Restenosis after percutaneous transluminal mitral commissurotomy is primarily driven by the progression of end-stage rheumatic valvular disease rather than re-fusion of the commissures.
Pathologic evidence links post-PTMC restenosis to rheumatic progression rather than re-fusion; hypothesis-generating for antifibrotic strategies in larger cohorts.
To clarify mechanisms of restenosis following percutaneous transluminal mitral commissurotomy (PTMC), we studied 253 patients (25% male) with PTMC using an Inoue balloon. Initial success (defined as either a mitral valve area >or= 1.5 cm(2) or more than twice the pre-PTMC valve area) was achieved in 95% of patients. During a mean follow-up period of 8 +/- 3 years, 12 patients underwent mitral valve replacement due to mitral valve restenosis. Visual inspection of the 12 resected valves with restenosis did not reveal fusion of the commissures. Histologically, all the resected mitral valves had evidence of end-stage rheumatic valvular disease, such as severe fibrosis and calcification. Deterioration of Wilkins echo score supported rheumatic disease progression in the leaflets and subvalvular region. Therefore, restenosis is not due to recurrence of fusion in commissures in these Japanese patients. Histologic and echocardiographic findings suggest that restenosis is based on end-stage valvular disease.
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Tsuji et al. (2002) studied this question.
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