Papillary muscle rupture (PMR) is a significant mechanical complication following myocardial infarction (MI), a condition associated with a high mortality. It results in severe mitral valve regurgitation (MR), often accompanied by cardiogenic shock and pulmonary edema, requiring both emergent medical treatment and surgical intervention. Surgical treatment includes either chordal sparing mitral valve replacement or mitral valve repair, which is associated with a high mortality. Mitral valve repair is believed to be superior to mitral valve replacement with respect to improving left ventricular function, albeit with risk of repair failure and resulting in increased cross clamp times. Concomitant coronary revascularization may improve both shortand long-term outcomes after surgery. With advances in medical innovations in the field of transcatheter devices, these devices may serve as a bridge to recovery or treatment in the setting of acute MR due to PMR.However, long-term data will be required to establish the non-inferiority of one treatment modality over the other. Management of these patients should be guided by a dedicated mitral heart team.

Background: This study aims to investigate the association of progression of tricuspid regurgitation following double-valve replacement by comparing the tricuspid valve repair and no repair groups, and to analyze outcomes of patients with non-repaired mild-to-moderate tricuspid regurgitation. Methods: Between January 2014 and September 2017, a total of 157 patients (74 males, 83 females; mean age: 51.7±13.7 years; range, 18 to 78 years) who underwent aortic and mitral valve replacements with/without concomitant tricuspid valve repair were retrospectively analyzed. The patients were divided into two groups: no-repair (n=78) and repair groups (n=79). The primary outcome measure was development of more than moderate tricuspid regurgitation during follow-up. Results: The data were evaluated according to propensity score matched analysis. The progression of tricuspid regurgitation was significantly increased in the no-repair group (p=0.006). Rheumatic etiology was independently associated with the presence of postoperative moderateto- severe tricuspid regurgitation (p=0.004, odds ratio: 3.40). There was no statistically significant difference between the groups in terms of the potential complications and mortality and survival rates. A multivariable subgroup analysis for the baseline mild-to-moderate tricuspid regurgitation without repair showed that rheumatic etiology was an independent factor for the progression of postoperative tricuspid regurgitation (p=0.01). Conclusion: Our study results demonstrated that rheumatic etiology was an independent marker for increased tricuspid regurgitation and it was also independently associated with increased tricuspid regurgitation in patients with mild-to-moderate non-repaired patients. The degree of tricuspid regurgitation was improved in the repair group during follow-up.