Etiology of Patent Ductus Arteriosus in Dogs

Abstract

Patent ductus arteriosus (PDA) is the most common congenital heart disease in dogs and usually causes heart failure and death unless corrected at a young age. Previous histologic studies in a line of dogs derived from Miniature Poodles with hereditary PDA identified varying degrees of hypoplasia and asymmetry of ductus-specific smooth muscle and the presence of aortalike elastic tissue in the ductus wall sufficient to cause patency. To determine if similar structural abnormalities cause PDA in other dogs, serial-section, 3-dimensional histology of ductal architecture was studied in 8 non-Poodle purebred dogs with PDA with no immediate family history of PDA. Morphologic abnormalities were observed in 7 of 8 dogs with PDA and essentially were the same as those in dogs known to have a hereditary form of PDA. These findings suggest that apparently sporadic PDA in these breeds is caused by a genetic defect in the structure of the ductus arteriosus that is similar or identical to that in the Poodle. The relatives of dogs with PDA, particularly parents, offspring, and siblings, should be screened for evidence of PDA. Dogs with PDA should not be used for breeding, regardless of breed.Key words: Congenital heart disease; Heredity; Histopathology; Pathogenesis; Smooth muscle hypoplasia. Patent ductus arteriosus (PDA) is the most common congenital heart disease in dogs. 1 Clinical and pathologic aspects of the disorder have been summarized recently. 2,3Increased prevalence of PDA in certain breeds indicated that genetic factors were involved in the pathogenesis of PDA, and a mixed-breed-Poodle line of dogs with hereditary PDA was developed.4 Histopathology in dogs with hereditary PDA consistently identified abnormalities in the wall of the ductus arteriosus (DA) that explained failure of DA closure after birth. The DA was shorter than normal, the ductus muscle mass (DMM) was hypoplastic and asymmetric, and segments of the DA wall that should have been muscular instead had a noncontracting, aortalike elastic wall. 5,6 Serial-section histology of fetuses predisposed to PDA identified 6 grades of abnormality characterized by asymmetrically reduced DMM and increased elastic tissue that correlated with increased PDA gene concentration in breeding experiments. 5 To determine if similar morphologic abnormalities cause PDA in other dogs, serial-section histology was performed on 8 unrelated purebred dogs with PDA representing 7 non-Poodle breeds. Materials and MethodsEight cardiopulmonary specimens with PDA were obtained from the postmortem examination service or from dogs donated for study. Included were 2 Collies and 1 each of the Cocker Spaniel, German Shepherd Dog, Keeshond, Pomeranian, Shetland Sheepdog, and Shih Tzu breeds. Their ages ranged from 10 days to 3 months except for the Shetland Sheepdog, for which age was not recorded.After gross examination and formalin fixation, each PDA and adjacent portions of the aorta and pulmonary artery were imbedded upright in paraffin so that the central part of the PDA could be section...

Echocardiographic Assessment of Cardiac Function by Conventional and Speckle‐Tracking Echocardiography in Dogs with Patent Ductus Arteriosus

“…[1][2][3][4] Ductal patency has been related to the absence of smooth muscle tissue in the ductal wall, which prevents effective constriction shortly after birth. 5 The main hemodynamic effect of a left-to-right PDA (L-R PDA) is volume overload of the left ventricle, as indicated by the increase in preload (increase in end-diastolic volume), which in turn increases contractility following Starling's law. 6,7 The left ventricle compensates by increasing stroke volume and eventually may develop eccentric hypertrophy to normalize wall stress.…”

Utility of Transesophageal Echocardiography for Transcatheter Occlusion of Patent Ductus Arteriosus in Dogs: Influence on the Decision-Making Process

“…Histologic sections of canine PDA document incomplete smooth muscle in the ductal wall, preventing normal constriction and commonly resulting in an asymmetrical lumen. 6 The most common PDA morphology (type II) tapers as the ductus communicates with the pulmonary artery, thereby providing a shelf of tissue useful for securely deploying an occlusion device. 7 Device embolization may be more likely if the PDA does not taper (type III) or if estimates of ductal dimensions are inaccurate prompting deployment of an inappropriately sized device.…”

Foramen Ovale and Ductus Arteriosus Patency in Neonatal Harbor Seal (Phoca vitulina) Pups in Rehabilitation

“…is hereditary, and failure of d.a. closure is due to hypoplasia of the musculature (Buchanan, 2003). Recent research in mice (Mus musculus) has suggested that an appropriate drop in prostaglandin levels is required, rather than an elevation, for closure of the d.a.…”