Imagine this clinical scenario: a dog with subaortic stenosis (SAS) is presented for treatment. The owner is keen for long-term survival, and you want to find the best intervention to improve physiological parameters and quality of life. Therefore, you explore the available evidence on medical and surgical treatments of aortic stenosis, and whether either treatment shows a longer survival time with improved clinical parameters.
Eight studies were critically appraised; one was a randomised controlled study, three were cohort studies, one was a case series and three were case reports.
Balloon valvuloplasty versus atenolol
In a randomised prospective study by Meurs et al. (2005), 38 large-breed dogs with severe SAS were studied, of which 10 dogs underwent balloon valvuloplasty (BAV) and were re-examined six weeks later to determine the feasibility of the procedure. Of the remaining 28 dogs, 15 dogs underwent BAV and 13 were medicated with atenolol. The BAV group had a mean preoperative pressure gradient (PG) of 147mmHg, which reduced to 86.7mmHg post-surgery. The atenolol group had a pre-treatment PG of 122.2mmHg, which reduced to 113mmHg after six weeks of atenolol. The median survival time of the dogs treated with surgery and those treated medically were almost identical: 55 months versus 56 months, respectively.
The median survival time of the dogs treated with surgery and those treated medically were almost identical: 55 months versus 56 months, respectively
High-pressure balloon valvuloplasty
A respective cohort study (Shen et al., 2017) investigated 22 dogs with SAS, with a mean transvalvular PG of 143mmHg (ranging from 80 to 332mmHg), that had undergone combined cutting and high-pressure balloon valvuloplasty (CB/HPBV). Dogs with an obtuse aortoseptal angle (AoSA) of more than 160° (4/22) had a greater decrease in PG following CB/HPBV compared to those with a more acute AoSA of less than 160°. By 12 months, PG was reduced by 76mmHg in dogs with obtuse AoSA (versus 28mmHg acute AoSA), suggesting that dogs with an obtuse AoSA may benefit more, and for a longer period, by undergoing a CB/HPBV procedure.
Propranolol and surgical resection
In a case report by Muir et al. (1989), a dog diagnosed with SAS was treated with 0.3mg/kg propranolol, which was gradually increased to 1.0mg/kg. Balloon dilation was then attempted to relieve the stenosis. At diagnosis, systolic PG was 100mmHg and post-dilation, the PG was similar at 90mmHg. The dog then underwent surgical resection of the stenosis, 10 days after the balloon dilation. Forty-eight hours after surgery, the heart murmur had reduced in intensity, although it was still easily audible. The dog died 20 days post-operatively. A post-mortem determined that death was not directly related to the surgery but still may have been cardiac in origin.
Open surgical correction
In a respective cohort study by Orton et al. (2000), 44 dogs were divided into a surgical and a non-surgical group, with the surgical group undergoing open surgical correction of the subaortic stenosis with the aid of cardiopulmonary bypass. All dogs in the surgery group were administered long-term atenolol, as were all but three dogs in the non-surgical group.
At two to four months post-operatively, the systolic PG for the surgery group was significantly lower, from 22 to 100mmHg. This equates to a 41 to 75 percent reduction
There was no significant difference in the early reduction of PG between the two groups. The PG recorded in the surgery group ranged from 54 to 232mmHg, while PG in the non-surgical group ranged from 51 to 272mmHg. At two to four months post-operatively, the systolic PG for the surgery group was significantly lower, from 22 to 100mmHg. This equates to a 41 to 75 percent reduction, but there was no comparative data reported for the non-surgical group. No benefit to survival was documented between surgical and medical intervention (5/22 dogs had recorded deaths related to surgical complications, and a further 6/22 recorded because of the disease itself).
In a case report by Hirao et al. (2003), a dog underwent surgical resection of the subvalvular stenosis. A decrease in preoperative left ventricular-aortic systolic PG from 90mmHg to 44mmHg and an increase in the diameter of the left ventricular outflow tract was found 203 days post-surgery. The dog died suddenly 10 months post-operatively, possibly related to its heart disease.
Modified Konno procedure
A final case report (Nelson et al., 2004) treated a dog with SAS with 0.8mg/kg atenolol. Eleven months after presentation, the systolic PG had increased to 240mmHg, but the atenolol dosage was deemed adequate and not altered. One year later, the dog presented with clinical signs of exercise intolerance and syncope, and a modified Konno procedure was performed involving the complete removal of the affected area of the septal outflow tract via right ventriculotomy. Eight days post-operatively, the systolic PG had reduced to 78mmHg, decreasing further after 24 months to 40mmHg.
In a case series by Komtebedde et al. (1993), four dogs had systolic apical murmurs and three had syncope/exercise intolerance, all with subvalvular SAS with a systolic PG of more than 70mmHg. Patients underwent cardiopulmonary bypass as well as a transverse aortotomy to surgically correct subvalvular SAS. Six dogs were alive and stable after a mean follow-up time of 15.8 months (with a range from 2 to 27 months). One dog died of chylothorax four months post-operatively. No dog experienced clinical signs of exercise intolerance or syncope post-operatively.
A cohort study by Eason et al. (2014) evaluated beta-blockers versus no treatment and found that beta-blockers had no demonstratable effect on survival time. Twenty-five dogs received atenolol, one received propranolol and one received sotalol. A high transvalvular PG of more than 130mmHg at diagnosis in both the treatment and control group was associated with a reduced survival time of 2.8 years, compared with 8.3 years for a transvalvular PG of 130mmHg or below.
Overall, intervention in dogs with moderate to severe SAS appeared to improve physiological parameters when compared to no treatment. Surgery had a greater effect on these parameters than medical management. The severity of clinical signs was reduced, but the risk of sudden cardiac-related death was not diminished according to several papers. However, the evidence is weak, relying on single case reports and retrospective studies.
Intervention in dogs with moderate to severe SAS appeared to improve physiological parameters when compared to no treatment […] The severity of clinical signs was reduced, but the risk of sudden cardiac-related death was not diminished
A further recurring issue with these studies is the lack of a negative control group, due to the ethical implications of not treating dogs with severe disease. Therefore, the difference made by interventions to the “natural” survival time of the patients cannot be accurately determined. Future research is required, including carrying out controlled randomised clinical trials to find a reliable recommendation for a specific treatment.