JPC SYSTEMIC PATHOLOGY

CARDIOVASCULAR SYSTEM

February 2025

C-M10

 

Signalment (JPC #2457059): A 9-year-old male castrated domestic shorthair cat

 

HISTORY: This cat presented with acute onset posterior paresis

 

HISTOPATHOLOGIC DESCRIPTION: Heart, cross section at the level of the ventricles: The left ventricular free wall and interventricular septum are thickened up to 7mm and the right ventricular wall is 2mm thick. Multifocally the left ventricular free wall, papillary muscle, and interventricular septum are characterized by increased interstitial fibrous connective tissue that surrounds, separates, and occasionally replaces often degenerate cardiomyocytes (interstitial fibrosis). There are occasional foci up to 1mm in diameter characterized by loss of cardiomyocytes with replacement by moderate amounts of collagen and rare adipocytes (replacement fibrosis). Adjacent to these foci, myofibers are often pale, swollen, and vacuolated with loss of cross striations (degeneration), less often they are shrunken and hypereosinophilic with a pyknotic nucleus (necrosis). Diffusely cardiomyocytes are enlarged 2-3 times normal with abundant eosinophilic fibrillar cytoplasm and a large, vesiculate nucleus (hypertrophy). Multifocally cardiomyocytes are irregularly arranged in right-angle branching or radiating "pinwheel" patterns (myofiber disarray). The tunica media of occasional myocardial small arteries and arterioles is expanded by hypertrophic smooth muscle cells (medial hypertrophy), while the tunica intima is expanded by fibrous connective tissue. There are rare luminal aggregates of polymerized fibrin (thrombi).

 

MORPHOLOGIC DIAGNOSIS: Heart, myocardium: Fibrosis, interstitial, chronic, multifocal, moderate, with myofiber hypertrophy, disarray, degeneration, necrosis and loss, and occasional myocardial arterial intimal and medial hypertrophy with rare thrombi, domestic shorthair, feline.

 

CONDITION: Hypertrophic cardiomyopathy

 

GENERAL DISCUSSION:

• Cardiomyopathy generally refers to idiopathic primary myocardial disease 
  • Diagnosis requires the absence of diseases that cause myocardial hypertrophy, such as significant valvular or vascular abnormality (congenital or acquired) and absence of hyperthyroidism (specifically in cats); presence of either of these results in “secondary cardiomyopathy”
• Cardiomyopathy is subdivided into dilated (DCM), hypertrophic (HCM), and restrictive (RCM) forms; some consider arrhythmogenic right ventricular cardiomyopathy (ARVC) as a fourth category (included under DCM by others)
• In cats, cardiomyopathy subtype frequency is: HCM>RCM>DCM>unclassified; HCM is the most commonly diagnosed cardiac disease of cats
• HCM: Diastolic dysfunction due to concentric ventricular hypertrophy (without dilatation) that is not attributable to other cardiac, vascular, or systemic disease; it is a heterogeneous disease with many phenotypes 

 

PATHOGENESIS:

• Cardiomyopathies can be divided into primary (i.e. genetic or suspected genetic origin) or secondary (known cause other than genetic)
• In cats, identified causes of cardiomyopathy include genetic, nutritional, +/- viral
• Genetic HCM: 
  • Autosomal dominant pattern of inheritance in Maine coons and Ragdolls with a mutation in the gene for myosin binding protein C3 (MyBPC3), a sarcomere protein, that results in myocyte hypertrophy, collagen synthesis, and myofiber disarray 
  • Autosomal dominant inheritance in American shorthair
  • Breed predisposition in British shorthair, Turkish Van, Scottish fold, Rex, Siberian, Sphynx, Bengal, Chartreux, and Norwegian Forest cats
• Nutritional: Taurine deficiency (DCM)
• Viral: Feline panleukopenia virus has been detected via PCR in cats with HCM, DCM, RCM, and myocarditis; feline immunodeficiency virus (FIV) in inflammatory cells infiltrating the myocardium of cats with HCM and myocarditis
• HCM is a diastolic disorder with a complex, poorly understood pathophysiology
  • Myocardiocyte damage of undetermined cause (e.g. genetic, hypoxic) à recruitment and induction of macrophages to release inflammatory and profibrotic mediators (IL-1, IL-6, IL-8, TNF-α, TGF-β, MMP-13, and TIMP-1) à cardiac remodeling, including progressive thickening of the left +/- right ventricular wall (concentric hypertrophy [increase in mass of ventricle without an increase in end-diastolic volume]) à decreased compliance of the ventricular myocardium but normal systolic myocardial contractile function à decreased ventricular filling during diastole (“diastolic failure”, decreased preload) à decreased cardiac output (CO), increased left ventricular diastolic pressure
    • increased back pressure into left atrium à left atrial dilation, left-sided congestive heart failure à pulmonary edema and/or pleural effusion
    • reduced blood flow velocity à abnormal blood flow, hypercoagulability + endothelial damage à 10-30% of cats with HCM develop atrial/iliac artery arterial thromboembolism (“saddle thrombus”) à posterior paresis
    • coronary vessel hypertrophy à luminal narrowing à myocardial ischemia à necrosis (myocardial infarction) à replacement fibrosis
    • in some cases, interventricular septum hypertrophy à papillary muscles displaced anteriorly which pulls on chordae tendinae à displacement of the anterior leaflet of the mitral valve into the left ventricular outflow tract à dynamic obstruction of the left ventricular outflow tract during systole (systolic anterior motion of the mitral valve) à unique “kissing lesion” in the left ventricular outflow tract only seen in cats with this form of HCM à further increased left ventricular pressure à further left ventricular concentric hypertrophy 
  • The increase in wall thickness and relative cardiac weight in feline HCM is not the result of true myocardial hypertrophy but due to a diffuse expansion of the interstitium by vessels, macrophages, and collagen as a consequence of degeneration and repair processes triggered by a still unknown cause
  • A recent study of feline HCM found that myocardial interstitial cell populations with CD34+ phenotype play a role in the pathogenesis of the disease (Rodríguez, Vet Pathol. 2022)

 

TYPICAL CLINICAL FINDINGS:

• Affected cats are usually young adult to middle-aged males
• Forward and/or backward (congestive) heart failure: lethargy, anorexia, dyspnea, tachypnea, coughing, hydrothorax, hydropericardium, ascites, pulmonary edema; sudden unexpected death is often the first manifestation
• Iliac thromboembolism (saddle thrombus): unilateral or bilateral pelvic limb ischemia, posterior paresis/paralysis with extreme pain, cyanotic nail beds and footpads, hyperkalemia
• Gallop rhythms, arrhythmia, murmur

 

TYPICAL GROSS FINDINGS:

• Concentric hypertrophy of left +/- right ventricles, narrowed ventricular lumen, atrial dilation +/- hypertrophy (symmetrical i.e. diffuse, or asymmetrical i.e. focal 
  • Hypertrophy is typically symmetrical (affects septum and free wall equally), or less often asymmetrical (focal or affecting the septum > free wall)
  • Myocardial hypertrophy is best identified by an increased heart weight to body weight ratio; in cats, normal is 3.83 +/- 0.2g/kg, cats with HCM have heart:body weight of 7.0 +/- 0.3g/kg; 
• End-stage HCM can progress to left ventricular dilatation with relative wall thinning
• Less common findings: Atrial thrombosis (+/-thromboembolism of caudal aorta/iliac artery), foci of ventricular fibrosis, endocardial fibrosis in the region of the left ventricular outflow tract

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Hypertrophied cardiomyocytes with vesiculate nuclei arranged in whorled or disorganized interweaving pattern (myofiber disarray) rather than parallel arrangement in the left ventricular free wall and interventricular septum +/- right ventricle; not specific to HCM, but are more severe in HCM than other conditions
• Variable, often extensive interstitial fibrosis especially of the inner 2/3 of the left ventricular free wall; rarely, scattered foci of replacement fibrosis due to myocardial infarction/necrosis +/- foci of cell-rich fibrosis with abundant small- and medium-caliber vessels
• Focal endocardial fibrosis and thickening
• +/- Intramyocardial artery medial hypertrophy (arteriosclerosis, “small vessel disease”, or “vascular dysplasia”)
• +/- Leukocyte infiltration: perivascular infiltrates of lymphocytes and histiocytes

 

ULTRASTRUCTURE:

• Disorientation and loss of myofibers
• Hypertrophied cardiomyocytes with large, pleomorphic nuclei with undulant membranes and prominent nucleoli, dense accumulation of Z-band material, lipofuscin granules; these findings are normal in feline cardiomyocytes but are more severe in cats with HCM 

 

ADDITIONAL DIAGNOSTIC TESTS:

• Echocardiography is the current gold standard to differentiate and classify feline cardiomyopathies
• Cardiac Troponin I (cTnI): Sensitive and specific marker for myocardial injury; increased levels in cats with HCM indicating ongoing myocardial damage; marked elevation in cats with systemic arterial thromboembolic disease 
• N-terminal proBNP (NT-proBNP), a relatively stable cleavage product of BNP which is secreted by ventricular myocytes due to stretch/volume/pressure overload, is increased in proportion to cardiac stretch and stress; it is a valuable screening test to distinguish between congestive heart failure and pulmonary disease in cats
• Masson’s trichrome and Movat’s pentachrome histochemical stains highlight fibrosis

 

DIFFERENTIAL DIAGNOSIS:

Other Cardiomyopathies in Cats:

• Dilated cardiomyopathy (DCM): Systolic dysfunction, rare in cats
  • Underlying cause unknown; often considered secondary to nutritional deficiency (taurine deficiency), toxicity (doxorubicin), severe volume overload, or rarely viral (feline panleukopenia virus); prevalence has decreased since the discovery of the link with taurine deficiency and subsequent dietary management
  • Systolic dysfunction: Decreased force of contraction, increased ventricular end-diastolic volume/afterload à atrial/ventricular dilation à decreased cardiac output, congestive heart failure
  • Gross findings: Dilation/enlargement of all heart chambers, and eccentric cardiac hypertrophy (increased ventricular volume and increased myocardial mass) or thin, flabby walls most often the left ventricle; increased heart to body weight ratio (5.4 +/- 0.3g/kg vs 3.83 +/- 0.2g/kg in normal cats, and vs 7.0 +/- 0.3g/kg in cats with HCM); thickened, opaque endocardium; expanded atrioventricular rings; atrial thrombosis; left or bilateral congestive heart failure (pulmonary edema, pleural effusion, ascites, chronic passive hepatic congestion); occasional arterial thromboembolism
  • Histologic findings: Often only minor changes, including variation in myocyte size, myocyte degeneration and necrosis, myocyte hypertrophy, variable (often mild, diffuse) interstitial edema and fibrosis +/- replacement fibrosis; no significant myofiber disarray
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC) variant of DCM: massive loss of myocytes with replacement by fatty infiltration and fibrosis; in humans, due to genetic defect in desmosomal proteins; occurs rarely in cats
• Restrictive cardiomyopathy (RCM): Decreased ventricular compliance with normal systolic function; also known as left ventricular endocardial fibrosis; a functional term rather than a disease entity
  • Impaired diastolic relaxation of one or both ventricles due to several possible causes of infiltrative disease à reduced diastolic ventricular filling (decreased preload) à decreased cardiac output
    • Causes of impaired diastolic relaxation: 
    • Left ventricular endomyocardial fibrosis: interstitial or endomyocardial fibrosis +/- variable leukocyte infiltration including eosinophils (fibrosis is possibly preceded by endomyocarditis (see C-M09), possibly due to infectious cause, fibrosis may be secondary to turbulent ventricular blood flow
    • Excessive moderator bands in the left ventricle (the trabecula septomarginalis, or moderator band, is normally only present in the right ventricle); likely congenital but manifests in adulthood
    • Others: Congenital endocardial fibroelastosis in Burmese cats (C-M03), amyloid deposition, in association with sarcoidosis, in association with hypereosinophilic syndrome
  • Rare, usually in older male cats
  • Clinical findings: Left-sided or bilateral heart failure, cardiac murmur, dysrhythmia
  • Gross findings: Normal sized ventricular profile with enlarged atria; severe ventricular endomyocardial fibrosis and thickening with marked atrial enlargement, slit-like left ventricular lumen, mural thrombosis, left or bilateral congestive heart failure, +/- excessive moderator bands
  • Histologic findings: 
    • Typical RCM: Endomyocardial replacement with granulation tissue and fibrosis of varying maturity; adjacent myocardium may contain mononuclear inflammatory cells (histiocytes, lymphocytes, plasma cells)
    • Excessive moderator bands: bands of Purkinje cells and dense, mature collagen covered by endothelium
• “Secondary Cardiomyopathy”: Compensatory cardiac concentric hypertrophy due to vascular or metabolic diseases: Hyperthyroidism, hypertension, aortic stenosis, PDA, patent foramen ovale, ventricular septal defects, etc.
• Muscular dystrophy: Due to lack of or abnormal dystrophin; dystrophin deficiency has been reported as an X-linked recessive disorder in cats, also termed “feline hypertrophic muscular dystrophy” and is comparable to Duchenne muscular dystrophy of humans (M-M06)

 

COMPARATIVE PATHOLOGY:

Cardiomyopathies in Other Species:

• Dogs:
  • DCM: Most common canine cardiomyopathy
    • Usually affects young to middle-aged giant and large-breed dogs (e.g. Saint Bernard, Irish Wolfhound, strela Mountain dogs, Great Dane), but also others such as Doberman pinscher, Boxers, Portuguese water dogs, Dalmatians, Newfoundlands, Scottish deerhounds, and some smaller dogs such as juvenile Portuguese water dogs and toy Manchester terriers
    • Causes are mostly unknown
    • Most are likely genetic; may be X-linked recessive in great Danes; autosomal recessive in Portuguese water dogs; autosomal dominant in boxer (or X-linked recessive), Irish wolfhound, and Doberman; familial tendencies in most affected breeds
    • Metabolic: Hypothyroidism has been noted as a reversible cause
    • Clinical signs: short history of left-sided congestive heart failure (cough, depression, dyspnea, syncope), weight loss, polydipsia, or sudden death, atrial fibrillation is the most common ECG abnormality, but ventricular tachycardia and VPCs are common in most Doberman Pinschers with DCM, prognosis is poor; arterial thromboembolism is NOT a feature as it is in cats
    • Histologic findings, two distinct forms:
  • 1) “Fatty infiltration-degenerative” type: Boxers and Doberman Pinschers; myocytolysis, myofiber degeneration, and atrophy with replacement by fibrosis and fatty infiltration
  • 2) “Attenuated wavy fiber” type: giant, large- and medium-sized breeds, including some Boxes and Doberman Pinschers; cardiomyocyte diameter is less than 6um (normal is 10-20um), with separation by clear spaces and minimal cellular infiltrates, most predominant in the left ventricular free wall
    • Differential diagnosis: DCM secondary to cardiotoxicity (doxorubicin, irradiation, ethanol, cobalt, lead, catecholamines, histamine, methylxanthines), infectious (e.g. canine parvovirus), and nutritional (taurine or carnitine deficiency - low blood taurine levels have been found in dogs fed certain lamb-rice commercial diets)
    • Variant form - Arrhythmogenic right ventricular cardiomyopathy: autosomal dominant inheritance in Boxers; right ventricular dilation or aneurysms are common; ventricular arrhythmias are common with left bundle branch block morphology; affected Boxers have a defect in striatin gene (a gene involved in trafficking of WNT pathway proteins, associated with an increase in β-catenin); arrhythmia may be intermittent and there may be no heart chamber enlargement 
    • HCM: Much less common, usually in large breed male dogs, and a heritable form has been suggested in pointers
      • Gross findings: interventricular wall thickness:left ventricular free wall ratio exceeds 1.2:1, there may be dynamic left ventricular outflow tract obstruction with associated thickened tunica intima adjacent to the mitral valve leaflet, thickened mitral valve leaflet, and/or malpositioned papillary muscles 
      • Histologic findings: +/- myofiber disarray, intimal and medial hypertrophy of medium-sized coronary arteries
    • Canine X-linked muscular dystrophy: Affected dogs can develop Duchenne cardiomyopathy (M-M06): Subepicardial interstitial fibrosis à cardiac insufficiency
    • Pheochromocytoma-associated catecholamine-induced cardiomyopathy characterized by multifocal cardiomyocyte necrosis, cardiomyocyte degeneration, myocardial hemorrhage, lymphohistiocytic myocarditis, and interstitial fibrosis
• Cattle: 
  • DCM in Holsteins and Canadian Holstein-origin cattle: likely autosomal recessive inheritance, possibly due to a nonsense mutation in the optic atrophy 3 (OPA3) gene that encodes a mitochondrial protein; results in right-sided congestive heart failure in young to mature cattle; histologically, mix of atrophied, hypertrophied, degenerate, and necrotic myofibers, fibrosis, fatty replacement
  • DCM in Japanese Black calves: likely autosomal recessive inheritance; short period of severe dyspnea with sudden death in calves <30 days old; marked cardiac enlargement with left ventricular dilation, signs of congestive heart failure; marked myocardial degeneration and necrosis with fibrosis especially of the papillary muscles; right ventricle also affected but less severe
  • Polled/horned Hereford calves: Congenital cardiocutaneous syndrome with distinctive haircoat (tightly curled, “wooly”) and cardiac dysfunction including arrhythmias; caused by a 7-bp duplication in NFkB interacting protein-1 gene; affected calves usually die by 12 weeks old
  • HCM: reported in Holsteins
  • Bovine generalized glycogenosis type II (Pompe’s disease): Generalized muscle weakness, occasional cases have left-sided heart failure with eccentric myocardial hypertrophy
• Rodents: Cardiomyopathy is common in aged mice, rats, and hamsters
  • Rats: RCM due to endocardial fibrosis is common in certain strains of aged laboratory rats (up to 80% prevalence in some strains) but also occurs in free-ranging rats; it affects both conventional and specific pathogen free rats; male > female; degeneration most prevalent in the papillary muscles of the left ventricle; interstitial fibrosis is an important feature; +/- cardiac insufficiency;  risk factors include male and heavier rats
  • Syrian hamsters: Cardiomyopathy is particularly common in aged animals; affected animals develop often-fatal cardiomyopathy-associated spontaneous atrial thrombosis and coagulopathy; females are affected younger than males
• Ferrets: Cardiac disease is common in pet ferrets, including the full spectrum of disease of dogs and cats, of which DCM and acquired valvular disease are the most common; regarding cardiomyopathies, DCM >> HCM >> RCM; pathogenesis in ferrets is unknown; HCM has a poor prognosis with frequent sudden death, DCM has a better prognosis with medical management
• Rabbits: Reported causes of secondary cardiomyopathy:
  • Coronaviral infection has been associated with pleural effusion disease and (secondary) cardiomyopathy in laboratory rabbits
  • Administration of ketamine/xylazine, detomidine/xylazine, or detomidine administration has been observed to cause multifocal myocardial degeneration and necrosis with fibrosis attributable to ischemia secondary to vasoconstriction
• Avians: HCM, DCM, and RCM. 
  • HCM: Characteristic microscopic lesions in severe cases of include, disarray, hypertrophy, and increased cytoplasmic basophilia of myofibers with interstitial fibrosis. 
  • RCM: Fibrosis; frequently the result of chronic pericarditis when inflammation and subsequent fibrous tissue contracts.
  • Pulmonary hypertension syndrome (PHS): Broiler chickens; classic example of RV hypertrophy and failure.
  • In chronic cases, the myocardium may have variable degrees of myofiber degeneration, hyaline deposits within myofibers, multifocal necrosis, edema, and fibrosis; these lesions resulting from pulmonary hypertension.
  • Spontaneous cardiomyopathy of turkeys (round-heart disease): a DCM in young turkeys; dilation of both ventricles (R>L)
  • The dilated RV wall is thin and flabby
  • Primary histo lesion - Focal myofiber degeneration (non-specific); enlargement of muscle nuclei and dilation of capillaries may be present 
  • In chronic cases, endocardial fibroelastosis +/- fibrocartilagenous tissue may occur in the LV
  • Cardiac lesions in adult turkeys are enlargement and hypertrophy of the LV
  • Furazolidone-induced cardiomyopathy can also cause dilated cardiomyopathy and similar lesions lesions to those of round heart disease of turkeys.
• Sea otters: Cardiomyopathy is common in Southern but not Alaskan sea otters; DCM is considered the end stage of this chronic condition histologically characterized by variably severe lymphocytic to pleocellular myocarditis with progressive myofiber loss and replacement fibrosis; exposure risk factors include domoic acid (DCM) and Sarcocystis neurona (myocarditis)
• California sea lions: Domoic acid is associated with cardiomyocyte degeneration and necrosis leading to secondary cardiomyopathy; domoic acid is suspected to be a direct cardiotoxin, interacting with cardiac glutamate receptors causing myocyte apoptosis; histologic lesions occur in the interventricular septum and left ventricle
• Striped skunks: Cardiomyopathy has been reported in captive animals
• Mongooses: DCM appears to be somewhat common in captive mongooses
• North American opossums: DCM and HCM are a serious health concern in captive animals, potentially related to obesity
• Cetaceans: Cardiomyopathy and myocardial degeneration are reported in pygmy and dwarf sperm whales; disease predominantly affects adult whales, male > female, of unknown pathogenesis; disease appears to be chronic progressive +/- HCM with end-stage DCM; limited mononuclear infiltrates are infrequent
• Nonhuman primates:
  • Apes (bonobos, chimpanzees, gorillas, orangutans): Cardiovascular disease is progressive with age and is the leading cause of death in captive great apes; idiopathic myocardial fibrosis and cardiomyopathy are a common cause of death in captive apes, +/- associated arteriosclerosis of intramural coronary arteries); this disease is sometimes seen in wild apes; histologic features include left ventricular hypertrophy, interstitial fibrosis, and polyploidy with convoluted nuclei; ventricular hypertrophy may be secondary to systemic hypertension 
• Humans:
  • genetic defects associated with cardiomyopathy include proteins associated with cardiac contraction (HCM), cytoskeletal proteins (DCM), or mitochondrial enzymes (DCM or HCM), and a carnitine transporter protein (DCM)
  • Specific genes identified in HCM include cardiac troponin T gene (cTnT), myosin heavy chain gene (MyHC), and cardiac myosin-binding protein C (MyBPC3) 

  

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