Ventricular Septal Defect in a foal

Ventricular Septal Defect in a foal


History: A 1 day old  foal had been unable to stand or nurse,  had contracted tendons (more severe in left forelimb),  and had been unable to sit sternal.  The foal also had parrot mouth.

Gross Findings:

The right ventricle of the heart was dilated and thickened. The right ventricular free wall measured 1 cm thick compared to the left ventricular free wall which measured 1.6 cm thick. A ventricular septal defect (0.8 cm diameter) was found high in the interventricular septum that communicated between the left ventricle 5 mm below the aortic valve, and right ventricle just below the right AV valve.


Right ventricular enlargement

Heart: Right ventricular enlargement



Ventricular Septal Defect from right side

Heart: Ventricular Septal Defect from right side



Ventricular Septal Defect from left side

Heart: Ventricular Septal Defect from left side


Jaw- Brachygnathia inferior (Parrot mouth)

Foal: Jaw- Brachygnathia inferior (Parrot mouth)


Ventricular septal defects are the most common congenital cardiac malformation in large animals.  The separation of the the right and left sides of the heart is formed from 3 parts of the embryonic heart- the muscular portion of the septum, the downward growth of the conotruncal ridges, and the membranous portion of the septum derived from the endocardial cushions.  A VSD can be related to any of these parts and therefore the position of the defect (high, low etc) is determined by which parts of the embryonic heart fail to form properly.  VSD’s most commonly involve the membranous septum and may involve portions of the muscular septum.

Detrimental effects of VSD’s are seen only postnatally.  In the developing fetus the left and ventricular pressures are equal and there is little flow across the defect.   After birth  pulmonary vascular resistance decreases causing the pressure in the right side of the heart to decrease resulting in a left to right shunt of blood through the VSD.  This causes increased pressure in the right ventricle which leads to concentric right ventricular hypertrophy and dilatation.   The increased blood circulated to the right side, and to the lungs, causes increased pulmonary hypertension and eccentric  and concentric hypertrophy of the left ventricle.  Eventually the hypertrophy of the right ventrical leads to shunt reversal (right to left) causing systemic hypoxia from flooding the systemic circulation with venous blood.


The Embryology of Domestic Animals.  Drew M. Noden, and Alexander DeLahunta.  Williams and Wilkins, 1985.

Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, 5th ed. Edited by M. Grant Maxie.  Elsevier 2007.

About Brian

Anatomic Pathologist, VetPath Services, Stone Ridge, NY- musculoskeletal, oral/dental, and sinonasal diseases
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