The present case series describes the spontaneous closure of an isolated congenital small restrictive perimembranous ventricular septal defect in two small breed dogs beyond 1 year of age. In the first case, the peak pressure gradient was 75 mmHg, which is lower than the value that defines a VSD to be restrictive (> 80 mmHg). In the absence of increased right ventricular systolic pressure, this value is most likely the result of underestimation of the systolic peak flow velocity because of a suboptimal Doppler angle. In the veterinary literature there are only two case reports describing a total of three dogs where a spontaneous closure of a ventricular septal defect took place [7, 8]. In Breznock’s report, in both dogs, the closure of the VSD was documented with physical examination and angiocardiography [8]. Both dogs were small breeds (a toy poodle and a miniature Schnauzer cross) and both of them underwent a successful surgical ligation of a concomitant left-to-right shunting patent ductus arteriosus at 8 weeks of age [8]. In these dogs, the murmur could not be detected at 12 and 16 months of age, respectively [8]. The other case report describes that a small VSD in a 5-month-old female Maltese dog, diagnosed with auscultation and color Doppler echocardiography, was spontaneously closed at 1 year of age, which is similar to the two cases described in this paper [7].

Spontaneous closure occurs frequently in humans, with higher incidence of muscular defects compared to perimembranous VSDs [6, 12,13,14,15]. Besides the anatomical localization, the size of the defect is an important factor, as smaller defects tend to close more often [6, 12]. In all the reported dogs, the defects were smaller than 2 mm [7, 8]. In humans, various mechanisms are described for spontaneous closure of VSDs, depending on the anatomical localization of the defect [12, 13, 15]. While closure of muscular VSDs are thought to be caused by the growth of the surrounding septum and fibrous tissue formation, perimembranous VSDs are suspected to be occluded as a result of right ventricular jet lesions, adherence of the tricuspid valve leaflets, aneurysm of the membranous septum and deposition of fibrin over the margins of the defect [12]. A membranous aneurysm may be a prelude to the spontaneous closing of small ventricular septal defects, where endocardial proliferation or hypertrophy appears around the defect on the right, like an aneurysmal protrusion of the membranous septum [14]. In addition to these mechanisms, in the case of perimembranous VSDs, when the defect is in close proximity to the tricuspid and aortic valves, reduplication of the tricuspid valve tissue and prolapse of an aortic valve leaflet have been described as the cause of spontaneous VSD closure [12]. The way in which turbulent blood flow results in a jet lesion and consequently a proliferation of endocardial fibrous tissue is similar to the mechanism described in the pathogenesis of double-chambered right ventricle and discrete subaortic stenosis [16]. The cause of closure of the VSDs in the present report cannot be known as both dogs remained alive and post-mortem examination has yet to be performed.

In humans, age appears to have a significant influence on the incidence of spontaneous VSD closure, while gender is less likely to affect this process [12,13,14,15]. Although spontaneous VSD closure can occur at any age in humans, it usually occurs during the first year of life or shortly thereafter [12, 17]. Interestingly similar to human patients, the age of VSD closure in all the five reported dogs (three from previously published reports and the two dogs from the present paper), took place shortly after 1 year of age [7, 8]. One possible explanation may be that the suspected endocardial fibrous proliferative changes do not occur until after the dogs have reached adult size and are no longer growing. Another possible explanation could be that proliferation starts early in life but takes more than a year to reach the extent which will close the VSD .

Both dogs in our report were intact females. One dog in Breznock’s case report was male and the sex of the other one was not reported [11]. The Maltese dog from the single case report was female [7]. Whether the seemingly female predisposition for VSD in the reported five dogs is a coincidence or if sex does influence this process, remains unknown. In human medicine, separate studies report conflicting gender predispositions [12, 18].

As both dogs in Breznock’s case report underwent surgical ligation of a left-to-right shunting patent ductus arteriosus several months before spontaneous closure of the VSD took place, the role of this surgery was discussed as a potential contributing factor [11]. Neither dogs in our case report had undergone a surgery of any kind or a general anesthesia before closure of the VSD, therefore a possible contribution of such a procedure remains impossible.

Disappearance of the murmur in a dog where previously a left-to-right shunting VSD was diagnosed can also result from the development of pulmonary hypertension (Eisenmenger’s syndrome), where the left and right ventricular systolic pressures equalize [3, 4, 19]. Performing an echocardiogram is therefore an important diagnostic test to identify the cause of murmur disappearance.

It is possible that VSDs in dogs close more often than is currently thought. One of the possible reasons why spontaneous closure of VSDs in dogs has not been more frequently reported may be the lack of serial cardiac auscultations and echocardiographic re-check examinations in these dogs. Small VSDs are known to have a good long-term prognosis that is presumably why regular monitoring of these dogs does not routinely take place.

In conclusion, the present report describes two female dogs, in which a congenital isolated small, restrictive perimembranous ventricular septal defect closed spontaneously shortly after 1 year of age.

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