Hi all, I hope you can help me with this case. I am a bit confused at the findings. Initially I thought it was PDA but the lack of volume overload remodelling just does not fit. However, I find something on the left short axis view…Please help:
Hi all, I hope you can help me with this case. I am a bit confused at the findings. Initially I thought it was PDA but the lack of volume overload remodelling just does not fit. However, I find something on the left short axis view…Please help:
This is 12 year old silky terrier. Male, not neutered. At 6 months old, a grade 2-6 pansystolic heart murmur is heard. At 1 year old, grade 4-6. No symptoms. Was started on enalapril. No xrays-ECG-echo. After a few years…enalapril stopped. After a few years, re’started. Dog has been on back enalapril for at least 3 years now. Patient is now starting to cough. At some point in 2010 dog had and ECG and Echo of which there is no report other than ¨nothing abnormal¨. Current findings:
Xrays: appears to have general mild enlargement, with increased ventricular contact with sternum aspect of the thorax. No obvious LA enlargement. On lateral view I fail to find a good descending aorta. On VD view I see a bulging main pulmonary artery. A mild vascular pattern. There might be mild peri-hilar pulmonary oedema…although I’m not too convinced.
ECHO:
-No LA enlargement. There appears to be a postvalvular aortic dilation.
-No significant mitral regurgitation nor abnormal mitral valves.
-there is mild tricuspid regurgitation, valves appear fairly normal to me. It is not significant since less than 2.5m/s
-There is significant Main pulmonary artery dilation and insufficiency.
-There is left and right ventricular concentric hypertrophy.
-On the left parasternal short axis/oblique view, I find a flow from aorta to somewhere I’m not sure…Which I thought it looks like PDA…but heart remodelling does not fit PDA…so Im very puzzled at the findings.
Please, I would appreciate anybody who could enlighten me with their knowdlege…
Comments
Would need to see the
Would need to see the complete study.
Here is a small paragraph from Small Animal Cardiovascular medicine on SAS:
Two-dimensional and M-mode echocardiographic findings are often normal in mildly-to-moderately affected individuals. Left ventricular hypertrophy is usually readily apparent only in moderately-to-severely affected dogs. In these cases, the M-mode echocardiogram demonstrates increased diastolic septal and left ventricular free wall thicknesses (left ventricular concentric hypertrophy) and a normal left ventricular shortening fraction. The narrowed subvalvular region can sometimes be identified while sweeping the M-mode transducer from the left ventricle to the level of the proximal aorta, but two-dimensional evaluation is more accurate for this purpose.11,12 Other findings may include poststenotic dilatation of the ascending aorta, secondary thickening of the aortic valve cusps, and midsystolic partial closure of the aortic valve cusps. In some cases of SAS, the mitral valve E-F slope decreases because of reduced compliance of the hypertrophied left ventricle.9 This should not be misinterpreted as mitral stenosis. Overall, M-mode examination alone is not very reliable for identification or confirmation of congenital SAS except in severe cases.
Some points:
1. PDA is a murmur (machinery) of both systole and diastole- not just pansystolic
2. Aortic stenosis explains the L sided concentric hypertrophy and possibly the right sided changes
3. Decrease in L ventricular and L atrial volume is due to the hypovolmia/decreased compliance
4. This also explains the post aortic and not sure about post pulmonic dilation.
I am not a cardiologist- but this is the best I can offer base on the 3 cine loops shown.
Maybe Peter or Eric can jump in here
Even if my though process is flawed- maybe we can get some comments.
We could have 2 defects causing the symptoms here
Given the PS the LV volume
Given the PS the LV volume may have poor return and pseudohypertrophy. If SAS is present the lvot velocity will be well into 4 m/sec or higher to have any secondary hypertrophy from that (personal cutoff no research on it) so if lvot velocities are foine the the lv hypertrophy is something else. More likely the “lvh” may be poor venous return to the left heart owing to the ps which would create a pseudohypertrophy of the LV and potentially the post aortic dilation but the post aortic dilation I see a lot in older dogs. i dont think the left heart is pathological clinically anyway for a 12 year old silky. Likely needs a balloon for the ps depnding on the rvot pressure gradients but likely pretty high since rv hyperophy is present and post pv dilation.