Key result
Atenolol significantly decreased mean and maximum pulmonary valve pressure gradients but did not alter less flow-dependent methods of assessment of pulmonary valve stenosis severity in dogs.
Why the study?
Does atenolol or butorphanol alter flow-dependent and less flow-dependent echocardiographic methods of assessing pulmonary valve stenosis severity in dogs?
Observational (n=27)
Single-blind
None
No
Does atenolol or butorphanol alter flow-dependent and less flow-dependent echocardiographic methods of assessing pulmonary valve stenosis severity in dogs?
Absolute Event Rate: 93.1% vs 108%
p-value: p=≤0.047
Atenolol reduces flow-dependent pressure gradients but does not alter less flow-dependent methods (velocity ratio, VTI ratio, iPVA) in dogs with pulmonary valve stenosis, supporting an integrative echocardiographic assessment.
Atenolol-associated gradient reductions may not reflect true severity change in canine PS; leaves open optimal echo parameters for assessment.
Background Velocity ratio, velocity time integral (VTI) ratio, and pulmonary valve area indexed to body surface area (iPVA) are methods of assessment of pulmonary valve stenosis (PS) severity that are less dependent on blood flow. Studies evaluating these methods are limited. Objectives To determine the effects of butorphanol, atenolol, and balloon valvuloplasty (BV) on velocity ratio, VTI ratio, iPVA, mean PG, and max PG. Animals Twenty-seven dogs with PS (max PG >50 mm Hg). Methods Prospective study. All dogs underwent an echocardiogram at baseline, 5-minutes after administration of butorphanol (0.2-0.25 mg/kg IV), and 2-to-4 weeks after atenolol (1-1.5 mg/kg q12h). Twenty-one of these were evaluated 24-hours after BV. Results There were no significant differences (P > .05) amongst any of the methods of assessment of PS severity after butorphanol. After atenolol, mean (SD) of mean (57.0 [21.0] mm Hg) and max PG (93.1 [33.8] mm Hg) were significantly decreased (P ≤ .047) compared with baseline (65.2 [26.2] mm Hg and 108 [44.4] mm Hg, respectively). After atenolol, there were no significant (P ≥ .12) differences in velocity ratio (0.29 [0.09]), VTI ratio (0.18 [0.05]), or iPVA (0.43 [0.16] cm2/m2) compared with baseline (0.30 [0.09], 0.19 [0.09], 0.44 [0.17] cm2/m2, respectively). Conclusions and Clinical Importance Atenolol might reduce mean and max PG but does not alter less flow-dependent methods of assessment of PS severity (velocity ratio, VTI ratio, and iPVA) in dogs with PS. Results support an integrative approach to assessment of PS severity that includes less flow-dependent methods, particularly in states of altered flow or right ventricular function.
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Nishimura et al. (2018) conducted an observational in Pulmonary valve stenosis (n=27). Atenolol vs. Baseline (within-subject) was evaluated on Pulmonary valve maximum pressure gradient (PV max PG) (p=≤0.047). Atenolol significantly decreased mean and maximum pulmonary valve pressure gradients but did not alter less flow-dependent methods of assessment of pulmonary valve stenosis severity in dogs.
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