Long-term outcomes of treatment for acute ischaemic mitral regurgitation: a mechanism-based approach

Acute ischaemic mitral regurgitation (aiMR) is a critical emergency in ischaemic heart disease, primarily diagnosed via echocardiography with Doppler and colour flow imaging, but treatment remains inconsistent due the diverse nature of valve dysfunction. This study addresses the need for mechanism-specific therapeutic strategies.

To assess the impact of aiMR pathophysiological mechanisms on long-term prognosis in patients receiving targeted therapies.

In this retrospective cohort study, we evaluated patients with aiMR admitted with acute coronary syndrome (ACS) to our centre from 2006 to 2024. Patients received either mitral valve replacement (MVR) or optimal medical therapy (OMT) based on TTE or TEE diagnostics. Three primary mechanisms affecting structural integrity and coaptation were identified: (1) left ventricular (LV) wall abnormalities by ischaemia in the papillary muscle causing leaflet tethering and eccentric regurgitation, (2) LV remodelling causing annular dilatation without direct leaflet motion abnormalities, and (3) papillary muscle rupture. Patients were classified by treatment type based on structural mechanism and followed up using medical records and telephone interviews.

Of 168 patients, 161 met inclusion criteria (69% male; median age 63 [57–69] years). Groups were distributed as follows: ischaemic papillary muscle dysfunction (n=106, 65.8%), LV remodelling (n=29, 18%), and papillary muscle rupture (n=26, 16.3%). No significant age or sex differences were observed among groups (p=0.425). Reperfusion therapy was not received in 80.1% of aiMR cases: ischaemic (84.9%), LV remodelling (65.5%), and rupture (76.9%) (ANOVA p=0.0618). STEMI occurred more frequently than NSTEMI, in 73.8% of cases, with rates by group as follows: ischaemic (80%), LV remodelling (69%), and rupture (53.9%) (p=0.619). Median follow-up was 132 days (IQR 13–1413), with Kaplan-Meier analysis extending to 1500 days. Survival outcomes were mechanism-dependent. In the ischaemic group, patients treated with OMT had a mean survival of 993 days (95% CI: 836–1150), whereas those undergoing MVR had a significantly shorter mean survival of 499 days (95% CI: 238–759) (Log-rank p=0.001). The LV remodelling group showed no significant survival difference between OMT and MVR (p=0.889). In the rupture group, patients receiving MVR had a significantly higher mean survival (1093 days, 95% CI: 816–1371) than those treated with OMT (mean 17 days, 95% CI: 1–34) (p=0.034).

Mechanism-based treatment for aiMR reveals significant survival variation across structural subtypes. While MVR improves survival in rupture cases, it shows poorer outcomes in ischaemic dysfunction compared to OMT. These findings underscore the importance of tailoring aiMR treatment to pathophysiological mechanisms for optimal long-term survival.