Key result
In a porcine model, free pulmonary regurgitation caused significant RV dilatation (RV end-diastolic area increased from 15 to 23 cm2/m2, P<0.0001) while tissue Doppler measures of RV contractility remained unchanged.
Why the study?
Does percutaneous pulmonary valve replacement improve Tissue Doppler derived measures of RV contractility in a porcine model of chronic severe pulmonary regurgitation?
Does percutaneous pulmonary valve replacement improve Tissue Doppler derived measures of RV contractility in a porcine model of chronic severe pulmonary regurgitation?
p-value: p=<0.0001
Tissue Doppler echocardiography may not be sufficiently sensitive to detect changes in RV contractility following chronic pulmonary regurgitation and percutaneous valve replacement in a porcine model.
Tissue Doppler may lack sensitivity for RV contractility changes after pulmonary regurgitation; leaves open need for alternative metrics in porcine models.
INTRODUCTION: Pulmonary regurgitation (PR) following repair of right ventricular (RV) outflow obstruction is related to slowly progressive RV dilatation and heart failure and will eventually require surgical intervention, but optimal timing of pulmonary valve replacement is challenging. Tissue Doppler based quantification of RV contractility may offer additional information in the management of these patients. METHODS: In a porcine animal model free PR was induced by percutaneous stenting of the pulmonary valve orifice (N = 23). After 1, 2, or 3 months of free PR percutaneous pulmonary valve replacement (PPVR) was performed. Tissue Doppler derived measures of global and regional myocardial contractility were obtained by transthoracic echocardiography, and compared to a sham-operated control group (N = 9). RESULTS: Free PR is associated with RV dilatation (RV end-diastolic area increased from 15 ± 3 to 23 ± 7 cm(2) /m(2) , P < 0.0001) and a decrease in RV fractional area change from 62 ± 10% to 57 ± 12%, P = 0.08, with no impact of duration of free PR. The isovolumic acceleration, regional strain, and strain rate were unchanged after free PR and after PPVR. No consistent relation of echocardiographic measures of contractility and response to PPVR could be identified. CONCLUSION: Echocardiographic measures of RV contractility remained unchanged, despite significant RV remodeling following chronic PR and PPVR persistently induced significant recovery in the majority of the animals. These results may imply that Tissue Doppler based measures of RV contractility may not be sufficiently sensitive to be a suitable adjunct to conventional echocardiography in the follow-up of patients with free PR in order to optimize timing of valve replacement.
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Kjærgaard et al. (2010) studied Pulmonary regurgitation (n=32). Free pulmonary regurgitation induced by percutaneous stenting followed by percutaneous pulmonary valve replacement vs. Sham-operated control was evaluated on RV end-diastolic area (p=<0.0001). In a porcine model, free pulmonary regurgitation caused significant RV dilatation (RV end-diastolic area increased from 15 to 23 cm2/m2, P<0.0001) while tissue Doppler measures of RV contractility remained unchanged.
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