Key result
The Ross operation was associated with a 79.7% freedom from any pulmonary homograft stenosis at 7-year follow-up, with the instantaneous hazard falling to zero after 4 years.
Why the study?
What is the incidence, location, and pathology of pulmonary homograft stenosis after the Ross operation?
Cohort (n=144)
What is the incidence, location, and pathology of pulmonary homograft stenosis after the Ross operation?
Pulmonary homograft stenosis after the Ross operation affects approximately 20% of patients at 7 years and appears to be driven by an early postoperative inflammatory reaction causing extrinsic compression.
May warrant early surveillance after Ross; leaves open whether anti-inflammatory strategies reduce homograft stenosis risk.
Background The Ross operation has several theoretical advantages. However, concern exists regarding evolving pathology in the pulmonary homograft. Methods and Results Consecutive patients (n=144; mean age 31 years, range 2 months to 64 years) undergoing the Ross operation were studied between 1993 and 2000. Echocardiographic examination of the pulmonary homograft was performed immediately after surgery, then at yearly intervals for a mean interval of 48 months. Fifteen patients (mean age 37 years) in whom echocardiography revealed peak pulmonary gradients ≥30 mm Hg (mean 46±18 mm Hg) underwent MRI with velocity mapping in a Picker 1.5-T magnet. No patient had more than mild pulmonary regurgitation. Four patients required reoperation for rapidly progressive pulmonary homograft stenosis; in all 4, there was macroscopic and microscopic evidence of a pronounced chronic adventitial reaction, with perivascular infiltration producing extrinsic compression. Freedom from any pulmonary homograft stenosis at 7-year follow-up was 79.7%, with instantaneous hazard falling to zero after 4 years. Freedom from reoperation at 7 years was 96.7%. In those studied with MRI, there was evidence of narrowing of the whole homograft or distal suture line in 14 of 15 patients, with obvious excess surrounding tissue in 11. Mean minimum diameter and peak velocity by MRI were 11±2 mm and 3.2±0.7 m/s, respectively. Multivariate analysis of patient-, surgery-, and homograft-related variables did not reveal any significant risk factors for development of neopulmonary stenosis. Conclusions Pulmonary homograft stenosis after the Ross operation is clinically important and appears to represent an early postoperative inflammatory reaction to the pulmonary homograft that leads to extrinsic compression and/or shrinkage.
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Carr‐White et al. (2001) conducted a cohort in Pulmonary homograft stenosis (n=144). Ross operation was evaluated on Freedom from any pulmonary homograft stenosis at 7-year follow-up. The Ross operation was associated with a 79.7% freedom from any pulmonary homograft stenosis at 7-year follow-up, with the instantaneous hazard falling to zero after 4 years.
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