levels in dogs with SAS were 833 pmol/L compared to 333 pmol/l for normal dogs. Although NT-proBNP is not specific for SAS, an elevated level should prompt additional diagnostic tests and echocardiography in particular.
Moderate to severe SAS is easily confirmed by 2D or Doppler echocardiography. Typical findings include concentric left ventricular hypertrophy, a subvalvular obstructing lesion, and poststenotic dilation of the aorta. The papillary muscles and endocardial surface of the ventricular myocardium often appear hyperechoic, presumably because of myocardial ischemia and replacement fibrosis or calcification. Structural changes in the mitral valve can often be appreciated and abnormal motion of the mitral valve (systolic anterior motion) can be detected in those dogs with coexisting mitral valve dysplasia and dynamic obstruction. Spectral Doppler measures the peak velocity of flow in the left ventricular outflow tract (LVOT). It is performed to assess disease severity; the results correlate closely with those obtained using invasive measures. Although Doppler-estimated pressure gradients between 80 and 100 mm Hg (peak flow velocities ranging from 4.5-5.0 m/s) are taken to indicate moderate LVOT obstruction and higher velocities more severe obstructions, these designations are somewhat arbitrary. Doppler color flow recordings are valuable for detecting and estimating the severity of any coexisting aortic or mitral valve insufficiency. The detection of mild SAS by echocardiography is often not possible as dogs with subtle abnormalities may escape detection by even the most accomplished examiners. A diagnosis of mild SAS is more secure when mildly elevated velocity measures are accompanied by disturbed flow, an anatomic lesion is visible, or velocity flow suddenly accelerates over a discrete region in the LVOT.
Treatment: Both moderate and severe cases of SAS are at risk for sudden death. Medical therapy with a beta blocker (e.g. atenolol at 0.5-1mg/kg BID) is the preferred treatment; mild exercise restriction is also recommended in severe cases. A number of surgical treatment options can be considered for dogs with moderate to severe SAS, but most are of uncertain value. Open resection of the obstructing lesion during cardiopulmonary bypass offers the best opportunity for reducing the systolic pressure gradient. Other surgical procedures employed to dilate or bypass obstructions have either failed to achieve a sustained reduction of the systolic pressure gradient or they entail an unacceptable risk of complication. Balloon valvuloplasty is no longer typically performed in most cases due to a lack of lasting beneficial effects and difficulty in adequately reducing the pressure gradient.
References:
Bussadori C, Amberger C, LeBobinecc G, Lombard CW. Guidelines for the echocardiographic studies of suspected subaortic and pulmonic stenosis. J Vet Cardiol 2000;2:15-22.
Kienle RD, Thomas WP, Pion PD. The natural clinical history of canine congenital subaortic stenosis. J Vet Intern Med 1994;8:423-31.
Oyama MA, Sisson DD. Cardiac troponin-I concentration in dogs with cardiac disease. J Vet Int Med 2004;18:831-39.
Reist-Marti SB, Dolf G, Leeb T, et al. Genetic evidence of subaortic stenosis in the Newfoundland dog. Vet Rec 2012;170:597.
Thanks Eric – but this is
Thanks Eric – but this is where I am confused as your book grades moderate SAS between 80-100mmHG where June Boon’s text would call this severe? So at 52mmHG is this mild or moderate? Should I rescan in 6 months to see if the heart is changing? Is this pet at risk for sudden death?
BTW, your book is very helpful – I use it all the time! I highly recommend it.
Thanks for the plug JP. Ive
Thanks for the plug JP. Ive always called SAS mild 2.5/3.5 m/sec, moderate 3.6-4.5 and severe > 4.5 so in that thought process yours is barely in moderate so I would call yours mild/moderate. The Curbside chapter on SAS was written by Peter and is going by Bussadori numbers. Everyone in Cardio world respects June Boon but not everyone uses her numbers especially the LA/AO which doesnt reflect chronic LA enlargement, for example. Its all semantics and hair splitting as the bottom line on your dog is at that pressure gradient he shouldnt be clinical. SAS cases usually live normal lives at velocities under 4 m/sec and I have yet to see one clinical til > 5 m/sec.
Go by tachycardia and velocities >4.5 when you start thinking clinical and consider treating wiht atenolol which is the only effective tx. That being said if he gets myocarditis or endocarditis or something else on top of it then thats a different issue. But if no complicating factors occur at these velocities I would just let him be a dog and be sure to prophy ABs before anesthetic procedures and dentals so nothing is given a chance to set up shop on that AV as endocarditis and make it worse. Check the echo every 6-12 months or earlier if the murmur grade increases or any ex intollerance.
Check our Randy’s thread regarding this la/ao issue as a side note on the June boon la/ao.
https://sonopath.com/forum/when-start-diureticspimopendan#comment-3936
Remember the global patient presentation dominates over numbers:)
Hi!
The problem is, that the
Hi!
The problem is, that the pressure gradients mentioned in Bussadori’s paper on SAS and PS and many other papers are extrapolated from human medicine. (mild 2.25-3.5, moderate 3.5-4.5, severe >4.5). Yet, human patients are quite relaxed when they are examined. Initially, severe stenosis in veterinary patients was considered from >125 mm Hg which is about 5.5 m/s.
What I would do now is: grade it like mentioned above and call anything above 5.5 m/s extreme stenosis. These patients usually have weak pulses and develop clinical symptoms.
Pls note that severe myocardial changes can affect the pressure gradient by reduction of myocardial performance.
Calculation of effective orifice area would be a good thing to do but is not that easy.
in a report, I would mention the pressure gradients and the myocardial changes as well as – if present – concomitant mitral dysplasia.
Re your patient:
The nyquist limit of the Color Doppler is set too low – this can cause overestitmation of the aortic regurgitation jet.
The PG is in the moderate range – this is unlikely to cause symptoms.
(There is some degree of poststenotic dilation)
The MR can cause problems once because of the high pressure within the ventricle.
I woudl not give any therapy at the moment but rescan the dog in a year.
Pls let me know if you have any questions
best regards
Peter
PS: hardly able to write on the keybord because I was bitten by a dog today 🙁
Even with a bite your entry
Even with a bite your entry is more articulate than anything I have written lately 🙂
Thank-you Peter – sorry about
Thank-you Peter – sorry about the bite : (
What nyquist would be optimal?
Jacquie