I have a couple of questions regarding SAM in HCM cats:
1. Do you grade the degree of SAM seen ie. mild vs severe and if so how do you do this – by the aortic max velocity and PG?
2. At what stage is atenolol indicated?
3. What changes would be expected to be seen on echoe when a patient is on atenolol for SAM (other than decreased HR)?
Thanks!
Jacquie
I have a couple of questions regarding SAM in HCM cats:
1. Do you grade the degree of SAM seen ie. mild vs severe and if so how do you do this – by the aortic max velocity and PG?
2. At what stage is atenolol indicated?
3. What changes would be expected to be seen on echoe when a patient is on atenolol for SAM (other than decreased HR)?
Thanks!
Jacquie
Comments
Big question and lots of
Big question and lots of differing opinions so I will defer to Peter on this mainly but this is what my team typically does whether right or wrong who knows.
Clinical signs (ex intollerance) and SAM: Tx atenolol
Resting HR > 200 and significant SAM: Tx atenolol or watch and recheck in 3-6 months
Other evidence of HCM, regional hypertrophy, fixed lvot obstriuction, remodeling, LAE and so forth: Tx atenolol +/- acei +/- Lasix if in chf but no atenolol in chf because they need the elevated HR to stay alive. Atenlol would come later if needed after stabilized.
I will actually check SAM early in the echo exam and then when he gets agitated and kicks up the HR then check it again…kind of a stress test.
Peter and I did case of the month (link for past cases of the month is under the current case of the month on the home page) on this a while back so check this out:
December 2011
Big question and lots of
Big question and lots of differing opinions so I will defer to Peter on this mainly but this is what my team typically does whether right or wrong who knows.
Clinical signs (ex intollerance) and SAM: Tx atenolol
Resting HR > 200 and significant SAM: Tx atenolol or watch and recheck in 3-6 months
Other evidence of HCM, regional hypertrophy, fixed lvot obstriuction, remodeling, LAE and so forth: Tx atenolol +/- acei +/- Lasix if in chf but no atenolol in chf because they need the elevated HR to stay alive. Atenlol would come later if needed after stabilized.
I will actually check SAM early in the echo exam and then when he gets agitated and kicks up the HR then check it again…kind of a stress test.
Peter and I did case of the month (link for past cases of the month is under the current case of the month on the home page) on this a while back so check this out:
December 2011
Hi!
Basically, there´s
Hi!
Basically, there´s currently no evidence at all showing any benefit from Atenolol treatment regaring time to onset of CHF or mortality. However, there´s no evidence against it´s use besides the fact that it should not be given in CHF or if there´s an increased risk for FATE. A recent study (JSAP 2009, Payne R et al) showed that there was no significant difference in mortality in asymptomatic cats with and without SAM. In human medicine, SAM is a very important factor because it causes significant clinical symptoms and is frequently associated with severely increased pressure gradients.
It has been shown in human medicine, that high heart rates are associates with worse outome in heart failure patients. One study by John Rush has shown a similar association in cats.
So, what I currently do is (no consensus, no evidence!!!):
Asymptomatic patients with SAM and high pressure gradients (>3.5 m/s): Atenolol
Asymptomatic patients with SAM, low pressure gradients and high heart rates (>200/min): Atenolol
Atenolol should be started at 6.25 mg/cat sid (evening). The heart rate should be re-measured after 1 week in the morning (approx 12 hrs later). If it´s still >180 /min, I give atenolol bid.
Asymptomatic patients without SAM and high heart rates: Diltiazem
If the left atrium exceeds 18 mm on 4 chamber views (end systole) I add Lasix and perhaps an ACEI. If it exceeds 20 mm (or less if speontaneous echocontrast is visible or if severe endocardial fibrosis is seen), I add plavix.
SAM is staged based on the pressure gradient (as you wrote). If you give atenolol, you can see a decrease in pressure gradients. BUt due to the fact that the pressure gradient can vary depending on stress, this change is not always obvious. It is unlikely to see other changes. It is important to disconinue Atenolol once the LA is really big or spontaneous echocontrast is visible. This is, because Atenolol can worsen left atrial dysfunction.
New substances aimed primarily at redicing the heart rate (ivabradine) have been studied but further clinical studies are necessary.
Note that therapeutic recommendations are always changing due to scientific progress.
I hope I could help!
Peter
Hi!
Basically, there´s
Hi!
Basically, there´s currently no evidence at all showing any benefit from Atenolol treatment regaring time to onset of CHF or mortality. However, there´s no evidence against it´s use besides the fact that it should not be given in CHF or if there´s an increased risk for FATE. A recent study (JSAP 2009, Payne R et al) showed that there was no significant difference in mortality in asymptomatic cats with and without SAM. In human medicine, SAM is a very important factor because it causes significant clinical symptoms and is frequently associated with severely increased pressure gradients.
It has been shown in human medicine, that high heart rates are associates with worse outome in heart failure patients. One study by John Rush has shown a similar association in cats.
So, what I currently do is (no consensus, no evidence!!!):
Asymptomatic patients with SAM and high pressure gradients (>3.5 m/s): Atenolol
Asymptomatic patients with SAM, low pressure gradients and high heart rates (>200/min): Atenolol
Atenolol should be started at 6.25 mg/cat sid (evening). The heart rate should be re-measured after 1 week in the morning (approx 12 hrs later). If it´s still >180 /min, I give atenolol bid.
Asymptomatic patients without SAM and high heart rates: Diltiazem
If the left atrium exceeds 18 mm on 4 chamber views (end systole) I add Lasix and perhaps an ACEI. If it exceeds 20 mm (or less if speontaneous echocontrast is visible or if severe endocardial fibrosis is seen), I add plavix.
SAM is staged based on the pressure gradient (as you wrote). If you give atenolol, you can see a decrease in pressure gradients. BUt due to the fact that the pressure gradient can vary depending on stress, this change is not always obvious. It is unlikely to see other changes. It is important to disconinue Atenolol once the LA is really big or spontaneous echocontrast is visible. This is, because Atenolol can worsen left atrial dysfunction.
New substances aimed primarily at redicing the heart rate (ivabradine) have been studied but further clinical studies are necessary.
Note that therapeutic recommendations are always changing due to scientific progress.
I hope I could help!
Peter