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| − | {{toplink
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| − | |backcolour = FFADB9
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| − | |linkpage =Cardiorespiratory System - Pathology
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| − | |linktext =Cardiorespiratory System
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| − | |maplink = Cardiorespiratory System (Content Map) - Pathology
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| − | |pagetype =Pathology
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| − | |sublink1=Heart and Great Vessels - Pathology
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| − | |subtext1=HEART AND GREAT VESSELS
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| − | }}
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| − | <br>
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| − | ==Functional Anatomy==
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| − | The endocardium is a smooth layer continuous with the lining of the blood vessels.
| + | #REDIRECT[[:Category:Endocardial Pathology]] |
| − | The endocardium also provides the structure to the valve leaflets.
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| − | Because of its close association with the blood, endocardium is particularly at risk of trauma and haematogenous infection.
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| − | Valvular disease is very rare in the cat, further discussion refers to canine disease.
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| − | ==Degenerative pathology==
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| − | ===Valvular Endocardiosis===
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| − | [[Image:heart valve.jpg|right|thumb|125px|<small><center>'''Heart Valve'''. Courtesy of A. Jefferies</center></small>]]
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| − | ''Incidence:''<br>
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| − | The most common cardiovascular lesion in dogs. In dogs over 9 years old 97% show lesions, of which approximatley 40% are clinically significant.
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| − | Often found at post mortem as an incidental age related change.
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| − | Aetiology is not currently known but breeds affected include chondrodystrophoid breeds E.g. Pomeranian. Males show a significantly higher prevalence of disease than females.
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| − | Potential genetic influence based on connective tissue degeneration. The disease appears similar to ''prolapsed mitral valve syndrome'' in humans which is associated with abnormalities in collagen metabolism.
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| − | ''Pathology:''<br>
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| − | [[Image:Endocardiosis2.jpg|right|thumb|125px|<small><center>'''Endocardiosis'''. Courtesy of A. Jefferies</center></small>]]
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| − | The pathological lesion occurs when collagen in the fibrosa layer of the valve leaflet degenerates and loose fibrelastic tissue and glycosaminoglycans are laid down in the spongiosa layer. This is mucoid or '''myxomatous degeneration'''. Endocardiosis is a sterile degenerative disease so no inflammatory infiltrate will be present, perhaps only a few chronic inflammatory cells E.g. lymphocytes.
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| − | The valve leaflet becomes thickened, the edges often rolling in on themselves. The lesions progress from small nodular areas to larger plaques to make the valve incompetent. Large lesions result in distortion of the valve leaflets and potentially rupture of the chordae tendinae.
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| − | [[Image:dilated left atrium.jpg|right|thumb|125px|<small><center>'''Dilated left atrium'''. Courtesy of T. Scase</center></small>]]
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| − | In most cases the mitral valve is affected, the tricuspd valve is less commonly involved and the semilunar valves even less commonly involved.
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| − | Incompetent valves allow mitral regurgitation and left atrial dilation. The regurgitant jet applies damaging forces on the atrial endocardium which may result in [[Endocardial - Pathology#Endocardial_Mineralisation|endocardial mineralisation]] and in extreme cases may facilitate left atrial rupture and haemopericardium.
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| − | ''Cinical Signs:''<br>
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| − | The eventual sequale of endocardiosis is left sided heart failure. The resultant increase in pressure within the pulmonary circulation will be seen as pulmonary oedema.
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| − | [[Image:endocardiosis3.jpg|right|thumb|125px|<small><center>'''Endocardiosis'''. Courtesy of A. Jefferies</center></small>]] | |
| − | The enlarged left atrium compresses the left main stem bronchus inducing a soft, moist '''cardiac cough'''. A cough is usually the first presenting sign noticed by the owner.
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| − | Exercise intolerance and dyspnoea may also be evident.
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| − | A harsh pansystolic murmur will often be evident, more intense over the left heart apex. A mid-systolic click may indicate the prolapse of AV-valves into the atria.
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| − | The left atrium enlargement will be clearly visible on radiographs and is identifiable on ECG.
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| − | ''Complications:''<br>
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| − | Further to the left sided heart failure the heart may not be able to adequately perfuse the coronary circulation resulting in focal myocardial necrosis and then fibrosis. This will impair conduction within the myocardium and potentially induce arrhythmias and further heart failure. In these cases syncope may be seen due to the arrhythmia.
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| − | ===Endocardial Mineralisation===
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| − | [[Image:Endocardial calcification.jpg|right|thumb|125px|<small><center>'''Endocardial mineralisation'''. Courtesy of A. Jefferies</center></small>]]
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| − | Associated with jet lesions from regurgitant or turbulent flow. Damaged endocardium allows the deposition of calcium and phosphorous.
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| − | This may also occur with elevated blood calcium; for example Vitamin D poisoning.
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| − | Seen in the left atrium with mitral regugitation and mitral endocardiosis.
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| − | ===Chronic Valvulitis===
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| − | Seen in the horse. Lesions are fibrous with sparse chronic inlammatory cells and scarring. Most significant lesions affect the mitral and tricuspid valves.
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| − | ==Inflammatory-Endocarditis==
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| − | Usually due to bacterial infection.
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| − | More common in cattle, pigs and sheep. Often due to a chronic bacteraemia or pyaemia, spread from adjacent myocardium is rare.
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| − | [[Image:Bacterial endocarditis.jpg|right|thumb|125px|<small><center>'''Bacterial endocarditis'''. Courtesy of A. Jefferies</center></small>]]
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| − | Organisms commonly isolated include:
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| − | *Cattle: [[Actinomycetes|Actinomyces pyogenes.]]
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| − | *Pigs: [[Erysipelothrix_rhusiopathiae|Erysipelothrix spp.]]
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| − | *Sheep: [[Streptococci|Streptococci.]]
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| − | ''Pathogenesis:''
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| − | Contributing factors include:
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| − | *Trauma: haemodynamic turbulence.
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| − | *Valve tissue ageing.
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| − | *Avascularity of valves; poor healing capacity.
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| − | *Tissue exposure; constant contact with blood-borne pathogens.
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| − | ===Vegetative endocarditis===
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| − | Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Needs sustained or recurrent bacteraemia. Some bacteria have particular adherence properties and may only need a single episode of bacteraemia to set up an endocarditis.
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| − | [[Image:vegetative endocarditis.jpg|right|thumb|125px|<small><center>'''Vegetative endocarditis (dog)'''. Courtesy of T. Scase</center></small>]]
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| − | ''Pathophysiology:''
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| − | Loose thrombi of platelets and fibrin form which build up to larger vegetations. Bacterial colonies are found within the mass. Attempts to organise the vegetation occur but complete healing very rarely occurs. The mass may become ulcerated. Progression to rupure of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium.
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| − | Valves may become stenotic, incompetant or both.
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| − | Death usually results from either embolisation of the vegetation or congestive heart failure due to significant valvular damage.
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| − | ''Species differences:''
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| − | *Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. Congestive right sided failure is manifested as ascites (including '''bottle jaw''') and embolisation to the lungs. Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
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| − | *Pig and dog: Lesions occur particularly on the mitral valve, perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.
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| − | ===Ulcerative endocarditis===
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| − | Commonly seen along with renal failure in dogs.
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| − | Uraemia irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the sunendocardial tissue with deposition of glycosaminoglycans.
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| − | Healing may occur by fibrosis or the lesion may progress to a necrotising endcarditis and, in extreme cases, left atrial rupture.
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| − | If renal sufficieny is re-established then healing of the endocardial lesion is possible.
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| − | ==Vascular Pathology==
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| − | ===Haemorrhage===
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| − | Seen as an incidental finding in horses and catte due to sudden death.
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| − | ===Atrial thrombosis===
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| − | Atrial dilation or fibrillation on dogs and cats allows abnormal eddying and stasis of blood within the atria. Thrombosis may occur with subsequent embolisation of thrombus and lodging in smaller vessels. This particularly occurs in the cat where thrombi lodge in the femoral artery. The platelets within the thrombus release vasoactive amines which potentiate the hypoxia by constricting collateral circulation to the hindlimb. The cat will present with an acute hind limb paralysis with the limbs affected being cold to the touch and without a femoral pulse.
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| − | Embolism elsewhere is usually clinically silent.
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| − | ===Blood cysts===
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| − | Haematoma formation within the AV-valve leaflets.
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| − | ==Proliferative Pathology==
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| − | ===Haemangioendothelioma===
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| − | Arise from the endothelial cells, usually of the right atrium and occasionally involving the right ventricle.
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| − | Often multiple with similar tumours in the [[Spleen - Anatomy & Physiology|spleen]].
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| − | ===Chemodectoma===
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| − | Tumour arising from the chemoreceptor cells of the aortic body. Usually benign although local enlargement causes clinical signs early on E.g. dyspnoea.
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| − | [[Image:sarcoma metastasis.jpg|right|thumb|125px|<small><center>'''Sarcoma metastasis'''. Courtesy of T. Scase</center></small>]]
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| − | The heart is also a site of secondary neoplasia, particularly mammary and thyroid adenocarcinomas and haemangiosarcomas.
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