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Missy's echo results

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  • Kelley
    Diagnosis: Congenital heart disease. Missy has a large atrial septal defect/ventricular septal defect (8 mm) a hole in the lower atrial septal and upper
    Message 1 of 4 , Feb 1, 2007
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      Diagnosis: Congenital heart disease. Missy has a large atrial septal
      defect/ventricular septal defect (8 mm) a hole in the lower atrial
      septal and upper ventricular septal wall where the chambers join which
      allows blood to shunt right to left and left to right in the heart.
      Her heart chambers are dialated and her pulmonary artery and veins are
      dilated. Her right ventricular wall is mildly thickened. The defects
      can lead to congenital heart disease (CHF) with fluid retention in the
      lungs, chest cavity and/or abdomen. Therefore I would recommend
      starting her on a low dose of furosemide.

      She called in a prescription of furosemide 10 mg/ml .3 mg once daily.

      The compounding pharmacy here says that can't be compounded
      transdermally because the molecule is too large.

      Comments? Is this as bad as it sounds to me?
    • nala nala
      Kelley, I am sorry that Missy s echo showed this kind of heart defect. There are few kitties and owners here who are dealing with VSD, although I don t recall
      Message 2 of 4 , Feb 2, 2007
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        Kelley,

        I am sorry that Missy's echo showed this kind of heart
        defect. There are few kitties and owners here who are
        dealing with VSD, although I don't recall off-hand any
        mentions of ASD or both. I am unfamiliar with the
        treatment of this heart defect.

        You mentioned that the vet "called in a prescription
        of furosemide 10 mg/ml .3 mg once daily."

        A oral dose of 0.3 mg furosemide would be impossibly
        small to give as a pill. In the liquid form you
        describe, that would be an oral dose of only 30
        microliters (0.03 ml) from a 10 mg/ml solution. You
        can measure an amount that small with a "tuberculin"
        syringe. I would double check the dosage with the vet
        and the pharmacy and make sure to get a syringe that
        can measure that kind of small volume. It would be
        easier to measure accurately if the solution were more
        dilute than that, for example a 1 mg/ml soultion.
        Then you would give 0.3 ml which might be more
        manageable.

        I've included a bit more info below my signature

        Best,
        Nala
        ----
        Here are some links that might help you get started :

        First a link to a short article that might be useful:
        www.ukvet.co.uk/ukvet/articles/
        Cardio_heartdisease_in_cats.pdf

        and from a meeting proceeding

        http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2002&PID=2526

        ATRIAL SEPTAL DEFECTS (ASD)
        ASD are uncommon congenital heart defects in small
        animals. They can appear as an isolated defect or they
        may be part of a complex malformation. Four types of
        ASD have been described: 1) ostium secundum, involving
        the region of the fossa ovalis; 2) ostium primum or
        partial atrioventricular canal defect, located in the
        lowermost portion of the interatrial septum and
        associated with endocardial cushion defects; 3) sinus
        venosus involving the superior portion of the
        interatrial septum; 4) coronary sinus, located in the
        posteroinferior angle of the atrial septum.

        Small ASD are not usually hemodynamically significant.
        Because the pressures between the two atria are
        similar, the shunt flow across an ASD does not
        generate murmur, but a murmur of relative pulmonic
        stenosis may be detected. Only right heart failure
        develops in severe cases.

        VENTRICULAR SEPTAL DEFECTS (VSD)
        Depending on the location, VSD are classified as: a)
        membranous/perimembranous, the most common type in
        dogs, b) outflow (infundibular/supracristal), c)
        inflow (atrioventricular canal), and d) muscular
        (trabecular). VSD can appear as isolated lesion or in
        association con others heart defects (i.e., PS,
        pulmonary atresia, truncus arteriosus and
        double-outlet right ventricle). Some defects can
        predispose to prolapse of the aortic valve into the
        defect.

        Pathophysiology: The physiologic consequences of a VSD
        are determined by the size of the defect and the
        relative resistance in the systemic and pulmonary
        vascular beds. If the defect is small ("restrictive"
        VSD), there is little or no functional disturbance,
        since pulmonary blood flow is increased only
        minimally. In contrast, if the defect is large ("non
        restrictive" VSD), the ventricular systolic pressures
        are equal and the magnitude of flow to the pulmonary
        and systemic circulation is determined by the
        resistances of the two beds. Initially, systemic
        vascular resistance excess pulmonary vascular
        resistance, so that left-to-right shunting
        predominates. As pulmonary flow increases, there is
        increased venous return to the left atrium and left
        ventricle, and the left ventricular diastolic pressure
        can increase. Left ventricular failure is likely when
        the left-to-right shunt is great. Over the time, the
        pulmonary vascular resistance usually increases, and
        the magnitude of left-to-right shunting declines. If
        the pulmonary vascular resistance equals or exceeds
        the systemic resistance the shunting of blood from
        left to right then ceases, and right-to-left shunting
        begins.

        Breed predispositions: English bulldog, Keeshond
        (genetic basis documented), English springer spaniel
        and Beagle are predisposed.

        Clinical assessment: Most animals that have survived
        through the first months without clinical signs, can
        tolerate the defect for many years without clinical
        signs. A harsh, holosystolic murmur, audible maximally
        over the ventral right thorax, often near to the
        sternum is present. Murmurs of the relative pulmonic
        stenosis or aortic regurgitation (prolapse of the
        aortic valve into the defect) may be audible with VSD.

        Thoracic radiographic findings in dogs with VSD are
        variable, but usually left atrial and ventricular
        dilation, pulmonary overcirculation, a dilated main
        pulmonary artery, and variable degrees of right
        ventricular enlargement are present. The ECG may show
        evidence of left, right or biventricular enlargement,
        depending on hemodynamic consequences of the shunt.
        Echocardiography is useful to confirm the diagnosis of
        a VSD and to help assess the severity of the defect.
        Spectral Doppler shows a high velocity jet (Vmax > 4.5
        m/sec) thorough a restrictive VSD and increased peak
        pulmonary artery velocity owing left-to right shunt.

        Clinical management: Definitive treatment of
        symptomatic or severe lesions requires surgery using
        cardiopulmonary bypass and is rarely performed.
        Pulmonary artery banding can be used to create
        supravalvular pulmonary stenosis and decrease the
        magnitude of left-to-right shunting in dogs with large
        VSD. If surgical correction or palliation is not an
        option, medical management of congestive heart failure
        may be required. Prophylactic antibiotic therapy
        should be considered in patients with VSD when there
        is known potential for hematogenous exposure to
        infectious organisms.

        ----





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      • nala_zq
        Kelley, this was meant for you . . . Hi My kitty has a cardiac cushion defect which covers the atrium and ventricle and means all her four chambers are in
        Message 3 of 4 , Feb 3, 2007
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          Kelley, this was meant for you . . .

          Hi

          My kitty has a cardiac cushion defect which covers the atrium and
          ventricle and means all her four chambers are in contact with each
          other. She is on Fortekor at 2.5mg each morning as she is only 6 months
          old. Her brothers all have a similar defect but not as bad.

          It sounds very similar to your kitty. My Milli is coping quite well and
          eating and playing like the others, although she often gets breathless.
          She was on furosimide but they took it off her as her lungs aren't
          congested. I also use the carnitine, co-Q supplements and this helped a
          lot.

          Lyn


          >
        • Lisa Clarizia
          Kelley, My Lilly has VSD, with thickening secondary to that defect. Her foster mom, Moriah took her to OSU where she was started on enalapril and a low dose
          Message 4 of 4 , Feb 3, 2007
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            Kelley,

            My Lilly has VSD, with thickening secondary to that defect. Her foster mom,
            Moriah took her to OSU where she was started on enalapril and a low dose of
            furosemide (lasix).

            Lilly is asymptomatic at this stage and the lasix was simply to prevent any
            fluid build up which *might* happen. I took her off this because I don't
            think (and my vet agrees) that prophylactic lasix is going to do any good at
            all. Cats, like humans, can develop a resistance to lasix over time,
            requiring higher and higher doses to be effective and frankly, if the cat is
            not in congestive heart failure (has no fluid in or around the lungs) it
            doesn't need lasix. Regular vet care, careful monitoring of breathing and
            behavior patterns will be enough to know when/if the cat will need
            diuretics.

            Aside from that, CHF is a catastrophic event in the sense that there's no
            such thing as having a little CHF. It happens when the disease has
            progressed to the point where there's a pathological pressure differential
            in the lungs, causing fluid to seep from the vessels and into the lung
            tissues. It's *not* something like humans taking low-dose aspirin to help
            prevent heart disease -- low dose lasix will *not* prevent CHF, all it is
            likely to do in the best possible scenario is delaying the symptoms of CHF
            from showing up by a matter of an hour or two. If and when CHF occurs it
            requires higher doses of lasix, possibly a second diuretic, and
            cardiac-specific drugs to counteract.

            I'm all for meds if they are going to help, but I think you may want to
            discuss this with your vet. Lilly is getting enalapril to help regulate her
            heart which is more likely to prevent fluid build up in the first place. As
            for how bad it sounds ... it's hard to say. Lilly, aside from a REALLY LOUD
            murmur has no outward signs on the disease and acts like any other cat.
            Some cats go for years with these defects, others don't and it's hard to say
            what will happen to any individual cat.

            The important thing is that you know what you're up against now and can do
            whatever you can to help Missy. A high-quality diet, supplements, and
            appropriate meds can all give her the best chance possible to live well and
            hopefully longer. As for the lasix -- if you're not comfortable going
            against your vet's advice right now, it will not hurt her short-term to get
            a low dose until you've had time to research this for yourself and decide
            what course of action you want to take. I'd suggest you look into
            enalapril. Enalapril, in this instance, is used as a "afterload reducer"
            and decreases left-to-right shunting and improves overall systemic blood
            flow and is recommended for both atrial and septal defects.

            Another issue you'll need to address is clot prevention -- all heart kitties
            are susceptible to forming clots, which can be life-threatening. There are
            different options for this, such as aspirin therapy (dubious benefits), low
            molecular weight heparins, plavix, and supplements such as nattokinase (an
            enzyme that 'eats' clots, Lilly gets this). Our septal defect kitties are
            even more a risk for these clots, so addressing this is something you can do
            that has a real chance at helping to prolong and improve Missy's life.

            I hope all this helps ... I know it's a lot of information and you're new to
            this. It can all be a little overwhelming at first!

            Lisa

            On 2/1/07, Kelley <moonvine@...> wrote:
            >
            > Diagnosis: Congenital heart disease. Missy has a large atrial septal
            > defect/ventricular septal defect (8 mm) a hole in the lower atrial
            > septal and upper ventricular septal wall where the chambers join which
            > allows blood to shunt right to left and left to right in the heart.
            > Her heart chambers are dialated and her pulmonary artery and veins are
            > dilated. Her right ventricular wall is mildly thickened. The defects
            > can lead to congenital heart disease (CHF) with fluid retention in the
            > lungs, chest cavity and/or abdomen. Therefore I would recommend
            > starting her on a low dose of furosemide.
            >


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