chapter 010-cardiovascular dx

7/28/2019 Chapter 010-Cardiovascular Dx

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Web Fig. 10-1 Schematic diagram showing serially connected pulmonary and systemic circulatory systems and how to trace the ow o blood.

A, Right heart chambers propel unoxygenated blood through the pulmonary circulation, and the let heart propels oxygenated blood through the systemiccirculation. B, Te direction o blood ow begins at the let ventricle o the heart, ows to the arteries, arterioles, capillaries o each body organ, venules,veins, right atrium, right ventricle, pulmonary artery, lung capillaries, pulmonary veins, let atrium, and then goes back to the let ventricle. RA, Right atrium;RV, right ventricle; LA, let atrium, LV, let ventricle. (From McCance, K: Pathophysiology: Te biologic basis or disease in adults and children, ed 6, St Louis, 2009, Mosby.)

Right pulmonary

artery

Left pulmonary

artery

Left pulmonaryvein

Left lungcapillaries

Aorta

RALA

RVLV

Systemiccirculation

Intestinalcapillaries

Renalcapillaries

Systemiccapillary beds

Heart

Right atrium

Right ventricle

Heart

Left atrium

Left ventricle

Hepaticportalsystem

Vena cava

Right lungcapillaries Liver circulation

Right pulmonaryvein

A

B

Aorta

Lungs

Arteries

Arterioles

Capillaries

Venules

Veins

Pulmonaryveins

Pulmonaryartery

Venaecavae

Veins ofeach organ

Venules ofeach organ

Arteries ofeach organ

Arterioles ofeach organ

Capillariesof each organ

STRUCTURE

MACROSCOPIC STRUCTURE

Cardiac Conduction System

e81CHAPTER 10 Cardiovascular System and Lymphatic Vessels

Copyright 2012, 2007, 2001, 1995, 1988 by Mosby, Inc., an affiliate of Elsevier Inc.


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Web Fig. 10-2 Normal cardiac muscle.Heart, let ventricular myocytes, longitudinal section, normal rat. Numerous densemitochondria (arrows) lie between myofbrils, which have prominent bands. N,Nucleus. EM. Uranyl acetate and lead citrate stain. (Courtesy School o VeterinaryMedicine, Purdue University.)

N

Web Fig. 10-3 Heart, fbrous stroma o the cardiac conduction system, goat.

A, Atrioventricular (AV) node. Te AV node (1) is composed o interconnecting nodal myofbers that are supported by loose collagenous and elastic fbrousstroma. Te node is embedded in adipose tissue (2) that is adjacent to the cardiac fbrous skeleton (arrows) that has undergone ocal chondroid metaplasia(3). Endocardium (arrowhead). H&E stain. A1, AV node, goat. Serial section oA. Note the overall deposition o collagen fbers (blue) in the structureslabeled 1 and 3 in Web Fig. 10-3,A. Massons trichrome stain. B, AV bundle. In this illustration, the AV bundle (1) travels diagonally through the center othe image rom the lower let to the upper right margins. It is supported by a loose to dense intervening interstitial collagenous stroma and is surrounded byadipose tissue (2). Cardiac cartilaginous skeleton (3). H&E stain. B1, AV bundle, goat. Serial section o B. Note the overall deposition o collagen fbers(blue) in the structures labeled in Web Fig. 3, B. Massons trichrome stain. (Courtesy Drs. A. Gal and J.F. Zachary, College o Veterinary Medicine, University oIllinois.)

1

A A1

B B1

2

3

1

2

3

MICROSCOPIC STRUCTURE

Myocardium

Cardiac Conduction System



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Web Appendix 10-1

NECROPSY ASSESSMENT OF HEART ANDVASCULAR STRUCTURES

Occasionally, normal eatures in animal hearts can be misinter-preted as lesions. Te epicardial lymphatic vessels, especially incattle, can appear as prominent white streaks that could be inter-preted as areas o necrosis. Te septal cusp o the tricuspid valve indogs is normally rather tightly attached to the ventricular septum.In young ruminants up to 2 to 3 weeks o age, the ductus arteriosusand oramen ovale can be probed patent, but unless the openingsare large, no signifcant shunting o blood is likely to occur duringlie. Te overall shape o normal hearts can vary rom the elongatedconical profle in the horse to the somewhat rounded shape in thedog. Cardiac weights vary greatly among species and breeds; pigshave relatively small hearts (approximately 0.3% o body weight)and dogs have relatively large hearts (rom 0.75% o body weightin nonathletic breeds to 1.25% in athletic breeds).

Postmortem alterations in hearts and vascular structures mustbe recognized and correctly interpreted. Rigor mortis occurs inmyocardium much as in skeletal muscles and produces contracted,rigid ventricular walls, which empties the more muscular let ven-tricle. Ater rigor passes, the ventricular walls relax.

Postmortem blood clotting produces red (currant jelly) clotsin the atria, right ventricle, and large vessels at the base o the heart.Postmortem blood clots are ound in these anatomic structures

Web Fig. 10-4 Postmortem chicken at arterial cast, dog.

Note how the clot conorms to the shape o the lumens o the vessels romwhich it was removed. Chicken at clots consist primarily o clotted plasmaand fbrin and other proteins o the coagulation cascade. Tey are otenindicative o anemia; however, in all animals their ormation by the separa-tion o the red blood cells rom the rest o the components o blood dependson the erythrocyte sedimentation rate (ESR). Separation can occur in allanimals in response to systemic inammation, which increases the ESR,but the horse normally has a high ESR because equine erythrocytes clumptogether in rouleau ormation, which increases the ESR. Tus dependingon the ESR, postmortem clots may be pale white to yellow ( chicken atclot) or shiny red (currant jelly clot) or sometimes a mixture. (Courtesy Dr.R.K. Myers, College o Veterinary Medicine, Iowa State University.)

Web Fig. 10-5 Focal hemorrhage and discoloration, intracardiac injec-tion, euthanasia solution, let ventricle, dog.

Euthanasia solution is oten injected into the let ventricle. In this case,solution was injected into the myocardium and caused a localized area ohemorrhage and discoloration. A mixture o euthanasia solution and bloodoten orm a brownish sludge in the ventricle. (Courtesy College o VeterinaryMedicine, University o Illinois.)

because they lack contractile elements (large vessels) or have lessmuscle mass (atria, right ventricle) to undergo contraction duringrigor mortis. In postmortem evaluations o the heart, it is importantto note the presence (or absence) o blood clots in the ventriclesand their appearance ( currant jelly versus chicken at) (Web Fig.10-4). Under normal conditions, because o its larger chamber

volume and thinner walls, a blood clot will be ound in the rightventricle, whereas little or no blood clot will be ound in the letventricle because o its smaller chamber volume and thicker walls.Animals with prolonged heart disease may lack adequate glycogenreserves in cardiac myocytes. As a result, the ventricular chambersmay ail to contract during rigor mortis, allowing a blood clot toorm in the let ventricle.

Occasionally, pale chicken at clots that contain reducednumbers o erythrocytes orm in animals with severe anemia, sys-temic inammatory disease, leukemia, or ater prolonged agonalperiods. Horses more oten have pale clots because o a rapiderythrocyte sedimentation rate termed rouleaux ormation. Post-mortem lysis o erythrocytes ollowed by imbibition o hemoglobinproduces diuse red staining o the endocardium and epicardiumand simulates the appearance o hemorrhage.

Usually 12 to 24 hours ater death, erythrocytes lyse, and theresultant imbibition o hemoglobin produces red discoloration othe normally white intima o blood vessels. Postmortem clottingmust be dierentiated rom thrombosis. Postmortem clots, oundin veins and large elastic arteries as red currant jelly type or occa-sionally as pale chicken at type, are readily removed by tractionor gentle ushing at necropsy, in contrast to thrombi, which areadherent. Postmortem contraction o muscular arteries because o




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Web Appendix 10-2EXAMINATION OF THE CARDIOVASCULARAND LYMPHATIC SYSTEMS AT NECROPSYAND TISSUE SAMPLING FORHISTOPATHOLOGIC EVALUATION

Ater the removal o the rib cage and exposure o the thoracicorgans, the pericardial sac should be incised and observations madeon the presence o pericardial thickening and adhesions and the

Web Fig. 10-6 Schematic diagram o the gross and microscopic examination o the heart.

Diagrams A to D illustrate the heart opened. Te numbers indicate the area and the shape o the blocks o tissue removed or histopathology. A, Rightventricle and right atrium. B, Right ventricular cavity and pulmonary outow tract. C, Let ventricle and let atrium. D, Let ventricle and aortic outowtract. 1, Right ventricular ree wall, atrioventricular valve, and atrium.2, Pulmonic valve, right ventricular outow tract, and pulmonary artery.3, Right auricularappendage. 4, Sinoatrial node. 5, Let auricular appendage. 6, Let atrioventricular valve, ventricle, and atrium. 7and 8, Let ventricular ree wall and papillarymuscles. 9, Atrioventricular node, right atrioventricular valve, and atrium. 10, Interventricular septum. 11, Aortic valve, let aortic outow tract, and aorta.(From Bishop SP: Necropsy techniques or the heart and great vessels. In Fox P, Sisson D, Moise N, eds: extbook o canine and eline cardiology, ed 2, Philadelphia, 1999,

Saunders.)

1

3

4

9Coronary

sinus

Caudalvena cava

Right atrium

Tricuspid valve

Right ventricle

A

2

Pulmonaryartery

Rightventricle

Tricuspid valveB

6

7,8

10

Left atrium

Mitral valve

Leftventricle Interventricular

septumC

5

11

Aorta

Left atrium

Interventricularseptum

Leftventricle

D

nature and amount o pericardial uid present. Samples o the uidusing aseptic techniques should be taken at this time or culture inecessary. Te heart and lungs should be removed together andexamined. Te great vessels are transected, and the entire heart isexamined to determine its overall shape, size, and color.

Te hearts o most animals are dissected to expose the endo-cardium and the our valves. A systematic approach should beollowed; usually the heart is opened in the direction o blood ow

with incisions through the right atrium and right ventricle to the

rigor mortis extrudes blood. Microscopically, these muscular arter-ies are devoid o blood, and their internal elastic lamina is wavy incross sections o the contacted vessel.

Other potentially misleading fndings at necropsy o young dogsand horses include diuse or patchy myocardial pallor that

subsequently ails to correlate with any detectable microscopicalterations. Also, the intracardiac injection o euthanasia solutionand other substances can cause hemopericardium and myocardialpallor rom tissue dissolution and rom crystalline deposits at thesite o solution deposition (Web Fig. 10-5).

e84 SECTION 2 Pathology of Organ Systems



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right ventricular apex and then along the right ventricular walladjacent to the interventricular septum into the pulmonary outowtract. Te let side is incised rom the atrium to the let ventricularapex to expose the endocardial suraces and mitral valve; subse-quently, the mitral valve leaet is incised to expose the outow tractinto the aorta. Ater all observed lesions and the weight o the heartare entered in the written record, the heart, dependent on the size,is placed in fxative solution or appropriate samples are taken andplaced in fxative (Web Fig. 10-6). It is important to obtain thebody weight and an accurate heart weight and then calculate thepercent heart weight to body weight ratio to determine i there isan increase or decrease in size o the heart.

Te hearts o small animals, such as rodents, birds, puppies,and kittens, are oten collected and placed intact in the fxativesolution.

Other procedures that can be perormed on hearts beore fxa-tion to quantitate hypertrophy and dilation include measurementso ventricular wall thicknesses, determination o weights o indi-

WEB TABLE 10-1 Experimental Models of Heart Failure

Experimental Model Experimental Method SpeciesPressure loading Pulmonary artery banding Rat, dog, pig, sheep, pony

Aortic constriction Rat, rabbit, dog, sheep

Supravalvular aortic constriction Dog

Aortic valve stenosis Rabbit, dog

Pulmonary valve stenosis Dog

Experimental hypertension Rat, dog

Volume loading Fluid overload Baboon

Aorta-to-vena cava fistula Rat, dog

Aortic valve incompetence Rat, rabbit

Atrial septal defect Cat

Myocardial infarction Sustained atrial pacing Dog

Coronary ligation Dog, pig

Controlled occlusionsubclavian-to-carotid shunt Dog

Coronary embolism Dog, calf, pig

Thrombus generation Dog

Chronic hypoxia Rat

Cardiomyopathy and other conditions Left ventricular Dacron patch Dog

Spontaneous cardiomyopathy Hamster, mouse, cattle, rat, turkey, cat, dog

Barbiturate overdose Dog

Furazolidone cardiomyopathy Turkey, duckling

Adriamycin cardiomyopathy Rat, dog, mouse, pig

Isoprenaline Rat

Noradrenaline Dog

Amphetamine Rat

Cobalt chloride Rat, pig

Vitamin E deficiency Rat, mouse, calf, lamb

Alcohol intoxication RatCoxsackie viral myocarditis Mouse

Viral encephalomyocarditis Mouse

Altered cardiac development and/or function Transgenic mice

Modified from Smith HJ, Nuttall A: Cardiovasc Res19:181-186, 1985.

vidual cardiac chambers and septum, and measurements o atrio-ventricular valve (AVV) ring circumerences.

Arteries, particularly the cranial mesenteric artery o the horseand caudal aorta in cats and veins, which have had intravenouscatheters, need to be assessed at the time o postmortem evaluation.Samples o diseased areas o veins, arteries, and lymphatic vesselsshould be placed in ormalin ater appropriate samples are submit-ted or virus, bacteria, or parasitic evaluation.

Ater fxation or at least 24 hours, tissue samples should beremoved rom standard heart sites or histopathologic evaluation(see Web Fig. 10-6). I gross lesions are apparent, representativesamples should be taken o those lesions. In small-sized hearts, thefxed specimen is bisected perpendicular to the long axis o theseptum to provide a sample or histopathologic study that includessections o all our chambers and interventricular and interatrialsepta.

Special sampling procedures are available or comprehensiveevaluation o the cardiac conduction tissue.




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Web Fig. 10-7 Epicardial hemorrhage, minoxidil cardiotoxicity, heart,let atrium, pig.

Note epicardial hemorrhage (upper let) and prominent small blood vesselswith swollen endothelial cells (arrows). H&E stain. (Courtesy School o Vet-erinary Medicine, Purdue University.)

Web Fig. 10-8 Hydropericardium, chicken.

Note the accumulation o clear yellow uid (transudate) in the pericardialcavity. Tis uid may occur as a result o hypoproteinemia, heart ailure, andvascular injury. I this accumulation is rapid, it compresses the heart (H)and great vessels, leading to a condition known as cardiac tamponade,which restricts venous return to the heart and reduces the end diastolicpumping volume o the heart. (Courtesy College o Veterinary Medicine, Uni-versity o Illinois.)

H

Web Appendix 10-3

CLINICAL DIAGNOSTIC PROCEDURES

Te array o diagnostic tools available to the veterinarian to detectand evaluate changes in cases o cardiac disease has grown dramati-cally in the past several decades, as many procedures have beenadapted rom use in human medicine. Procedures include physicalexamination, radiography, electrocardiography, echocardiography,angiocardiography, and cardiac catheterization. Cardiac myocardialdamage can be detected by increased activity o serum enzymes andisoenzymes, such as creatine kinase (CK), lactate dehydrogenase

(LDH), troponin (n), troponin I (nI), and aspartate amino-transerase (AS), which are specifcally leaked rom injuredcardiac muscle cells. Also, increased plasma concentrations oplasma natriuretic peptides (A type [atrial] ANP and B type[brainBNP) may indicate cardiac disease. Tese hormones are syn-thesized and released by cardiac muscle cells in increased amountsduring cardiac dysunction. In research studies o cardiac diseasesin animals, endomyocardial biopsies have been used to assess thelight microscopic and ultrastructural alterations during the courseo the disease.

FUNCTION

PERICARDIUM

Disturbances of Circulation

Hemorrhage

EffusionsHydropericardium




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Web Fig. 10-10Visceral gout, heart, pericardium, chicken.

White urate deposits are present on the epicardial surace. (Courtesy Collegeo Veterinary Medicine, Te Ohio State University; and Noahs Arkive, College o

Veterinary Medicine, Te University o Georgia.)

Web Fig. 10-9 Epicardial calcifcation, heart, right ventricle, mouse.

A, Note the prominent white mineral deposits over the right ventricle (RV).B, Te basophilic mineral deposits are present epicardially and in the outermyocardium (let). H&E stain. (Courtesy School o Veterinary Medicine, Purdue University.)

RV

A B

Cell Degeneration and Death

Epicardial Calcification

Gout




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Web Fig. 10-11 Chronic passive congestion, doxorubicin cardiotoxic-ity, congestive heart ailure, liver, ascites, rabbit.

Note the light-red-stained transparent uid in the peritoneal cavity (ascites)and the mottled liver (L) characteristic o chronic passive congestion. (Cour-tesy School o Veterinary Medicine, Purdue University.)

L

Web Fig. 10-12 Cardiac dilation, doxorubicin cardiotoxicity, heart,

rabbit.All cardiac chambers are dilated. (Courtesy School o Veterinary Medicine,Purdue University.)

Web Fig. 10-13 Myocardial vacuolar degeneration, chronic doxorubi-cin cardiotoxicity, heart, section o myocardium, dog.

Te aected myocytes have prominent sarcoplasmic vacuolation (arrows).Plastic-embedded, toluidine bluestained section. (Courtesy School o Veteri-nary Medicine, Purdue University.)

Web Fig. 10-14 Sarcoplasmic vacuolation, chronic doxorubicin car-diotoxicity, heart, section o myocardium, dog.

Te prominent sarcoplasmic vacuolation (V ) is produced by distention oelements o sarcoplasmic reticulum. Even though the myofbrils have exten-sive lysis, mitochondria (arrowheads) are intact. EM. Uranyl acetate andlead citrate stain. (Courtesy School o Veterinary Medicine, Purdue University.)

MYOCARDIUM

Cell Degeneration and Death

Hydropic Degeneration




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Web Fig. 10-15 Myofbrillar lysis, urazolidone cardiotoxicity, heart,ventricular myocardium, duckling.

Aected myocytes have extensive dissolution o myofbrils with scatteredree myoflaments and dense clumps o Z-band material (arrowheads).Other organelles appear normal. EM. Uranyl acetate and lead citrate stain.(Courtesy School o Veterinary Medicine, Purdue University.)

Web Fig. 10-16 Myocardial necrosis, monensin toxicosis, necroticmyocyte, heart, longitudinal section, cal.

Te necrotic myocyte (center) has disrupted myofbrils, damaged mitochon-dria with matrical densities, and several invading macrophages (M). F,Fibrin. EM. Uranyl acetate and lead citrate stain. (Courtesy School o Vet-erinary Medicine, Purdue University.)

Web Fig. 10-17 Myocardial necrosis, electric shock overdose by def-brillator, heart, dog.

Te dark shredded segments o myocytes are due to acute contraction bandnecrosis. Te time interval between defbrillation and the fxation o theheart was 24 hours. Plastic-embedded, toluidine bluestained section.(Courtesy School o Veterinary Medicine, Purdue University.)

Web Fig. 10-18 Myocardial necrosis, monensin toxicosis, heart,section o myocardium, cal.

Necrotic myocyte has disrupted contractile material invaded by a macro-phage (M). Te basal lamina o the necrotic myocyte is noted by arrow-heads. EM. Uranyl acetate and lead citrate stain. (Courtesy School oVeterinary Medicine, Purdue University.)

Myofibrillar Degeneration Myocardial Necrosis




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WEB BOX 10-1 Toxicants Affecting Blood Vessels

ARTERIESToxicants that produce arterial medial smooth muscle proliferation:

Ergot (Claviceps purpurea), ergotamine.

Fescue (Festuca arundinacea) parasitized by endophytic fungi(Epichloe typhina, Acremonium coenophialum).

Toxicants that induce arterial medial calcification:

Vitamin D (dietary excess or cholecalciferol-containing

rodenticides).

Calcinogenic plants (Cestrum diurnum, Trisetum flavescens,

Solanum malacoxylon, Solanum torvum).

Toxicants that induce necrosis of arterial medial smooth muscle and

medial hemorrhage:

Epinephrine, norepinephrine, digoxin, theobromine, minoxidil,

hydralazine, fenoldopam mesylate, phosphodiesterase

inhibitors, endothelin receptor antagonists, dopamine

receptor agonists, others.

Toxicants that alter arterial connective tissue to produce aneurysms:

-Aminopropionitrile (Lathyrussp. product). Penicillamine, aminoacetonitrile.

Toxicants that induce arterial intimal proliferation:

Ergotamine, methylsergide, estrogen and/or progesterone-

containing oral contraceptives, other.

Toxicants that induce arterial fibrinoid necrosis:

Organic mercury, lead.

VEINSToxicants that induce venous hyaline degeneration:

Phenylbutazone.

CAPILLARIESToxicants that incite microangiopathy:

Cadmium, cyclophosphamide.

BLOOD LYMPHATIC VASCULAR SYSTEMS

Blood Vessels

INFLAMMATION

Thrombosis and Embolism

Coronary and Other Arteries

Web Fig. 10-19Arterial thrombosis, subacute, interlobular artery,kidney, dog.

An interlobular artery contains a thromboembolus, which has frmlyattached to the vessel wall. Note the large size o the thromboembolus whencompared to the luminal diameter (see bottom let corner) o the artery.Tis fnding suggests that it is growing in size via the mechanisms oVirchows triad and the adherence o platelets and fbrin to the initialembolus. (Courtesy College o Veterinary Medicine, University o I llinois.)




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HYPERTROPHIC CARDIOMYOPATHY: CATSMaine Coon cats: Autosomal dominant

Ragdoll cat: Autosomal dominant (?)

British shorthair cat: Autosomal dominant (?)

DILATED CARDIOMYOPATHY: DOGSPortuguese water dog: Autosomal recessive

Doberman Pinscher dog: Autosomal dominant

Irish wolfhound dog: Autosomal dominant (recessive?)

Newfoundland dog: Autosomal dominant

Great Dane dog: X-linked recessive (?)

CARDIOMYOPATHY WITH X LINKED MUSCULARDYSTROPHYDOGSIrish terrier, golden retriever, Dalmatian, Shetland sheepdog, Samoyed,

Pembroke Welsh corgi, Japanese spitz, Alaskan malamute dog:

X-linked recessive

ARRHYTHMOGENIC RIGHT VENTRICULARCARDIOMYOPATHY: DOGBoxer dog: Autosomal dominant

CARDIOMYOPATHY WITH CURLY HAIRCOAT: COWPoll Hereford cow: Autosomal recessive

DILATED CARDIOMYOPATHY: COWHolstein-Friesian cow: Autosomal recessive with X-linked muscular

dystrophy

CARDIOMYOPATHY WITH MUSCULARDYSTROPHY: HAMSTERSyrian golden hamster: Autosomal recessive

VALVULAR ENDOCARDIOSIS (MYXOMATOUSVALVULAR DEGENERATION)Cavalier King Charles Spaniel: Polygenic trait

Dachshund: Polygenic trait

AORTIC STENOSIS (SUBVALVULAR)Newfoundland: Polygenic trait

TETRALOGY OF FALLOT: CONOTRUNCAL DEFECTSKeeshond: Simple autosomal locus with partial penetration in

heterozygous and complete penetrance in homozygotes

PATENT DUCTUS ARTERIOSUS

Poodle: Polygenic trait

PULMONIC STENOSISBeagle: Polygenic trait

TRICUSPID DYSPLASIALabrador retriever: Autosomal dominant with reduced penetrance

WEB BOX 10-2 Inherited Cardiovascular Diseases of Animals

DISORDERS OF DOMESTIC ANIMALS

Web Fig. 10-20 Hypertrophic cardiomyopathy, heart, ventricular myo-cardium, cat.

A, Note the pattern o interwoven cardiac myocytes, indicating myofberdisarray, and the hypertrophic myocytes (compare with Figs. 10-20 and10-51). Te number o fbroblasts is increased in the interstitium. H&Estain. B, Normal cardiac myocytes arranged in parallel bundles. (CourtesyDr. L Borst, College o Veterinary Medicine, University o Illinois.)

MYOCARDIUMHypertrophic cardiomyopathy (hypertrophy)




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Web Fig. 10-21 Intimal body(arrow), intestine, muscular artery, horse.

Intimal bodies are distinctive small, mineralized masses within the suben-dothelium o small muscular arteries and arterioles o horses. Tey are anincidental fnding and have no pathologic signifcance. H&E stain. (CourtesyDr. M.D. McGavin, College o Veterinary Medicine, University o ennessee.)

DISORDERS OF HORSES

Arterial Intimal Calcification

Web Fig. 10-23 Fibrinoid necrosis, mulberry heart disease, vitaminEselenium defciency, heart, section o myocardium, pig.

Te aected arteriole (let) has intraluminal masses o fbrin (F) andentrapped erythrocytes. Fibrin masses are present in the vessel wall, and theadjacent interstitium has edema and hemorrhage. Note scattered erythro-cytes (E). EM. Uranyl acetate and lead citrate stain. (Courtesy School oVeterinary Medicine, Purdue University.)

FE

E

DISORDERS OF PIGS

Dietary Microangiopathy

Web Fig. 10-22 Myocarditis, East Coast ever, heart, cow.

Te multiple white-beige areas in the let ventricular wall are infltrates omononuclear inammatory cells. (Courtesy School o Veterinary Medicine,Purdue University.)

DISORDERS OF RUMINANTS

East Coast Fever (Theileria parva)

Web Fig. 10-24Vasculitis with inarction (arrows), neuroparenchyma,edema disease (enterotoxemic colibacillosis), brainstem, pig.

Some strains oEscherichia coli produce a Shiga-like toxin that causesnecrosis o smooth muscle cells in small arteries and arterioles in the centralnervous system (CNS), leading to vasculitis and inarction. Te toxin bindsto specifc receptors on endothelial cells (see Chapter 4), and this bindingcan initiate a chain o inammatory and immunologic reactions that leadto vascular damage. H&E stain. (Courtesy Dr. M.D. McGavin, College o Vet-erinary Medicine, University o ennessee.)

Cerebrospinal Angiopathy

Web Fig. 10-25 Fibrin thrombi, disseminated intravascular coagula-tion, lung, alveolar septal capillaries, horse.

Fibrin thrombi (arrows) occlude two alveolar capillaries. H&E stain. (Cour-tesy School o Veterinary Medicine, Purdue University.)

African Swine Fever



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Web Fig. 10-27Verminous arteritis, diroflar iasis, pulmonary artery,dog.

A dead adult Diroflaria immitis (DI) parasite in the lumen o the pulmo-nary artery is surrounded by pyogranulomatous inammatory cells adhered

to the wall (let) o the artery. Note the loss o the endothelial cells on thelet side o the artery. H&E stain. (Courtesy School o Veterinary Medicine,Purdue University.)

DI

Web Fig. 10-28 Chronic endarteritis, diroflariasis, lung, pulmonaryartery, dog.

Several intact adult Diroflaria immitisare in the lumen. Note the thickenedfbrotic intima (arrow). H&E stain. (Courtesy School o Veterinary Medicine,Purdue University.)

Heartworm DirofilariasisDISORDERS OF DOGS

Fibrocartilaginous Embolism

Web Fig. 10-26 Fibrocartilaginous emboli, multiocal inarction,spinal cord, dog.

Note the poorly stained (pale red to clear) areas in the let hal o the spinalcord aecting both dorsal and ventral gray horns and all uniculi. Te ventralgray horn is aected on the right side. Tese areas are inarcts caused byocclusion and blockage o blood ow in arterioles supplying blood to theseareas by fbrocartilaginous emboli. Emboli are thought to cross rom thevenous side to the arterial side o the circulatory system in vascular anas-tomoses that orm in metaplastic and degenerative cartilage as occurs inintervertebral disk disease. H&E stain. (Courtesy Dr. M.D. McGavin, Collegeo Veterinary Medicine, University o ennessee.)




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Buergelt CD: Equine cardiovascular pathology: an overview,AnnHealth Res Rev 4:109, 2003.

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Kierszenbaum AL: Histology and cell biology: an introduction topathology, ed 2, St Louis, 2006, Mosby.

King JM, Roth L, Haschek WM: Myocardial necrosis secondaryto neural lesions in domestic animals, J Am Vet Med Assoc180:144-148, 1982.

Lewis W, Haase C, Raidel S et al: Adverse eects o drugs on thecardiovascular system. In Silver MD, Gotlieb AI, Schoen FJ,editors: Cardiovascular pathology, New York, 2001, ChurchillLivingstone, p. 541.

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Web Fig. 10-29 Polyarteritis nodosa, mesenteric arteries, rat.

Te aected segments o the arteries are thick, red, hemorrhagic, and tortu-ous (arrows).(Courtesy School o Veterinary Medicine, Purdue University.)

Web Fig. 10-30 Periarteritis and arteritis (polyarteritisbeagle painsyndrome), beagle dog.

Note the accumulation o lymphocytes and macrophages around the arte-riole. H&E stain. (Courtesy Dr. P.W. Snyder, School o Veterinary Medicine,Purdue University.)

Polyarteritis




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chapter 010-cardiovascular dx

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