Repeat crossclamp after failed initial degenerative mitral valve repair is safe and successful.

Objective: Surgical risk and long-term outcomes when re-crossclamp is required during degenerative mitral valve repair are unknown. We examined the outcomes of patients who required re-crossclamp for mitral valve reintervention. Methods: Adults undergoing mitral valve repair for degenerative mitral valve disease at a single center from 2007 to 2021 who required more than 1 crossclamp for mitral valve reintervention were included. Outcomes including major morbidity and 30-day mortality were collected. Kaplan-Meier analysis characterized survival and freedom from recurrent mitral regurgitation. Results: A total of 69 patients required re-crossclamp for mitral valve reintervention. Of those, 72% (n = 50) underwent successful re-repair and the remaining underwent mitral valve replacement (28%, n = 19). Major morbidity occurred in 23% (n = 16). There was no 30-day mortality, and median long-term survival was 10.9 years for those undergoing re-repair and 7.2 years for those undergoing replacement (P = .79). Midterm echocardiography follow-up was available for 67% (33/50) of patients who were successfully re-repaired with a median follow-up of 20 (interquartile range, 7-37) months. At late follow-up, 90% of patients had mild or less mitral regurgitation. Of those re-repaired, 2 patients later required mitral valve reintervention. Conclusions: Patients requiring re-crossclamp for residual mitral regurgitation had low perioperative morbidity and no mortality. Most patients underwent successful re-repair (vs mitral valve replacement) with excellent valve function and long-term survival. In the event of unsatisfactory repair at the time of mitral valve repair, attempt at re-repair is safe and successful with the appropriate valvar anatomy.

Subpopulations of M-MDSCs from mice infected by an immunodeficiency-causing retrovirus and their differential suppression of T- vs B-cell responses.

Monocytic (CD11b(+)Ly6G(±/Lo)Ly6C(+)) myeloid derived suppressor cells (M-MDSCs) expand following murine retroviral LP-BM5 infection and suppress ex vivo polyclonal T-cell and B-cell responses. M-MDSCs 3 weeks post LP-BM5 infection have decreased suppression of T-cell, but not B-cell, responses and alterations in the degree of iNOS/NO dependence of suppression. M-MDSCs from LP-BM5 infected mice were sorted into four quadrant populations (Ly6C/CD11b density): all quadrants suppressed B-cell responses, but only M-MDSCs expressing the highest levels of Ly6C and CD11b (Q2) significantly suppressed T-cell responses. Further subdivision of this Q2 population revealed the Ly6C(+/Hi) M-MDSC subpopulation as the most suppressive, inhibiting T- and B-cell responses in a full, or partially, iNOS/NO-dependent manner, respectively. In contrast, the lower/moderate levels of suppression by the Ly6C(+/Lo) and Ly6C(+/Mid) M-MDSC Q2 subpopulations, whether versus T- and/or B-cells, displayed little/no iNOS dependency for suppression. These results highlight differential phenotypic and functional immunosuppressive M-MDSC subsets in a retroviral immunodeficiency model.