Congenital cardiovascular pathology

Question 1

Congenital atrial defects

Answer 1

Persistent foramen ovale

Septal defects

Question 2

Congenital ventricular defects

Answer 2

Septal defects

Question 3

Congenital vascular defects

Answer 3

Patent ductus arteriosus (PDA)

Pulmonic stenosis

Aortic stenosis

Persistent IV right aortic arch

Dextraposition of aorta

Transposition of great vessels

Question 4

Congenital complex defects

Answer 4

Tetralogy of fallot

Question 5

Miscellaneous congenital defects

Answer 5

Haematocysts

Valvular dysplasia

Endocardial fibroelestosis

Ectopia

Question 6

Patent ductus arteriosus breed predispositions

Answer 6

Chihuahua, bichon frise, English springer spaniel, Pomeranian, poodle, keeshond, and Shetland sheepdog

In poodles it is inherited

Question 7

PDA

Answer 7

Shunts blood from pulmonary artery to aorta

Gives rise to pulmonary hypertension

At first blood is shunted from the left to the right ventricle and this may lead to reversal of flow through the PDA and clinical development of cyanosis.

Right and left ventricular hypertrophy and cardiac failure are secondary effects.

Question 8

Persistent foramen ovale and atrial septal defect

Answer 8

(Cattle)

The most frequent is failure of closure of the foramen ovale

True septal defects of the interatrial septum arise either due to failure of growth of septum secundum or failure of separation of right pulmonary veins and anterior vena cava.

Pulmonary hypertension may develop leading eventually to reversal of flow through the atrial communication.

Question 9

Breed disposition of persistent foramen ovale

Answer 9

Greatest frequency of persistent foramen ovale is in boxer, Doberman pinscher, and Samoyed.

Question 10

Ventricular septal defects

Answer 10

Cat and cattle.

A common defect in animals.

It is a failure of complete development of the interventricular septum (membranous or muscular).

It occurs more commonly in the upper portion of the interventricular septum (membranous).

Postnatally the effect of these defects depends on the size of the opening.

There is often a left to right shunt.

Left ventricular output is maintained by an increased end diastolic volume and increased contractility.

The right ventricle is confronted by a large systolic and diastolic load.

Both ventricles undergo hypertrophy.

Question 11

Breed disposition for VSD

Answer 11

In dogs it is most likely in English Bulldogs, English Springer Spaniels, and West Highland White Terriers

Question 12

Tetralogy of fallot

Answer 12

Dog.

It is a complicated cardiac anomaly with four (tetrad) anomalies:
§ ventricular septal defect,
§ pulmonic stenosis,
§ dextraposition of the aorta.
The fourth lesion, hypertrophy of the right ventricle is secondary or compensatory.

Invariably results in clinical signs of fatigue, cyanosis and polycythemia due to hypoxia.

Growth is usually retarded.

Question 13

Breed predisposition for tetralogy of fallot

Answer 13

Inherited in Keeshond dogs and is frequent in English bulldogs

Question 14

Anomalies from failure of normal valvular development

Answer 14

Pulmonic stenosis

Subaortic stenosis

Dysplasia of tricuspid and mitral valves

Question 15

Breed predisposition for pulmonic stenosis

Answer 15

It is inherited in beagles, English bulldog, Chihuahua and probably in other breeds.

Question 16

Pulmonic stenosis

Answer 16

The defect can be due to deformity of the valves themselves (valvular stenosis) or as a formation of a circumferential band of fibrous or muscular tissue beneath the valve (subvalvular stenosis).

There is post stenotic dilatation of the pulmonary trunk.

Concentric right ventricular hypertrophy is present because of the increased systolic pressure generated within the ventricle.

Question 17

Breed predisposition of subaortic stenosis

Answer 17

Dog and pig.

It appears to be inherited in German shepherd, boxer and Newfoundland dogs.

Question 18

Subaortic stenosis

Answer 18

thickness and endocardial valvular fibrosis that encircles the left ventricular outflow below the aortic valve.

Secondary lesions develop such as ventricular concentric hypertrophy, foci of myocardial necrosis and post stenotic dilation.

Question 19

Dysplasia of tricuspid and mitral valves

Answer 19

Cat (tricuspid valve).

Valve leaflets are distorted and chordae tendinae shortened and thickened.

Valve leaflets are distorted with enlarged annulus, short thick chordae tendinae and malpositioned papillary muscles.

Right atrium is enlarged due to valvular insufficiency leading to regurgitation of blood through the incompetent valve.

The right ventricle becomes hypertrophied.

Question 20

Anomalies from malpositioning of the great vessels

Answer 20

Persistent right aortic arch

Question 21

Persistent right aortic arch

Answer 21

Dog.

Arises when the right IV aortic arch, rather than the left, develops.

With the aortic arch in this position the ductus arteriosus compresses the oesophagus against the trachea (ligamentum arteriosum).

When the animal consumes solid feed vomiting and regurgitation occur.

Proximal dilation (megaoesophagus) develops due to oesophageal obstruction.

This condition therefore presents as a digestive rather than a circulatory problem.

Question 22

Miscellaneous cardiac congenital anomalies

Answer 22

Not common

Endocardial fibroelastosis

Portocaval shunts

Question 23

Endocardial fibroelastosis

Answer 23

Cat.

Burmese and Siamese kittens.

Inherited disease characterised by prominent, white, inelastic, thickened endocardium.

The left ventricle is especially affected with proliferation of fibroelastic tissue.

Left atrium is dilated and left ventricle becomes progressively hypertrophied and dilated.

Question 24

Portocaval shunts

Answer 24

Dog.

Blood bypass the liver dealing to hyperammonaemia due to failure of hepatic degradation of nitrogenous products.

Neurological signs develop resulting in hepatic encephalopathy.