Cardio. HCM Chap 41 Flashcards

1
Q

Types of cardiomyopathies in cats:

A

four basic types of cardiomyopathy:

1) DCM
(2) HCM
(3) restrictive cardiomyopathy (RCM
(4) arrhythmogenic right ventricular cardiomyopathy

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2
Q

Genetics, what do we know?:

A

HCM in humans is a genetic disease, and this disorder has been associated with hundreds of mutations of genes that encode sarcomeric proteins

The mutations responsible for familial HCM in Maine Coon cats and in Ragdoll cats have been identified
finding and the occurrence of HCM in related purebred and mixed breed cats support a genetic basis

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3
Q

RCM
presumed pathophys.
Echo findings

A
  • impaired ventricular filling in the absence of myocardial hypertrophy
  • term generally is applied when there is atrial enlargement associated with a ventricle that has normal or nearly normal appearance

endomyocardial fibrosis and myocardial functional deficits that impair relaxation are the presumed explanations
-may represent the sequelae of endomyocardial inflammation

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4
Q

Diastolic Dysfunction requires what two things:

A
  • ability of the ventricle to fill at low diastolic pressures depends on the rate of the active, energy-requiring myocardial relaxation (lusitropy)
  • mechanical properties that determine compliance

lusitropy and compliance

Impaired myocardial relaxation and dimin-
ished chamber compliance alter the pressure-volume relationship = diastolic pressures are high when ventricular volume is normal

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5
Q

Systolic Anterior Motion of the Mitral Valve - explain pathophys.
% of cats with HCM:
prognostic relevance:

A

Systolic anterior motion (SAM) of MV is echocardiographically detected in approximately 65%

  • abnormal drag forces are responsible for systolic movement of the valve leaflets toward the septum secondary to abnormal papillary muscle orientation
  • mitral leaflets toward the septum results in dynamic—left ventricular outflow tract obstruction
  • concurrent mitral valve regurgitation
  • labile phenomenon
  • explain the fact that the intensity of the associated murmur may vary from moment to moment
    px. not been defined - LVOFT obstruction caused by SAM has been associated with poor prognosis in humans

results of three retrospective studies of feline HCM suggest that SAM confers a more favorable px. but hard to conclude given retrospective nature

SAM is likely the most important cause of cardiac murmurs in cats with HCM

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6
Q

FATE
Site:
risk factor:

A

left atrium—appendage—more commonly the site of thrombus formation
aortic trifurcation
left atrial enlargement and spontaneous contrast

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7
Q

clinical syndrome of FATE solely from arterial occlusion?

A

no, experimental ligation of the distal feline aorta does not reproduce the clinical syndrome
-available evidence suggests that vasoactive mediators, notably PGs & serotonin, released from thrombus

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8
Q

Auscultation:

A

gallop sound signifies diminished ventricular compliance
S4 - atrial contraction into stiff ventricle
(vs. S3 DCM blood filling floppy heart)
murmur SAM

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9
Q

Describe radiographic findings:

A

radiographic cardiomegaly
patchy interstitial to alveolar pattern distributed diffusely through the lung
prominent pulmonary veins
large pleural effusions associated with HCM

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10
Q

Echo dx:

A

end-diastolic thickness of the interventricular septum or left ventricular posterior wall is less than 6 mm in healthy cats
.:. > 6mm suggesting hypertrophy

Left atrial enlargement resulting from diastolic dysfunction and sometimes concomitant mitral valve regurgitation

respiratory signs rarely result from cardiomyopathy in patients with normal atrial size

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11
Q

Why is BP inportant:

A

RO systemic hypertension in compensatory hypertrophy

-feline HCM is a diagnosis of exclusion

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12
Q

Pro BNP assay

A

two studies generally were concordant; NT-BNP concentration identified respiratory distress caused by feline cardiomyopathy with high sensitivity—near 90%—and a somewhat lower specificity that was in the high 80s

this was assay that had to be sent out Fox Oyama study

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13
Q

Tx FATE:
mortality not as a result of euthanasia, associated with FATE is close to ____during initial hospitalization

and euthanasia is elected for ____ of cases during hosp.

Surgical vs thrombolytics:
Conservative tx:

A

challenging, syndrome is associated with a poor px.
30%
30%
thrombectomy, transcatheter thrombectomy, and the use of fibrinolytic drugs such as streptokinase and tPA

none of these interventions is obviously superior to

Heparin is often administered in the 48 to 72 hours after an embolic event in the hopes that this treatment will prevent enlargement of the thrombus

LMWH an advantage over unfractionated heparin has not been demonstrated. Optimally, monitoring of the activated clotting time or prothrombin time is used to
guide unfractionated heparin therapy.

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14
Q

px importance of temp.:

return to normal limb function:

A

hypothermia associated with reduced survival. retrospectively acquired data predicted 50% short-term survival for patients with a body temperature of 37.2°C (98.9F)

if it occurs, may take weeks
consequences of dermal or even muscular necrosis

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15
Q

Prevention of future embolic events:

Prophylaxis of FATE presents a particularly difficult bc embolism is the first indication of cardiac disease in approximately ____%:

incidence of FATE in patients known to have cardiac disease is relatively low ___%.

A

aspirin vs clopidogrel vs LMWH
clopidogril > aspirin

80%

<20% of patients

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16
Q

Tx of acute CHF:

A

Furosemide 2 to 4 mg/kg observed for 40 to 60 minutes. Frequent administration of low doses (0.5 to 1 mg/
kg intravenously [IV] q1h) until respiratory signs resolve may provide a means to prevent excessive diuresis.

CRI of furosemide may be considered
noteworthy that the clinical profile of heart failure resulting
from feline cardiomyopathy is similar to that of feline endomyocarditis. The latter is an idiopathic disorder that is associated with pneumonitis. Diuresis is unlikely
to improve clinical status.

Nitroglycerin (NG) is an organic nitrate that is sometimes used with furosemide as an adjunctive therapy that may further reduce ventricular filling pressures
-NG causes venodilation as well as dilation of specific arteriolar beds, including those of the coronary circulation.

In veterinary medicine, NG is used principally as a veno-
dilator that increases venous capacitance, therefore causing a decrease in ventricular filling pressures

17
Q

Tx chronic CHF:

A

β-Adrenergic antagonists such as atenolol indirectly improve ventricular filling by lowering HR.

slowing the rate may improve coronary perfusion

it is likely that abnormal ventricular stiffness related to hypertrophy and fibrosis is at least partly responsible. It is therefore unclear whether heart rate reduction in
patients in which heart rate initially is normal can decrease venous pressures.

Relevant studies are lacking, and the optimal heart rate for patients with heart failure caused by feline HCM is not known.

β-Adrenergic antagonists may have a particular role when dynamic left ventricular outflow tract obstruction is caused by SAM and when tachyarrhythmias complicate the clinical picture

18
Q

“funny” (If) sodium channel antagonists

A

ivabradine may have value as they slow heart rate but

do not exert a negatively inotropic effect

19
Q

diltiazem

two benefits:

A

benzothiazepine calcium channel antagonist, only a modest slowing effect on heart rate but is believed to
speed myocardial relaxation

may dilate coronary arteries and improve diastolic function by improving coronary perfusion

no effect on outflow tract obstruction caused by SAM

20
Q

pimobendan
beneficial:
risk:

A

lusitropic effect of pimobendan may be beneficial
HCOM
“off-label”