• Cause: underreported in rabbits; however, the incidence in other species ranges from 7-15%. In one study of 59 pet rabbits with cardiovascular disease, one had a ventricular septal defect (VSD).
• Signs: variable. Small restrictive VSD (restrictive – a small amount of blood shunted through the VSD) may be an incidental finding post-detection of a right parasternal murmur on physical examination. Others may be found concomitantly with other diseases, such as tetralogy of Fallot, atrial septal defects, patent ductus arteriosus, aortic stenosis, etc. Additionally, patients can present with stunted growth or congestive heart failure secondary to VSD.
• Diagnosis: ultrasound, echocardiography.
• Treatment: none in restrictive VSDs that are not causing symptoms. In non-restrictive symptomatic patients, occlusion devices and coronary artery banding have been reported in other species but not described in rabbits.
• Prognosis: normal life expectancy in small restrictive VSDs; poor if there is right to left shunting or congestive heart failure. Prognosis also varies depending on whether the VSD is occurring in isolation or with another congenital defect.

• Small defect: usually asymptomatic and an incidental finding associated with a loud right-sided systolic parasternal murmur.
• Large defect: usually causes a soft systolic murmur and is associated with delayed growth, left-sided congestive heart failure Heart: congestive heart failure, lethargy, and exercise intolerance.
• Cyanosis: secondary to right to left shunting.

• Congestive heart failure.
• Dead.
• Cyanotic.

• Usually, young; this can be noted later in life, especially in asymptomatic patients.

• None reported in rabbits.

• Case reports describe the condition in New Zealand White rabbits and Japanese white mixed breed New Zealand White. However, due to the lack of data, VSDs are thought to occur in other breeds. In one study of 59 pet rabbits with cardiovascular disease, one had a VSD, but breed was not described.

Restrictive

• Cost of echocardiogram, thoracic radiography, and consultation/physical examination to diagnose the condition.

Symptomatic patients

• Cost of thoracotomy and coronary artery banding in cases where treatment is pursued.
• Cost of repeated echocardiography, chest radiography and diuretic medication if surgery is not performed.
• Cost considerations for patients with heart failure or who are not pursuing treatment should include hospitalization visits to treat CHF.
• Post-operative cost considerations include re-check echocardiograms.

• Depends on the size of the defect.
• In severe cases, ISACHC class IV heart failure treatment with oxygen, sedation and IV diuretics may be needed.
• If pleural effusion is present in thoracocentesis.
• Concurrent treatment of other associated congenital diseases.

⚠️Symptomatic rabbits are particularly unstable, and resuscitation status should be determined and equipment ready in the event of cardiac arrest.

• Congenital condition caused by disturbances in septal formation or displacement of the ventricular outflow tract during gestation.
• In humans, myocardial infarction has been reported to cause VSD formation, but this is unreported in veterinary medicine.
• In humans, blunt chest trauma can uncommonly cause VSD in the peri membranous region adjacent to the AV valves or in the apical muscular portion of the septum (this has not been reported in rabbits).

General

• Heredity is seen in other species but is unknown in rabbits.

• Failure of septal closure or displacement of the ventricular outflow tract during embryological development leaves a connection between the left and right ventricles.
• Myocardial infarction (in humans – unknown if this occurs in rabbits) of the septal wall can lead to ischemia of the septal wall. With ischemia, we see loss of cardiomyocytes and thinning of the wall. Myocardial thinning can tear before the development of the fibrous scar tissue, leading to the formation of a VSD.
• Due to the higher pressures in the left ventricle, blood is shunted from the left to the right ventricles.

Restricted VSD

• Small VSDs have “restricted” blood flow due to the small orifice, and the high pressure of the left ventricle is not transferred to the right; thus, patients can remain asymptomatic.
• More apical VSDs shunt blood into the right ventricle, while more basilar ones may shunt blood directly into the right ventricular outflow tract.

Non-restricted VSD

• Increased blood flow into the right side of the heart leads to pulmonary over-circulation and increased blood return to the left side of the heart.
• With large volumes of blood being diverted into the right ventricle, we see increased return to the left side of the heart via the pulmonary vasculature, which can lead to left atrial and ventricular dilation.
• With increased blood return to the left ventricle and reduced abilities to compensate for this, the left atrial pressures increase, which can lead to congestive heart failure [heart: congestive heart failure].
• Large VSDs can equalize the left and right ventricular pressures, resulting in loss of shunting from left to right (laminar – low-grade murmur) or, in some cases, reversal of flow leading to right-to-left shunting.
• Increased right ventricular pressure in equalizing VSDs can result pulmonary hypertension.
• In right-to-left shunting, deoxygenated blood is transferred into the left-sided systemic circulation which can result in cyanosis.
• In rare cases of right-to-left shunting, polycythemia may be noted.
• It is hypothesized that in rare circumstances, small VSDs, if orientated in the right direction, can cause jet lesions in the right ventricle, causing the formation of a scarred ridge leading to the development of a double chamber right ventricle.

• Starts at birth.
• Small, restricted defects often do not result in the development of heart disease.
• Large defects progression is variable, with severe cases presenting clinical signs within months of birth (based on other species as there is no data in rabbits).

Refereed papers

• Recent references from PubMed and VetMedResource.
• Ozawa S, Guzman D S M, Keel K & Gunther-Harrington C (2021) Clinical and pathological findings in rabbits with cardiovascular disease: 59 cases (2001–2018). J Am Vet Med Assoc 259 (7), 764-776 PubMed.
• Di Girolamo N, Palmieri C, Baron Toaldo M et al (2018) First description of partial atrioventricular septal defect in a rabbit. J Exot Pet Med 27 (4), 5-9 VetMedResource.
• Bomassi E, Misbach C, Tissier R et al (2015) Signalment, clinical features, echocardiographic findings, and outcome of dogs and cats with ventricular septal defects: 109 cases (1992–2013). J Am Vet Med Assoc 247 (2), 166-175 PubMed.
• Vörös K, Seehusen F, Hungerbühler S et al (2011) Ventricular septal defect with aortic valve insufficiency in a New Zealand White Rabbit. J Am Anim Hosp Assoc 47 (4), e42-49.
• Orcutt C L & Malakoff R (2020) Cardiovascular disease. In: Ferrets Rabbits & Rodents. 250-257 PubMed.