Endocardial and Myocardial Diseases

what is endocardiosis also referred to as?

myxomatous mitral valve disease (MMVD)

what is endocardiosis?

the valve cusps of the AV valves become shorter, nodular, and shiny. If the valve cusps become markedly shortened, then the valve loses its ability to prevent blood from regurgitating back from the ventricle to the atrium

which valve is usually most effected by endocardiosis?

left AV valve, resulting in dogs present with clinical signs of LSCHF (pulmonary congestion and edema)

what do you look for during PM examination of dogs with endocardiosis?

Look for evidence of ‘jet lesions’ → the presence of ‘flares’ of mineralization on the endocardial surface of the atrium is good evidence that blood was regurgitating back through the valve

May also find dilation of the atrium

what is endocarditis?

an inflammatory lesion of the endocardium.

what causes endocarditis?

bacteria attaching to and colonizing in the endocardium and stimulating an inflammatory reaction

what is endocarditis predisposed to by?

the more circulating bacteria, the higher chance of endocarditis AND the more turbulence, the higher chance of endocarditis

are production or companion animals more likely have to high numbers of circulating bacteria that can predispose them to endocarditis?

production animals (ex: foot abscesses, mastitis, metritis)

which bacteria cause endocarditis most often?

staphylococci and E. coli (presumably as these bacteria most commonly circulate in the blood)

what happens once bacteria colonize on a valve?

aggregation of fibrin, which then trap RBCs (aka exophytic lesions referred to as vegetations)

what is the prognosis for animals with endocarditis?

in some cases, animals can die suddenly if the vegetations become so large that they block the valve orifice and prevent the flow of blood through the heart

can vegetations interfere with valve functions? if so, how?

yes! they can partially block the valve and causing stenosis or interfering with normal valve closure, allowing blood to regurgitate through the valve

what sequelae occur from endocarditis?

septic emboli (what happens next depends on side of heart the endocarditis developed in) and valves heal by fibrosis (resulting in shortening of valves, causing blood to regurgitate through the valve and development of congestive heart failure)

where do septic emboli from endocarditis in the left side of the heart end up?

they will travel through the systemic circulation, most likely to cause infarcts in the myocardium, kidneys or brain

where do septic emboli from endocarditis in the righ side of the heart end up?

they will travel through the pulmonary circulation and result in lung abscesses

what can result from a thrombus developing in the atrium?

if it is large enough, it will block the flow of blood through the atrium or AV valve (causes rapid death) OR

the thrombus sits in the atrium and emboli break off and travel in circulation

which atrium is most commonly affected by atrial thrombosis?

left atrium; emboli will travel in circulation and cause infarcts in the kidney, heart, or infarction of the hindlimbs in cats (aka saddle emboli)

what is endocardial mineralization

most frequently seen as ‘jet lesions’ due to regurgitation of blood through a valve

in which species is endocardial mineralization most often seen

cattle with Johne's disease but function of the heart is not altered!

what is hypertrophic cardiomyopathy (HCM) defined by?

thickening and stiffening of the ventricle walls, almost always affecting the left side of the heart

what are the four key components of HCM?

thickened walls of the ventricle; reduced ventricle chamber volume; dilated atrium; loss of competency of AV valves

why does HCM result in the perfect conditions for an atrial thrombus to form?

a dilated atrium with slow-moving blood and an incompetent AV valve that is shooting up fast-moving blood every time the heart beats. Worse, the heart is beating more rapidly. This creates lots of turbulence. 

what is primary HCM in felines?

it has a genetic components; seen in cats ~4yo

the larger the cat, the better the chances of developing primary HCM

which cat breeds are predisposed to primary HCM?

giant breeds, mostly Maine coon and Norwegian Forest cats

what is secondary HCM in cats?

results from hyperthyroidism (but exact mechanism is unknown)

thyroid hormone seems to act on the myocardium in an irreversible way

what are the four ways that cats show signs of HCM?

sudden death; aortic ‘saddle’ thromboembolism; congestive heart failure; and death during anesthesia

what is dilated cardiomyopathy (DCM)?

the chamber of the ventricle expands, stretching the myocardium like a balloon

as the muscle gets thinner, the strength of the myocardial muscle weakens; resulting in loss of sufficient blood pressure generation to pump blood through the circulation

is DCM more common in cats or dogs?

dogs! the larger the dog, the better the chances of getting DCM

are there any breed predispositions to developing DCM?

high rates of disease seen in giant breeds of dogs such as great Danes, Irish wolfhounds, and Scottish deerhounds

BUT some smaller breeds have a strong genetic predisposition, such as Boxers and Dobermans

are there any deficiencies linked to development of DCM in some breeds?

dietary deficiencies can be seen as co-factors → grain-free diets have been linked to DCM!!

describe the expected radiographic findings of the heart of a dog with DCM

The heart is markedly enlarged and occupies most of the thorax. It has a rounded (globoid) appearance, with both ventricles appearing enlarged

what necropsy findings can be associated with DCM?

the heart is enlarged and round, and often the wall is so thinned it 'collapses' under its own weight. A cross-section of the heart reveals marked dilation of the chambers and thinned myocardium.   

what kind of processes that cause necrosis of skeletal muscle can also causes necrosis of cardiac muscle?

white muscle disease caused by vitamin E/selenium deficiency and ionophore toxicity

what happens to the heart if large numbers of myocytes die?

the heart completely loses the ability to pump blood and death will be rapid;

necrotic cells are progressively replaced by fibrosis, which decreases heart’s contractility power, reducing blood pressure that can be generated and the ability of the heart to pump blood around the body

when do we see infarction (a ‘heart attack’) in animals?

infarctions in animals are rare compared to humans;

they may occur secondary to emboli breaking off from endocarditis lesions involving the aorta or left AV valves, secondary to subaortic stenosis, or due to emboli breaking off from an atrial thrombosis

what virus can cause viral myocarditis?

parvovirus in puppies less than two weeks old (super rare though!)

what is it hard for bacteria to colonize the myocardium?

rich vascularization of the tissues allows rapid recruitment of neutrophils and large quantities of oxygen; neither of which is good for bacterial survival

when might we see bacterial myocarditis?

In feedlot cattle, Histophilus somnus causes pneumonia, meningoencephalitis, and myocarditis, but we rarely see disease due to this bacteria in New Zealand. Occasionally, higher bacteria such as mycobacteria can infect the heart. 

when do we see parasitic myocarditis?

Cysticercus ovis (the intermediate stage of Taenia ovis - sheep measles) can develop in the myocardium;

Toxoplasma gondii is a rare cause of fatal myocarditis in young puppies and kittens