Acute MR frequently develops in clinically vulnerable patients, including those with advanced age, extensive coronary disease, and in some cases severe ventricular dysfunction, often accompanied by renal impairment and evolving multiorgan injury. Mitral valve repair or replacement has been regarded as definitive therapy, while medical therapy and mechanical circulatory support (MCS) have served primarily as stabilization measures, relying on diuretics, ventilatory support, vasodilators, and vasoactive agents to reduce pulmonary congestion and hemodynamic compromise. However, medical stabilization is often constrained by hypotension and renal hypoperfusion, with progression to cardiogenic shock frequently necessitating MCS. Surgical intervention remains an important therapeutic option in acute MR, but outcomes vary by mechanism and timing. While PMR generally mandates urgent surgery, early mortality exceeds 20% in emergency settings and approaches 30% to 40% in unstable patients.2 In contrast, surgical correction of functional ischemic MR is associated with lower operative mortality when performed electively; however, randomized and observational data have failed to demonstrate a survival advantage of repair over replacement, largely due to high rates of recurrent MR after repair.3 In such patients, the feasibility of urgent surgical intervention may be limited, and delays inherent to operative triage may prove clinically consequential.

Within this context, transcatheter edge-to-edge repair (TEER) has emerged as a potential means of addressing a long-standing treatment gap providing rapid, lesion-directed MR reduction without cardiopulmonary bypass and extending transcatheter therapy beyond traditional elective indications into acute, high-risk settings. In the unstable patient, TEER functions primarily as a hemodynamic therapy: rapid reduction in regurgitant volume can decrease left atrial pressure, relieve pulmonary venous hypertension, improve forward cardiac output, and facilitate de-escalation of vasoactive therapy and ventilatory support. In acute MR, mortality is frequently determined by early hemodynamic collapse and hypoxemia rather than by late valve-related morbidity. Therefore, an intervention capable of meaningfully reducing regurgitation promptly and without cardiopulmonary bypass may change outcomes.

Registry data have been central in establishing TEER as a feasible option in acute post-MI MR. In EREMMI, 44 consecutive high-risk patients treated in 11 European centers underwent TEER with a high technical success rate (86.6%).4 The IREMMI registry extended these findings to unstable presentations: among 93 patients, 53.8% were in cardiogenic shock, but procedural success remained high (90% in shock vs 93% without shock).5

A comparative investigation of conservative, surgical, and percutaneous treatments for acute MR by Haberman et al.,6 included 471 patients with at least moderate-to-severe secondary MR following acute MI managed in 21 centers. Although patients selected for intervention were clinically more unstable, mitral valve intervention was associated with substantially lower in-hospital mortality (11% vs 27%) and lower 1-year mortality (16% vs 35%) compared with conservative therapy (adjusted hazard ratio, 0.28). Among the 205 patients undergoing intervention (106 surgical, 99 percutaneous), procedural success was similarly high (92% vs 93%), but mortality was lower with percutaneous repair than surgery (in-hospital 6% vs 16%, 1-year 17% vs 31%), supporting TEER as a feasible alternative pathway for high-risk patients with prohibitive operative risk.

In parallel, broader shock-focused evidence has reinforced the relevance of TEER beyond the post-MI subgroup. A study investigating urgent TEER for severe MR with degenerative flail leaflet in 17 critically Ill patients demonstrated procedural success in 16 patients with similar mortality rates between the urgent and elective groups.7 In a large registry analysis of patients with significant MR and cardiogenic shock undergoing TEER, device success was achieved in 85.6%, with significant MR reduction in 88.2%.8 Importantly, successful MR reduction was associated with substantially lower 1-year mortality (34.6% vs 55.5%), supporting the concept that TEER may offer a clinically meaningful benefit even in critically ill shock populations and shift perception toward TEER as a component of shock-directed care.

These registry findings are further supported by a systematic review and meta-analysis.9 In 24 studies including 5428 patients with severe MR and cardiogenic shock treated with TEER, pooled device success was 86% and MR ≤ 2+was achieved in 89%, with a 30-day mortality rate of 14%. In the acute MI subgroup, device success remained high (81%), although with higher early mortality (20% at 30 days), highlighting that while TEER is technically feasible in cardiogenic shock, outcomes remain strongly influenced by the underlying acute MI context.

Acute MR is not a single disease entity, and this complexity is central to understanding the role of acute mitral TEER. The mechanism determines anatomy, procedural feasibility, durability, and prognosis. Consequently, recent expert consensus has emphasized the need for integrated and mechanism-based management strategies in severe MR complicating MI rather than reliance on a binary operative decision.10

In the post-MI setting, 2 broad mechanistic phenotypes predominate. The first is acute secondary (functional) MR related to ischemic ventricular dysfunction, remodeling, and leaflet tethering. The second is acute primary (mechanical) MR due to PMR and/or chordal disruption. These phenotypes may present similarly yet represent fundamentally different valvular pathologies. A uniform approach is problematic: it may exaggerate the expected benefit of TEER in mechanically disrupted valves, while delaying or denying TEER to high-risk patients with favorable anatomy.

This mechanistic distinction is increasingly supported by clinical outcome data. An etiology-based analysis by Haberman et al.11 provides direct evidence that TEER can be performed in severe acute post-MI MR, including patients with extreme hemodynamic compromise. Among 176 patients, procedural success was high and MR reduction was comparable among mechanisms (87% in PMR vs 92% in secondary MR). However, PMR was characterized by greater acuity and worse outcomes, including higher conversion to surgery (22% vs 3%), with MR etiology remaining the strongest predictor of in-hospital death after adjustment (odds ratio, 6.71). A recent systematic review focused on acute post-MI M-TEER reinforces the notion that feasibility does not imply uniform prognosis among mechanisms.12 Among 8 studies (n=1148), procedural success was consistently high (86.6%-100%) for both primary and secondary MR, but outcomes diverged substantially by etiology: in-hospital mortality was 6% to 14.4% in secondary MR compared with 30% in primary MR related to PMR/papillary muscle dysfunction. These findings reinforce that in acute MR, TEER should be deployed with mechanism-specific expectations: stabilizing physiology in PMR when no immediate surgical option exists, while enabling definitive MR reduction in selected patients with acute functional MR.

The most challenging and clinically consequential phenotype remains papillary muscle injury and rupture complicating MI. While complete papillary PMR represents a true surgical emergency, papillary muscle injury exists along a spectrum, ranging from partial rupture or chordal disruption to complete structural failure. Emergent surgery is frequently constrained by profound instability, operative risk, and evolving organ dysfunction. Consequently, TEER has been explored as rescue therapy or as a bridge-to-surgery strategy in patients who might otherwise be treated conservatively with an exceptionally poor prognosis. In a dedicated analysis of TEER for papillary muscle injury following acute MI, 23 critically ill patients underwent salvage TEER, with cardiogenic shock present in 87% and frequent need for mechanical support.13 Procedural success was achieved in 87%, with meaningful MR reduction and a marked fall in left atrial V-wave. Despite extreme baseline acuity, 70% were discharged, although a subset required subsequent surgical mitral valve replacement. In this cohort, only 39% of patients had complete PMR with the rest having either partial PMR or chordal rupture. These findings are consistent with the systematic review by Calì et al.,14 which concluded that TEER is feasible in post-MI PMR but is most often deployed as rescue or bridge therapy rather than definitive treatment. Overall, these data support the feasibility of TEER in selected papillary muscle injury scenarios while reinforcing the need for realistic expectations regarding durability, recurrence, and reintervention risk.

These convergent data suggest that TEER is increasingly positioned not merely as a procedural alternative, but as a mechanism-directed strategy capable of reshaping acute MR care (figure 2). However, this paradigm shift should not be reduced to TEER-vs-surgery competition. The more consequential transformation is that TEER changes the structure and timing of clinical decision-making. Historically, management was often reduced to 2 options: urgent surgery for those who could tolerate it, and supportive care for those who could not. TEER has introduced a third pathway: urgent reduction of MR without cardiopulmonary bypass, with the intent of definitive therapy in acute functional MR or stabilization/bridging in acute mechanical MR.

Figure 2.

Suggested algorithm for the management of acute severe mitral regurgitation. MI, myocardial infarction; MR, mitral regurgitation; TEE, transesophageal echocardiography; TEER, transcatheter edge-to-edge repair; TTE, transthoracic echocardiography.

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This shift is already influencing Heart Team practice. Acute MR management is increasingly approached as a time-sensitive syndrome requiring rapid phenotyping (functional vs mechanical), structured imaging with early transesophageal echocardiography, integration with MCS when required, and prompt valve-directed therapy when anatomically feasible. The implications of this approach extend beyond procedural success. In cardiogenic shock, MCS can stabilize systemic perfusion and provide procedural safety; however, unless the regurgitant lesion is treated, MCS may function as an incomplete strategy. Ty directly reducing MR, TEER may facilitate liberation from MCS and enable recovery trajectories that would be otherwise unattainable.

However, caution remains essential. The current evidence base is dominated by observational registries, administrative datasets, and meta-analyses of nonrandomized cohorts, all of which are inherently vulnerable to confounding by indication and selection bias. Timing relative to MI, severity of shock, deployment and type of MCS, and institutional expertise vary substantially among reports. Moreover, acute MR after MI is frequently treated as a single label despite marked heterogeneity in valve mechanism, anatomical suitability for leaflet approximation, left atrial size, and competing determinants of outcome such as infarct size, right ventricular failure, and systemic inflammatory response. These limitations do not diminish the clinical relevance of the existing data; rather, they emphasize that interpretation must remain mechanism-aware and that clinical pathways must be defined by phenotyping, not by procedural availability.

The field is therefore approaching an inflection point. TEER should no longer be viewed as an exceptional measure reserved for patients in whom surgery is not feasible, or as a simplistic competitor to emergent operative repair. Instead, TEER must be integrated into a structured, Heart Team-driven approach in which the first priority is rapid definition of the mechanism and the second is timely MR reduction when anatomically feasible. Within this paradigm, TEER may serve different objectives among phenotypes: in acute functional MR, it may become early definitive therapy in prohibitive surgical candidates; in papillary muscle injury, it may serve as rescue therapy or as a bridging intervention designed to stabilize physiology, reduce pulmonary venous hypertension, and facilitate subsequent definitive treatment. This phenotype-specific approach is now reflected in the 2025 European Society of Cardiology/European Association for Cardio-Thoracic Surgery guidelines for the management of valvular heart disease, which continue to favor surgical repair or replacement for PMR as a primary structural lesion, while supporting the use of M-TEER in acute ventricular secondary MR, particularly following MI, in which MR reduction may also facilitate weaning from MCS.15

What is now required is prospective validation and standardization. In acute MR, procedural success should not be defined solely by MR grade at procedure completion. Clinically meaningful endpoints should reflect the pathophysiology of acute MR and shock: de-escalation of vasoactive support, liberation from mechanical ventilation, discontinuation of MCS, survival to discharge, and durable recovery trajectories rather than short-term technical metrics. Future studies should explicitly stratify by mechanism and incorporate standardized hemodynamic and imaging protocols. Prospective randomized evidence is now needed, and ongoing trials such as EMCAMI (Early transcatheter mitral valve repair after myocardial infarction, NCT06282042) will be critical to define patient selection, optimal timing, and robust endpoint definitions for TEER in acute post-MI MR.

Severe acute MR should be approached as a time-critical syndrome requiring rapid stabilization, early definition of mechanism, and coordinated Heart Team decision-making. Surgery remains the standard therapy for PMR as a primary structural lesion, while TEER has an emerging role in selected patients with acute ventricular secondary MR, particularly when rapid regurgitation reduction may stabilize hemodynamics or facilitate weaning from MCS. Importantly, transcatheter intervention is not universally applicable and is limited by anatomical complexity, small left atrial dimensions, and dependence on institutional expertise. The evolving paradigm therefore reflects not a shift from surgery to transcatheter therapy, but a mechanism-based, patient-specific strategy integrating medical therapy, circulatory support, and timely valve intervention to improve outcomes in acute MR.

This editorial received no external funding.

M. Shuvy is a clinical proctor for Abbott and Edwards Lifesciences. I. Amsalem declares no conflicts of interest.