Study Limitations
The study end point was reoperation, which limited the conclusions drawn about bioprosthesis failure rates. First, the valve failure rates may be lower than actual with this approach, as patients may be lost to valve-related mortality,26 inoperable status,19 out-of-province reoperations, and non-operative management of failing aortic valves rather than referral for reoperation. Indeed, studies that focus only on reoperation rates systematically underestimate the real incidence of SVD.27 Thus our approach underestimates valve failure rates, resulting in lost statistical power in comparing SVD by valve type. Overall event rates were low, limiting statistical power as well as the potential generalizability of the results.
This has also caused the Cox proportional hazards model to fail to show significance of smoking on prosthesis reoperation, which is otherwise a known predictor of SVD27. This precluded us from examining other known predictors of SVD, or to make a meaningful distinction between SVD and non-SVD mechanisms.
Echocardiogram data can reveal specific cause of valve failure, such as SVD, non-structural VD, or infective endocarditis.28Such data would demonstrate more accurate rates of prosthesis failure requiring reoperation.