Abstract 4141995: Impact of myocardial infarction on aortic and mitral bioprosthetic valve degeneration

Background: Studies have previously suggested that myocardial infarction (MI) have an impact on native aortic valve stenosis progression as well as inducing pathobiological changes in native mitral and tricuspid native valve leaflets. Inflammation, renal failure, and hypertension have been identified as potential factors accelerating structural valve degeneration (SVD). However, the impact of MI on bioprosthetic valve and SVD is unknown. Hypothesis: MI accelerates the progression of bioprosthetic valve degeneration. Methods: A retrospective cohort analysis of patients who underwent a bioprosthetic aortic or mitral valve replacement at Quebec Heart and lung Institute was done. Patients were identified through a keyword search in institutional medical records and through the local cardiac surgical database (n = 158). Inclusion required a bioprosthetic valve in aortic (n = 146) or mitral (n = 12) position, with or without history of MI after surgery and at least two echocardiograms within 5 years post-MI, along with available echocardiograms performed ≥6 months prior to the MI. Patients were matched for baseline and prosthetic valve characteristics and divided into two groups 1) No MI (controls, n= 79), 2) MI (cases, n= 79). Echocardiograms were reviewed for valve mean and maximal gradient as well as valve area derived from the continuity equation. Results: At baseline, the two matched groups had comparable characteristics and echocardiographic data. The annualized progression of prosthetic valve area was higher in the MI group (-0.04 ± 0.16 cm 2 /y vs 0.00 ± 0.11, p = 0.039). This was mostly driven by patients with aortic valve replacement (aortic valve area -0.05 ± 0.14 cm 2 /y vs 0.01 ± 0.11, p = 0.0077). Using a mixed linear model, the presence of MI had a significant interaction with the decline of aortic valve area and indexed aortic valve area (p = 0.0057, p = 0.0041). There was no difference in mean or maximal gradient between the two matched group. Annual progression rate of indexed bioprosthetic aortic valve area was faster in men compared to women in the whole population (-0.061 ± 0.01 cm 2 /m 2/ y vs -0.01 ± 0.02 cm 2 /m 2/ y for men and women, respectively; p = 0.009). Conclusion: This study suggests that bioprosthetic valve stenosis may be accelerated following a myocardial infarction. These findings could be explained by the same fibrotic mechanisms observed in native valves. More studies are needed to understand the underlying mechanisms and clinical impact.