SysPath - Cardiology

Differentials for an enlarged cardiac silhouette?

Cardiomegaly, tumour, or pericardial effusion (pericarditis, hydro or hemopericardium).

What is the heart’s capacity for healing?

Limited, so it compensates via dilation, hypertrophy, or activation of neurohumoral mechanisms.

What happens when blood volume expands?

Increased secretion of atrial natriuretic peptide (ANP), which increases Na+ / water excretion & vasodilation.

What are the neurohumoral mechanisms?

A depression in cardiac output leads to release of NE (increased heart rate & vasoconstriction), decreased renal blood flow (increased renin, increased salt/water reabsorption & vasoconstriction), & increased ADH (increased water retention & blood volume).

When does dilation occur in the heart?

Acute volume overload.

What happens to the structure of the heart during dilation?

Myocardial fibres stretch, increasing contractile force, stroke volume, & cardiac output, but at the cost of decreased tension.

When does hypertrophy occur in the heart?

Chronic volume overload.

Primary cardiac hypertrophy (cardiomyopathy)

Genetic or idiopathic myocardial disease.

Secondary cardiac hypertrophy

As a result of sustained increase in workload, or as a result of trophic signals (such as hyperthyroidism).

Eventual result of cardiac hypertrophy

Impaired intrinsic contractility, decreased compliance, & impaired ventricular relaxation.

Eccentric vs. concentric hypertrophy

Eccentric: volume overload (increased preload), causing thin ventricular wall and distended ventricle.

Concentric: pressure overload (increased afterload), causing thick ventricular wall and reduced ventricle.

Gross changes of cardiac hypertrophy

Broadening of right side’s base, increased length of left side, general globose appearance.

Three stages of cardiac hypertrophy

1. Initiation (cell size increase).

2. Compensation (stable hyperfunction, no symptoms).

3. Deterioration (degeneration of cardiomyocytes & fibrosis due to loss of ventricular contractility).

What is heart failure?

When the heart is unable to pump sufficient blood to meet tissue demands. Can be backwards (inability to empty venous reservoirs) or forwards (decreased outflow via great vessels).

Symptoms of congestive (backwards) heart failure

Ascites, pleural effusion, pulmonary edema & dyspnea.

Symptoms of low output (forwards) heart failure

Syncope, lethargy, hypotension & weak pulse.

Mechanism of congestive heart failure

Diastolic filling pressures result in decreased venous return & increased hydrostatic pressure, edema, & congestion. Can occur acutely during shock or at the end stage of chronic heart disease.

Extracardiac consequences of right sided congestive heart failure

Systemic venous congestion causing generalised edema & chronic, passive hepatic congestion, leading to nutmeg liver.

Extracardiac consequences of left sided congestive heart failure

Pulmonary venous congestion causing pulmonary edema & intra-alveolar macrophages that phagocytose RBCs (appear blue in histology due to iron consumption), known as “heart failure cells”.

Shunts of fetal circulation

Ductus venosus, ductus arteriosus, and foramen ovale

Ductus arteriosus

Connects the fetal pulmonary artery to the aorta. Closes functionally within hours of birth, but can take weeks to close structurally (ligamentum arteriosum).

Patent Ductus Arteriosus (PDA)

Failure of the ductus arteriosus to close.

Symptoms of patent ductus arteriosus

Continuous murmur, bounding femoral pulse, arrhythmia, left congestive heart failure.

Haemodynamics of patent ductus arteriosus

Blood shunts left to right, increasing flow to the lungs. Leads to increased venous return to the left heart, causing volume overload & LV eccentric hypertrophy. In rare cases can cause pulmonary hypertension, pressure overload in the RV leading to concentric hypertrophy.

Eisenmenger syndrome

Shunt reversal (right to left) causing cyanosis (+ erythrocytosis, exercise intolerance), due to increased pulmonary resistance & hypertrophy / arteriopathy.

Patent foramen ovale

Communication between RA and LA. If the left atrial pressure is higher than the right it will remain closed, if vice versa it can open.

Atrial septal defect

Fixed opening due to failed development of the interatrial septum.

Haemodynamics of atrial septal defect

Blood shunts from LA to RA, increasing RV blood volume, causing overload & RV eccentric hypertrophy.

Ventricular septal defect

Communication between RV & LV. A “high” VSD is a defect in the membranous septum, a “low” VSD is a defect in the muscular septum.

Haemodynamics of ventricular septal defect

Blood shunted from LV to RV, increasing volume in the RV & pressure equalisation across the ventricles, leading to uniform hypertrophy. Rarely causes shunt reversal / cyanosis.

Valvular dysplasia

Causes valvular insufficiency (regurgitation).

Appearance of dysplastic valves

Short, misshappen leaflets, rolled edges, abnormal chordae tendinae, fusion of leaflets/chordae to wall, or thick or atrophied papillary muscles.

Most common feline congenital heart anomaly

Mitral valve dysplasia, which may cause insufficiency / stenosis.

Haemodynamics of valvular dysplasia

Valvular insufficiency causes systolic regurgitation, leading to volume overload of both atrium & ventricle, causing atrial dilation & eccentric ventricular hypertrophy.

Pulmonic stenosis

Narrowing of the valvular orifice, via a constricting band of fibrous / muscular tissue or fusion of the leaflets. Rarely, can obstruct the right outflow tract.

Haemodynamics of pulmonic stenosis

Stenotic valve restricts outflow, causing pressure overload in RV & RV concentric hypertrophy, leading to right heart failure.

Post-stenotic arterial dilation

Distal to the stenosis, the vessel will dilate to accommodate the increased pressure.

Subaortic stenosis (SAS)

Narrowing of aortic valve orifice, often in aorta. Stenotic site is usually a constricting band of fibrous / muscular tissue.

Haemodynamics of subaortic stenosis

Stenotic valve restricts outflow, causing pressure overload of the LV and concentric hypertrophy. If severe can cause arrhythmias and sudden death or congestive left heart failure.

Jet lesions

Endocardial fibrosis, indicating damage to the intima due to turbulent blood flow.

Tetralogy of Fallot

Ventricular septal defect, overriding aorta, pulmonic stenosis, & right ventricular hypertrophy.

Haemodynamics of Tetralogy of Fallot

Stenotic valve restricts outflow, causing pressure overload in RV & concentric hypertrophy, & along with a right to left shunt through the ventricular septal defect causes cyanosis. Animals usually die due to hypoxia & hyperviscosity.

Ectopia cordis

Heart is located at an abnormal site, such as extrathoracic, intraabdominal, or pre-sternal locations.

Pericardial effusion

Enlargement of the pericardial sac, caused by excess fluid, progressive hemorrhage, exudate, or cardiac enlargement.

Pericardiocentesis

Only way to cure tamponade, by entering the pericardium with a needle & removing fluid.

Hydropericardium

Transudate - clear fluid with low cellularity & protein. Acute pericardial surfaces remain smooth & shiny.

Pathogenesis of hydropericardium

• Increased hydrostatic pressure (RH failure).

• Decreased osmotic pressure (hypoproteinemia).

• Increased vascular permeability (sepsis, vasculitis). May cause visible fibrin / protein in fluid.

• Decreased lymphatic drainage (obstruction by tumor).

Hemopericardium

Accumulation of blood caused by atrial / aortic rupture (due to hemangiosarcoma, chronic valvular regurgitation leading to atrial dilation, puncture, or idiopathic).

Pericarditis

Diffuse, suppurative, fibrinous pericardial inflammation.

Symptoms of suppurative pericarditis

Causes jugular vein distension, murmur, decreased GI motility, distended pericardium, & pericardiocentesis reveals fetid yellow fluid.

Traumatic reticuloperitonitis

A metal object penetrates the reticular wall, diaphragm, and pericardium, causing the pericardium to be filled with fibrinosuppurative exudate.

Etioloigic organisms of swine fibrinous pericarditis

Glaesserella parasuis or Streptococcus suis. Cause fibrinous polyserositis (peritonitis, pericarditis, arthritis, meningitis).

Result of chronic pericarditis

Organising fibrinous pericarditis, where organisation of exudate leads to fibrosis & adhesions. Encases the heart in fibrous tissue leading to limited diastolic expansion (RH failure).

Acquired localised endocardial fibrosis

Causes turbulent blood flow which damages the endocardium. Most common in the atria, associated with valvular insufficiency. Grossly the endocardium appears focally thickened with a rough surface.

Acquired diffuse endocardial fibrosis

Secondary to prolonged cardiac dilation & can impair diastolic expansion. Grossly, the endocardium appears diffusely thickened with a rough surface.

Endocardial mineralisation

Abnormal deposition of calcium / mineral in the endocardium & arteries. Grossly, the endocardium is roughened with pale yellow plaques.

Valvular cysts

Common in calves but have no clinical significance. Can be hematocyst or lymphocyst. May rupture and disappear.

Myxomatous valvular degeneration (endocardiosis)

Common in elderly dogs, primarily affecting the mitral valve. May or may not cause symptoms. Characterised by nodular valvular thickening (of loose, myxomatous tissue) with a smooth, shiny surface.

Consequences of severe myxomatous valvular degeneration

Mitral valvular insuffiency, LV eccentric hypertrophy, left atrial dilation or rupture, & left congestive heart failure.

What to do if you suspect the chordae tendinae have ruptured

Open the left atrium, remove the blood, fill the ventricle and atria with water, & rhythmically compress the heart.

Endocarditis

Frequently caused by bacteria, can be valvular or mural (myocardial). Grossly can be vegetative (mass of exudate/fibrin attached to valve), or ulcerative (denuded endocardium). Causes pyrexia, lameness, murmurs.

Etiologic agents of vegetative valvular endocarditis

• In cattle, Trueperella pyogenes, usually affecting the right AV valve due to venal caval thrombosis.

• In pigs, Streptococcus suis or Erysipelothrix rhusiopathiae.

• In horses, Streptococcus equi, Actinobacillus equuli.

• In dogs, Staphylococcus aureus, Streptococcus, Bartonella.

• In cats, Bartonella, Streptococcus.

Common sequelae of vegetative valvular endocarditis

Thromboembolism (tricupsid / pulmonic endocarditis leading to pneumonia; mitral / aortic leading to renal infarcts).

Congestive heart failure, due to valvular dysfunction.

Myocardial necrosis

Appears histologically as loss of striation, hypereosinophilia, swelling, & nuclear condensation. May have mineralisation in cardiomyocytes.

What happens to the heart during myocardial necrosis?

Cardiac muscle has no repair capacity, so necrotic tissue (consumed by macrophages & neutrophils) is replaced by fibroblasts, leading to scarring.

Ischemic myocardial necrosis

Caused by myocardial infarcts (think humans, atherosclerosis), is rare in animals.

Toxic myocardial necrosis

Caused by cardiotoxins, such as ionophores, antineoplastic medications (Doxorubicin, Cyclophosphamide), toxic plants, or in horses, Cantharidin (blister beetle toxin).

Nutritional myopathy (White Muscle Disease)

Affects artiodactyls, causing skeletal and/or cardiac muscle necrosis (RV in lambs, LV in calves). Often manifests as sudden death in stressed, rapidly growing animals. It can cause birth defects or abortion. Can only be treated early on.

What causes nutritional myopathy?

Selenium & vitamin E deficiency. Causes decreased scavenging of the free radical byproducts of normal cardiac metabolism, leading to peroxidation of cell membranes, thus cardiac/skeletal muscle necrosis & mineralisation.

Neurogenic myocardial necrosis (Brain heart syndrome)

Brain trauma can lead to myocardial necrosis, possibly due to catecholamine (nor/epinephrine, dopamine) release.

Myocarditis

Usually occuring as part of a systemic disease. Appears grossly as pallor. Can be suppurative, lymphocytic, eosinophilic, hemorrhagic, or granulomatous.

Parvoviral myocarditis

Caused by canine parvovirus, which targets rapidly dividing cells. Causes enteritis, & rarely myocarditis in newborn puppies.

Histophilosis (Histophilus somni)

Main cause of myocarditis in cattle on feedlots. Causes vasculitis & myocardial infarction, often including the papillary muscles. May also cause multifocal myocardial abscesses.

Cardiomyopathy

Primary myocardial abnormality, resulting in cardiac hypertrophy & electrical disturbances that can cause congestive heart failure. Is genetic or idiopathic as a result of mutations in cardiac proteins & enzymes.

Hypertrophic cardiomyopathy

Common in cats. Causes lethargy, discomfort, dyspnea, tachypnea, or acute hindlimb paralysis. Often it has no overt signs other than a murmur, but occasionally causes sudden / anesthetic death. Grossly, the heart appears enlarged (can be symmetric or asymmetric), most often affecting the LV, with concentric hypertrophy & left atrial dilation.

Complications of hypertrophic cardiomyopathy

Stiff fibres, impaired ability to accept diastolic flow from the left atrium, & normal systole until end-stage. 10-20% of cats will get saddle thrombus. Rarely, ventricular fibrosis & atrial thrombosis is visible grossly.

Secondary hypertrophic cardiomyopathy

Non-genetic, often caused by feline hyperthyroidism. Leads to concentric biventricular hypertrophy (compensatory).

Dilated cardiomyopathy

Common in large breed dogs. Causes dyspnea, depression, weight loss, syncope, murmur / arrhythmia, ascites, or sudden death. Grossly, appears as increased heart mass with biventricular eccentric hypertrophy / arterial dilation, with thin flabby walls & attenuated papillary muscles.

Functional & microscopic findings for dilated cardiomyopathy

Characterised by progressive cardiac dilation, decreased contractile force, systolic dysfunction. Histologically appears as subtle changes (wavy cardiomyocyte attenuation, degeneration, fibrosis).

Secondary dilated cardiomyopathy

As a result of taurine deficiency, causing eccentric hypertrophy in dogs, cats, & foxes. Correlated with exotic, grain-free pet foods high in pulses.

Diagnostics of restrictive cardiomyopathy

A functional diagnosis of cats, based on ECGs. Causes left ventricular stiffness that impairs diastolic function & atrial enlargement, with regular ventricular thickness & systolic function. Murmurs / arrhythmias are common. Leads to left congestive heart failure.

Gross appearance of restrictive cardiomyopathy

LV fibrosis (endo/myocardial), with atrial enlargement & possibly mural thrombi. Some cases may be end-stage HCM.

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Primarily in boxer dogs (Striatin gene mutation), causing ventricular arrhythmias, syncope, heart failure or death. Grossly, appears as RV eccentric hypertrophy & replacement of RV/LV cardiomyocytes by adipose or fibroadipose.

Examples of other primary myocardial abnormalities

Excessive LV moderator bands (false tendons) in cats, usually incidental.

Congenital endocardial fibroelastosis in Burmese cats, causing diffuse endocardial fibrosis, LV eccentric hypertrophy, & show abnormal collagen / elastic deposits in the myocardium.

Arteriosclerosis

Degenerative hardening of elastic arteries (i.e. aorta), causing elasticity loss & reduced lumen. Branching sites are commonly affected (possibly due to turbulence?).

Grossly, appears as raised white intimal plaques. Histologically, appears as fibrosis in the intima, smooth muscle hypertrophy, & mineral deposition.

Atherosclerosis

Formation of cholesterol plaques in the intima & media of larger elastic arteries. In humans causes heart attacks (coronary) & stroke (carotid/cerebral), but is rare in animals except in dogs due to hypothyroidism, & aged psittacines.

Grossly, appears as prominent thick yellow arteries. Histologically, appears as plaques composed of foamy lipid macrophages, cholesterol clefts, fibroblasts, & smooth muscle.

Arterial hypertrophy

Hypertrophy of smooth muscle in muscular arteries, leading to loss of elasticity & occlusion of the lumen. Often caused by hypertension & increased volume flow.

Brisket Disease (arterial hypertrophy)

Chronic exposure to high altitudes causes alevolar hypoxia, leading to pulmonary arterial constriction, medial hypertrophy, increased vascular resistance & eventually RV hypertrophy & failure.

Aneurysms

Localised weakning & dilation of elastic arteries (& possibly veins). Can be saccular (spherical dilation, resembling balloon) or dissecting (intimal tear causes blood to enter the intimomedial space). They are prone to rupture.

Common causes of aneurysms

Strongylus vulgaris: horses (cranial mesenteric artery, aorta).

Spirocerca lupi: dogs (aorta).

Copper deficiency: mares & dogs (uterine artery).

Vasculitis

Inflammation of the vasculature, caused by systemic infection, hypersensitivity reactions (Ag-Ab complexes), toxins, or adverse drug reactions. Often cause hemorrhage, edema, thrombosis, & infarcts.

Fibrinoid necrosis (Mulberry Heart Disease).

Vascular necrosis with microscopic deposition of acidophilic, proteinaceous material (fibrin, Ab, complement, platelets) in the artery walls.

Mulberry Heart Disease: pigs, as a result of vitE/selenium deficiency leading to decreased free radical scavening, fibrinoid necrosis & thrombosis, causing cardiac hemorrhage & necrosis.

Verminous arteritis

Strongylus vulgaris larvae migrate through the aortic & mesenteric artery walls, inducing inflammation. Adults live in intestines.

Arteritis of Dirofilaria immitis

Adults live in pulmonary arteries, & are detected in the blood. Cause proliferative endoarteritis, arteriosclerosis, pulmonary hypertension & RH failure.

Phlebitis

Vein inflammation, often co-occuring with thrombosis (thrombophlebitis). Often iatrogenic in the jugular (venipuncture), femorally (prolonged prostration of large animals), in the vena cava of cattle or as omphalophlebitis.

How does rumenitis lead to phlebitis / thrombosis?

Grain overload leads to rumenitis, where bacteria cross the mucosa & drain via the portal system to the liver, causing hepatic abscesses. They rupture through the vena cava & cause phlebitis & thrombosis (pieces may break off, causing tricupsid endocarditis or embolic pneumonia leading to hemoptysis).

Hemangioma

Benign endothelial tumour. Common in dogs, often in the skin but can occur in any tissue.

Hemangiosarcoma

Important in dogs. Common in right atrium (auricular), spleen. Masses are dark red & bloody. Can cause cardiomegaly, heart failure, or cardiac tamponade. Readily metastasise to other organs, & appear histologically as spindle-shaped neoplastic cells lining irregular, bloody channels.

Chemodectoma

Tumour of aortic chemoreceptors. Usually benign & non-functional, forming masses within the pericardial sac at the base of the heart. May block lymphatics, causing pericardial effusion or heart failure (compression of atria / vena cava). Bradycephalic breeds predisposed, may also have carotid body tumours (in the neck). Appears as grey-white nodular mass surrounding the great arteries.

Mesothelioma

Diffuse pericardial involvement common. Causes pericardial effusion, possibly with concurrent pleural / peritoneal involvement.