Hypertrohpic Obstructive Cardiomyopathy ( HOCM)

4 responses to “Hypertrohpic Obstructive Cardiomyopathy ( HOCM)”

1. Do you have a good M Mode of

   Do you have a good M Mode of the L ventricle. In the 3rd still picture 

   showing SAM the IVS and VFW did not look all that thickened to me.

   If there is not concentric hypertrophy but rather eccentric hypertrophy or even no hypertrophy I would consider starting this cat on diuretics and +/- Pimobendan (off label)

   I don’t know that you can diagnose CHF on Echo alone.

   I know there are financial constraints- but a chest x-ray and EKG are indicated.

   OK – I put my 2 cents in here. Wait and see what others have to say.

2. yeh he has a 2 cm left atrium

   yeh he has a 2 cm left atrium which is kocking on the door to chf depends if wet lung or not from traditional definition of chf. In my opinion many would tx differently here. Correct you are not supposed ot use b blockade in chf because they need th elevated HR to stay alive basicly. So what I do with these is BID lasix and stat and acei 0.25-0.5 mg/kg and sit on it for about a week and then reecho. Im a proactive plavix user too so I would add that. If you reduce the volume overload and starlings laws come back home the HR may drop under 200 on its own but if the vlume overload reduces to say an LA of 1.6 or so and the HR is still > 200 then I would add atenolol. Again its just how I have managed these cats and many may do it differently but the key is minor adjustments… treat what you can see and here I see volume overload and have always lived by treat the volume issue first then see if the heart gets happier or not before trying to control the rate.

   note the contractility is not elevated here even if the LV is thick… Im eyeballing a 35% fs or so which is a tendency toward restrictive cmy… but things change once volume issues are adjusted and fs% may go up to true hcm range > 45-50%.

   Hope this helps

3. Thank you for the

   Thank you for the feedback.

    

   Here are the LV measurements. Based on the measurements for LVIDd, there is no evidence of volume overload but FS% is ~30%. Base on the ‘lowish’ FS%, so i still presumed volume overload is present due to the large atrium?

    

4. Thank you for the updated

   Thank you for the updated images.

   Below is Dr Chris Stauthammers take on treatment of HCM.

   Congestive heart failure:

   Acute Therapy:

   Cats that present in respiratory distress secondary to CHF require prompt and aggressive

   therapy. The primary treatment is parenteral furosemide. Most cats also benefit from

   supplemental oxygen (e.g., oxygen cage). Topical nitroglycerine may also be applied, but

   its efficacy in cats is unknown. Cats with significant pleural effusion require

   thoracocentesis. It is important remember that cats with severe heart failure are usually in

   severe respiratory distress, and must be managed with the utmost care and with minimal

   stress. Stress and excessive handling exacerbate dyspnea, and this can prove fatal.

   Chronic Therapy:

   After resolution of the acute crisis, the therapeutic objective is to prevent a recurrence of

   pulmonary edema. Furosemide is the most important and efficacious drug available to

   achieve this objective. Most cats require life-long furosemide therapy. However,

   furosemide can occasionally be discontinued, usually in those cats in which the heart

   failure that was precipitated by a reversible event (e.g., fluid or corticosteroid

   administration). Cats are more sensitive to furosemide than dogs, and are more likely to

   develop azotemia or electrolyte abnormalities with overzealous administration. Cats with

   pleural effusion may require periodic thoracocentesis.

   Two classes of drugs have been advocated to improve left ventricular filling in feline

   cardiomyopathy; calcium channel blockers and-blockers. Published information that

   addresses this issue in an objective manner is scant. However, an abstract was presented

   at the 2003 ACVIM Forum from a prospective, double-blinded, multicenter study

   evaluating chronic therapies for CHF in cats with either HCM or restrictive/unclassified

   cardiomyopathy. Cats were entered into the study after having survived an acute episode of

   CHF. In addition to furosemide, the cats were randomly assigned to receive placebo, a

   calcium channel blocker (extended-release diltiazem), a beta-blocker (atenolol), or an ACE

   inhibitor (enalapril). Cats receiving atenolol did significantly worse than cats receiving

   placebo (in terms of time to recurrence of CHF or death). The cats receiving diltiazem had

   a similar outcome to cats receiving placebo, but there was a relatively high incidence of

   side effects (predominately gastrointestinal signs). Cats receiving enalapril appeared to

   have a better outcome than cats receiving placebo, but this difference did not achieve

   statistical significance in this study.

   Based on these results, we currently recommend that cats in CHF be treated with either

   furosemide alone, or furosemide and an ACE inhibitor (e.g., enalapril or benazepril). The

   ACE inhibitor is carefully added to a cat’s treatment protocol once it is eating well and is

   not azotemic. In addition to furosemide and an ACE inhibitor, therapy aimed at

   preventing systemic arterial thromboembolism (e.g., aspirin or clopidogrel) is

   recommended in cats with HCM (see arterial thromboembolism lecture). Positive inotropic

   medications (digoxin, pimobendan) are not recommended as myocardial contractility is

   generally normal and these medications may exacerbate the diastolic dysfunction and

   myocardial hypoxia. Positive inotropic