Cardiac

• Heart disease clinical signs may be predominantly cardiac (e.g. exercise intolerance, syncope) or related to changes in other organs (e.g. respiratory distress). Malfunction of the left or right side of the heart results in very different pathophysiological effects (understanding of this is directly relevant to the clinical diagnosis of cardiac disease):

  Left– leads to pulmonary congestion/oedema.

  Right – leads to systemic venous congestion.
• Left cardiac failure:

  upstream- pulmonary congestion and oedema

  downstream- decreased output
• right cardiac failure:

  upstream- systemic congestion and ascites

  downstream- decreased output to the lungs and then the systemic circulation
• HCM and DCM are the result of pathological changes to the cardiomyocytes themselves. In HCM and DCM the hypertrophy and dilation are not associated to increased functional demand (i.e. increased afterload or preload), but are instead the result of cardiomyocyte derangement.
• The endocardium lines the cardiac chambers, and is a component of the valve cusps.
• atrioventricular valves = atrial (left) & tricuspid (right)

  semilunar valves = aortic (left) & pulmonic (right)).
• Parasitic lesions - in the UK, a parasite which commonly causes vascular lesions of significance is the equine large stongyle (roundworm), Strongylus vulgaris. The larvae and immature adults migrate through and along arterial walls causing intimal damage and arteritis. Lesions are encountered in the ascending aorta, roots of the cranial mesenteric, ileocaecal and renal arteries.
• Heart disease can be primary or secondary:

  Primary- due to functional derangement of the heart itself

  Secondary- due to extracardiac derangement, either systemic or organ specific e.g. systemic hypertension in renal disease, pulmonary hypertension following pulmonary fibrosis.

   

  Pathological changes can follow increased demand:

  • Increased preload due to increased volume of blood entering the heart during diastole (causes regurgitation and shunting)
  • Increased afterload due to increased resistance against which the heart must pump blood during systole i.e. pressure overload
• Pathogenic causes of heart disease:

  • Pump failure due to weak contractility or impaired filling
  • Obstruction to forward flow due to valvular stenosis , vascular narrowing or systemic/ pulmonary hypertension
  • Regurgitant blood flow due to valvular incompetence
  • Shunted blood flow, mostly as a result of congenital defects (septal or vascular)
  • Rupture in the heart or a major vessel
  • Cardiac conduction disorders leading to arrhythmia and pump failure
• Compensatory mechanisms of the heart can be morphological:

  • Cardiac dilation (increased volume capacity)
  • Cardiac hypertrophy (increase in cardiomyocyte size as they cannot divide)

  Or functional:

  • Increased cardiac rate
  • Blood redistribution via peripheral vasoconstriction
  • Increased blood volume

   

  Acute and manageable increases in preload e.g. during exercise result in transient heart dilation to accommodate the extra blood. Force of contraction, stroke volume and cardiac output also increase.
• Concentric hypertrophy- response to increased afterload where ventricular volume is increased. More power is needed to eject blood so there is hypertrophy alone with no change in end diastolic volume.
• Chronic hypertrophy eventually leads to myofiber degeneration and interstitial fibrosis. Dilation can compensate to a limit, at which point cardiomyocytes degenerate and the heart decompensates.
• Eccentric hypertrophy- response to increased preload increasing ventricular blood volume. There is hypertrophy and DILATION as there is more blood entering the ventricle.
• The effectiveness of cardiac compensatory mechanisms depends on location, extent and duration of the pathological lesion. Clinical disease occurs when compensation fails. Long periods of compensation can result in cardiomyocyte hypoxia as capillary density cannot keep up with demand. In this case, cardiomyocytes degenerate and are replaced by fibrosis.

   

  Irrespective of the initial type of hypertrophy, cardiac dilation may occur as compensation fails.
• Congenital cardiac defects may be either inherited or acquired (genomic defect arises in the fertilised zygote)

  Acquired: (not exhaustive)

  -          Infections, especially in early pregnancy e.g. bluetongue

  -          Physical e.g. hypoxia, hyperthermia, mechanical trauma, ionising radiation

  -          Nutritional deficiencies e.g. vitamin A

  -          Chemicals or toxins e.g. thalidomide

   
• Common cardiac congenital diseases include:

  1.      Septal defects, affecting chamber development and partitioning

  2.      Great vessel abnormalities, affecting valve origins

  3.      Valvular dysplasias

  4.      Persistent embryonic structures e.g. persistent right aortic arch
• Atrial defects e.g. Persistent foramen ovale. Atrial septal defects shunt from the left A to the right A, resulting in right atrial dilation and an increased right V preload and eccentric right V hypertrophy.

   

  Ventricular defects. Can be part of a more complex transposition syndrome. Usually located high on the septum, below the aortic valve. Result of failure of the inter-ventricular septum to join with the endocardial cushions. Shunting is usually from the left V to the right V, causing increased right V preload and eccentric right V hypertrophy.
• Normally the ascending aorta and pulmonary artery develop from a spiral partitioning of the truncus arteriosus. This spiral partitioning accounts for the intertwined relationship of the roots of the great vessels in the adult heart.
• Congenital defects of the truncus arteriosus:

  Transposition defects of the roots- usually affect the aorta, displacing normal positioning . Most common is dextro-rotation where the aorta is misplaces to lie over the right ventricle

   

  Persistent truncus arteriosus – the normal spiral position into aorta and pulmonary artery does not complete, resulting in one large artery into which both left and right ventricles empty.
• Semilunar valve stenosis – is a congenital condition with abnormal development of semilunar valve primordia, causing distortion and stenosis (or formation of a band of muscular or fibrous tissue in the outflow tract- subvalvular stenosis)

  • Aortic stenosis increases left ventricular afterload, causing left ventricular concentric hypertrophy and aortic poststenotic dilation
  • Pulmonary stenosis increases right ventricular afterload, causing right ventricular concentric hypertrophy and pulmonary artery poststenotic dilation
• The tetralogy of fallout involves Various congenital defects occuring together, causing several malformations:

  Ventricular septal defect, pulmonic stenosis, right ventricular hypertrophy and dextro-rotated aorta (over RV and VSD): there is an increase in right ventricular afterload with shunting from the right ventricle to the left ventricle (causing systemic hypoxia)
• For up to two weeks in the pig, sheep and horse, ductus arteriosus patency may be normal. Persistence is pathological.

   

  Patent Ductus Arteriosus is a shunt from  the aorta to the pulmonary artery, with an increase in right ventricular afterload and subsequent right ventricular concentric hypertrophy. This results in pulmonary overperfusion.
• Persistent overperfusion causes chronic injury to the delicate pulmonary vasculature and may lead to arteriosclerosis and a gradual increase in pulmonary resistance. Once resistance in pulmonary circulation exceeds the pressure of systemic circulation, shunt reversal occurs. E.g. in persistent ductus arteriosus, deoxygenated blood flows from the pulmonary artery into the aorta (eisenmenger’s syndrome -> systemic hypoxia)
• In the embryo, six pairs of branchial arches present, but normally only the left 4th arch persists (aortic arch). Persistent brachial arch results in constriction of the oesophagus due to anomalous vascular rings or associated structures, causing megaoesophagus with regurgitation of undigested food.

  Most common aortic arch syndrome is persistent right aortic arch. The vascular ring forms between the ductus arteriosus  (brachial arch L6) and the anomalous root of the aorta.  (persistent right arch R4)

  Other forms are double aortic arch and anomalous subclavian arteries
• Valvular dysplasia usually affects atrioventricular valves. The two presentations:

  • Valve leaflets are replaced by a fenestrated web-like structure
  • Short chordae tendinea with small papillary muscles
• The pericardium is a thin, fibrous, inelastic sac with an internal serous membrane lined by flattened mesothelial cells. It encloses the heart and roots of the great vessels. Any fluid accumulation causes a compressive effect (tamponade), affecting the thinner right side preferentially.
• Non-inflammatory fluid accumulation in the pericardium:

  1.      Hydropericardium: true serous transudate, usually as a result of congestive heart failure. May also be seen with neoplasms, anaemia, uraemia and hypoproteinaemia

  2.      Hemopericardium: accumulation of blood in the pericardium. Usually associated with rupture of large vessels or dilated atria due to AV valve regurgitation.

  3.      Idiopathic pericardial haemorrhagic effusion: relatively common in dogs, predominantly large breeds.  Presents as slowly developing right sided heart failure followed by left side
• Inflammation of the pericardium is pericarditis

  May result in restriction of ventricular movement => acute or chronic circulatory failure. Possible pathogenesis:

  1.      Haematogenous spread, secondary to septicaemia

  2.      Traumatic penetration by foreign bodies (from the oesophagus or reticulum) or fractured rib

  3.      Extension of infection from surrounding tissues (lungs, pleura, mediastinum or myocardium)

  Pericarditis is associated with inflammatory exudation, and can be fibrinous (due to increased vascular permeability) or suppurative (with pus formation).
• Cases of chronic pericarditis often result in sequelae, possible outcomes are:

  1.      Resolution –without further functional/morphological consequences.

  2.      Adhesion - of fibrin from exudate, forms adhesions between the epicardium and pericardium. These adhesions may become fibrous

  3.      Constriction/atrophy - if the condition is insidious, gradual tamponade and cardiac atrophy may occur: constrictive/restrictive pericarditis

  4.      Myocarditis – Extension of pericarditis into the myocardium (usually associated with traumatic reticulopericarditis in cattle)
• The myocardium is made up of cardiomyocytes forming myocardial bundles arranged in layers and bands. Blood is supplied from the coronary arteries which arise from behind the aortic valve cusps in the sinuses of vasalva. The straited muscle is very well supplied with a ratio of capillary: cardiomyocyte approx. 1:1. Myocardial disease and damage must be widespread and severe before clinical signs are observed.  If severe, myocardial disease results in heart failure (acute or chronic). Cardiomyocytes cannot divide, and compensation attempts are by hypertrophy of surviving muscle.
• Myocardial diseases can be functional, from metabolic disturbance, infarction, inflammation, parasitic, nutritional or a cardiomyopathy.
• Functional overload:

  Myocardial hypertrophy (increase in cell size) may result from a physiological response (e.g. increased exercise) or a pathology (e.g. valvular stenosis, systemic hypertension of renal disease etc)

  Dilation may occur where the disease process is too rapid to allow for compensation.
• Metabolic disturbances:

  • Fatty infiltration: replacement of muscle bundles by adipocytes, no degeneration.
  • Hydropic degeneration – cell injury, intracellular accumulation of fluid. ATP production decreases, membrane pumps fail
  • Fatty degeneration: fat accumulates within cardiomyocytes due to inability to metabolise normally. May result from myocardial hypoxia or toxicity
  • Hyaline degeneration: necrosis
  • Calcification: a dietary excess of vitamin D (incl. plants with vitamin D analogs) or calcium therapy
• visceral gout is a myocardial metabolic disturbance which occurs in reptiles and birds (who produce uric acid as their nitrogen end product). Uric acid precipitates in myocardium (and other tissues) as urate tophi crystals when there is a high protein diet and/or dehydration.  
• Myocardial infarction: relatively uncommon but occurs usually as the result of an embolism of coronary vessels. Could be sterile, septic or neoplastic.  Small focal areas of myocardial degeneration may be associated with intimal lesions of the intra myocardial arterioles in the canine heart but these lesions and similar ones in the horse do not seem to be clinically significant.
• Myocarditis: inflammation of the myocardium, usually following a bacterial, viral or protozoal infection. Usually results in acute cardiac failure.
• Acute  (suppurative) myocarditis occurs most often as a result of septic emboli being released from non-cardiac suppurative foci lodging in the heart (e.g. umbilical abscesses, joint-ill, mastitis). May also extend from endocardium or pericardium, or septic emboli from valvular endocarditis entering the coronary vessels.
• Acute (non-suppurative)myocarditis occurs resulting from septicaemia or viraemia e.g  pasteurellosis, leptospimrosis, Foot and Mouth disease, canine viral hepatitis, parvovirus in puppies, encephalomyocarditis virus in pigs.
• Chronic myocarditis occurs where cardiomyocytes are lost and replaced by fibrous tissue. May become granulomatous in cattle and sheep and a sequel of earlier sub-clinical acute myocarditis in dogs and cats
• Myocardial parasitism: parasitic larvae may encyst in the myocardium in heavy infestations. They generally elicit little or only localised host response. Species include cestodes, protozoa (forming sarcocysts), toxoplasma, neospores and tryptanomiasis