The major findings of this pilot study carried out in patients with severe primary mitral regurgitation are as follows: (i) pathological mitral valves express both MAO-A and -B isoforms with a predominance of MAO-A, (ii) MAOs contribute to local oxidative stress, which is potentiated by ANG2, (iii) both MAO expression and oxidative stress are decreased ex vivo by either an MAOI or ARB, an effect that was more prominent in the samples harvested from patients with several comorbidities. This evidence concerns the gene MAOA and mitral valve insufficiency.