Pathology of Valvular and Myocardial Diseases Flashcards
what are two ways that the heart can compensate for changes in load
dilation and hypertrophy
how does dilation affect filling and ejection
increases chamber size to improve filling
increases amount ejected UP TO A POINT
if too much dilation –> decreased contraction ability
how does hypertrophy affect filling and contractility
- concentric: decreases filling, increases contractility
- eccentric: increases filling, decreases contractility
concentric hypertrophy
sarcomeres added in parallel to increase wall thickness
caused by increased pressure (afterload)
eccentric hypertrophy
sarcomeres added in series to increase wall length
caused by increased volume (preload)
pathologic hypertrophy
when hypertrophy exceeds physiologic state and becomes pathologic
concentric pathologic hypertrophy
causes diastolic dysfunction from decreased compliance
increases EDP and decreases conduction
eccentric pathologic hypertrophy
causes systolic dysfunction from decreased contractility
growth occurs in random directions = loss of coordinated contraction
intracardiac consequences of hypertrophy
reduced heart function
fibrosis, dysrhythmias, increased myocyte mass, decreased contractility and CO
if CO < demand –> heart failure
extra cardiac consequences of hypertrophy
fluid accumulation and ischemia
what is the most common cause of heart disease in animals
valvular disease
what is the most common cause of valve disease in animals
AV valve disease (MV, TV)
sign of AV valve disease
regurgitation
valve forms incomplete seal causing blood to back flow from ventricle to atrium
sequela to AV valve disease
atrial dilation + ventricular hypertrophy
AV valve dysplasia
congenital malformation of the valve
nodular: rounded, thickened tissue
imperforate: valve leaflets never separated
tricuspid valve dysplasia
causes regurgitation
common in labradors
mitral valve dysplasia
causes regurgitation
common in cats and cavalier King Charles spaniels
AV valve endocardiosis
degeneration of the valve at a faster than normal rate
usually myxomatous
usually mitral valve
myxomatous mitral valve endocardiosis
smooth, firm/rubbery, multi nodular tissue that blends into adjacent valve tissue
causes regurgitation and turbulent flow leading to jet lesions
jet lesions
endocardial thickening in response to turbulent flow
AV valve endocarditis
infectious inflammation of the valve
usually bacterial
usually mitral valve
(except cows: tricuspid valve)
bacterial MV endocarditis
proliferative, granular or friable (fibrin) material that adheres to the valve surface
what bacterial causes valvular endocarditis in pigs, horses, and cattle
pigs: strep. suis OR E. rhusiopathiae
horses: strep. equi OR actinobacillus equuli
cattle: trueperella pyogenes OR E. coli
what causes bacterial endocarditis
- aseptic jugular catheter placement
- sustained bacteremia that attaches to valve (endocardiosis predisposes)
- immunosuppression
- congenital valve defects
outcome of bacterial endocarditis
usually fatal due to significant vascular injury and remodeling
can cause embolisms when pieces of bacteria break off as flap closes/opens and gets trapped in next capillary bed
sign of semilunar valve disease
stenosis
narrowing of vessels leaving the heart –> increases vascular resistance –> increases afterload
sequela to SL valve disease
concentric hypertrophy + post-stenotic vessel dilation
also causes jet lesions from turbulent flow
primary myocardial disease
disease that is intrinsic to the myocardial fiber
usually idiopathic
progressive and irreversible
dilated cardiomyopathy
enlargement and dilation of the ventricles and atria
causes eccentric hypertrophy and systolic dysfunction
what species and which chamber is most commonly affected by DCM
dogs
left ventricle
what kind of drugs would you want to use to treat DCM
positive inotropes
(increase contractility)
arrhythmogenic right ventricular cardiomyopathy (ARVC)
subset of DCM characterized by loss of myocytes with fatty infiltrate
causes eccentric hypertrophy with fatty infiltration (not fibrosis)
usually right ventricular
hypertrophic cardiomyopathy
thickening of the ventricular wall from concentric hypertrophy leading to diastolic dysfunction
how does HCM cause arrhythmias
myocytes are laid down irregularly w/ fibrosis –> poor conduction –> arrhythmias
what species and chamber is most commonly affected
cats
left ventricular > IVS > right ventricle
what kind of drugs would you use to treat HCM
drugs that decrease HR
(allows for more time to relax/fill during diastole)
what is a common sequela of HCM in cats
saddle thrombus
caused by blood stasis and congestion in lungs
signs: 5 Ps (pain, paresis/paralysis, pulselessness, poikilothermia, pallor)
restrictive cardiomyopathy
fibrous tissue deposition within the endocardium and sub endothelium surrounding the ventricular lumen
causes a diastolic dysfunction due to NO compliance
usually idiopathic
what species and chamber are most commonly affected by restrictive cardiomyopathy
cats (also dogs, cattle, pigs)
left ventricular
secondary myocardial disease
myocardial disease that occurs as a result of an exogenous force (hypertension, nutrition, etc)
most are REVERSIBLE by removing primary disease
feline hyperthyroidism
thyroid tumors leading to thyrotoxic heart disease
specific to CATS only - dogs do not get clinical thyroid tumors (but if they do then most are malignant)
are cat thyroid tumors more often benign or malignant
benign but release free T4
follicular adenomas, multi nodular hyperplasia
what lesions is seen with feline thyrotoxic heart disease
concentric hypertrophy WITHOUT fibrosis
similar to HCM grossly and clinically but NO collagen deposits on histology
vitamin E/selenium deficiency causing secondary myocardial disease
low vit E/Se causes decreased protection from oxidative damage –> lipid peroxidation –> dec energy available for heart
what lesion does vitamin E/Se deficiency cause in pigs
mulberry heart disease
fibrinoid vascular necrosis leading to hemorrhage
(hemorrhage + pallor)
taurine deficiency causing secondary myocardial disease
taurine = essential AA in cats
without taurine –> “feline DCM”
eccentric hypertrophy
reversible w/ taurine supplementation
toxic myocardial necrosis
toxins leading to death and necrosis of cardiomyocytes
- cardiac glycosides
- ionophores
- blister beetles
- doxorubicin
cardiac glycoside toxicity
causes direct damage to cardiomyocytes
species: horses
ex. oleander
ionophore toxicity
increases Ca uptake in cells –> increased sensitivity causes myocardial necrosis
species: horses
ex. monensin
blister beetle toxicity
causes myocarditis, hemorrhagic enteritis, cystitis
species: horses
doxorubicin toxicity
antibiotic that has cumulative dose related toxicity - once max dose is given, patient can not have this medication again in its life
species: small animals
myocarditis
inflammation of the myocardium; many infectious etiologies (bacterial, viral, fungal, protozoal, parasitic)
parvoviral myocarditis
rare complication of parvovirus resulting in infection of the myocardium
affects puppies 3-8 weeks old
presents as sudden death months after Parvo recovery
what is the heart’s responses to injury
LIMITED regenerative capacity
- myocyte loss –> fibrosis
- remaining myocytes –> hypertrophy
effect of fibrosis on heart function
decreases compliance and conduction
(dec. contractility and arrhythmias)
what is heart failure
end point for many diseases; occurs when compensatory mechanisms are not enough to meet demand
forward failure
decreased cardiac output
backward failure
increased vascular stasis and congestion
left sided heart failure
pulmonary edema
blood congests from LA –> PV –> lungs
starling forces (inc. hydrostatic pressure) drives effusion out of vessels
gross lesion of L-HF
brown, enlarged, fluid filled lungs
brown b/c of alveolar macrophages that infiltrate to consume fluid and RBCs –> converts HgB into hemosiderin –> brown color
clinical signs of L-HF
exercise intolerance
increased respiratory effort at rest
cough
crackles
syncope
right sided heart failure
hepatomegaly, ascites or pleural effusion, peripheral edema, jugular distention
blood congests from RA –> cranial and caudal vena cava –> jugular vein and liver
causes species specific fluid accumulation
R-HF fluid accumulation in dogs, cats, and LA
dogs: ascites
cats: pleural effusion
LA: subcutis (SQ edema)
nutmeg liver disease
chronic hepatic congestion from R sided heart failure
