Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Follow-Up and Surveillance

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nehal Eid, M.D.[2]

Follow-Up and Surveillance

Follow-up after mitral transcatheter edge-to-edge repair (M-TEER) for ventricular secondary mitral regurgitation (MR) must address both valve performance and the underlying heart failure with reduced ejection fraction (HFrEF). Atrial functional MR (AFMR) represents a distinct secondary-MR phenotype; limited mechanism-specific surveillance considerations are noted separately.

In COAPT, 73.6% of device-treated patients had died or been hospitalized for heart failure by 5 years, whereas device-specific safety events occurred in only 4 of 293 treated patients (1.4%) and all occurred within 30 days. Long-term surveillance should therefore emphasize recurrent MR, iatrogenic mitral stenosis, right-heart and heart-failure trajectory, and continued optimization of guideline-directed medical therapy (GDMT).[1]

Discharge and multidisciplinary handoff

Discharge should be a structured transition involving the valve team, heart-failure clinicians, primary cardiologist, and rehabilitation services. Medication reconciliation should address GDMT, diuretics, rhythm therapy, antithrombotic treatment, blood pressure, renal function, nutrition, and plans for cardiac rehabilitation. Any unanticipated clinical change, including stroke, worsening renal function, hemodynamic instability, or arrhythmia, should permit prompt access to the extended multidisciplinary team.[2]

Before discharge:

  • Document the device type, number and location of implanted devices, residual MR, mean transmitral gradient with heart rate, mitral valve area, pulmonary artery systolic pressure (PASP), right-ventricular function, tricuspid regurgitation (TR), and any iatrogenic atrial septal defect (iASD).
  • Record the intraprocedural hemodynamic result and any procedural complication that should alter surveillance intensity.
  • Provide a device card, written antithrombotic plan, dental/endocarditis instructions, medication-titration plan, and scheduled valve and heart-failure follow-up.
  • Establish post-procedural Kansas City Cardiomyopathy Questionnaire (KCCQ), New York Heart Association (NYHA) class, weight, blood pressure, renal function, electrolytes, and hemoglobin as clinical reference values.

Clinical and imaging schedule

The ACC/AHA guideline recommends an initial post-procedural transthoracic echocardiography (TTE) study after valve intervention (Class 1, LOE B-NR). This baseline study should ideally be performed 1–3 months after intervention, when loading conditions have normalized; an in-hospital study may be obtained when clinically necessary or for convenience. Periodic surveillance imaging and annual clinical follow-up are separately recommended (Class 1, LOE C-EO). For transcatheter mitral repair, the guideline specifies baseline imaging followed by annual TTE at a Comprehensive Valve Center without a defined stopping point.[3][4]

MVARC states that comprehensive follow-up TTE is typically recommended at 1 month, 6 months, and annually thereafter.[5] ASE recommends TTE at day 1, 30 days, and 6–12 months; early studies assess complications and the acute result, whereas the later study assesses durability, chamber remodeling, and pulmonary pressures.[6]

Regulatory follow-up requirements are more intensive than the guideline minimum. Multimodality appropriate-use criteria note that post-procedural assessment determined by FDA requirements involves echocardiography before discharge and at 1, 6, and 12 months, followed by annual imaging through 5 years, with TTE rated appropriate.[7] The schedule below therefore synthesizes guideline, trial-standard, imaging-consensus, and regulatory sources rather than representing one validated protocol.

Early surveillance is clinically important. In the CUTTING-EDGE registry, the median interval from M-TEER to mitral surgery for failure was 3.5 months (interquartile range 0.5–11.6 months), and approximately three-quarters of operations occurred within the first year.[8]

Composite post-M-TEER surveillance schedule
Time point Recommended assessment Principal objectives
Before discharge Clinical assessment and TTE after anesthesia effects have resolved and at blood pressure at least equal to the patient's basal state Establish residual MR, mitral valve area, mean gradient with heart rate, device position, TR, PASP, RV function, pericardial status, and iASD; document complications and discharge medications
Approximately 1 month Early valve and heart-failure review with TTE Detect early recurrent MR, single-leaflet device attachment, device thrombus, rising gradient, iASD, renal deterioration, worsening TR, or failure to improve clinically
1–3 months Guideline baseline TTE under stable, normalized loading conditions; this may coincide with the 1-month study Establish the longitudinal reference for residual MR, mean gradient with heart rate, mitral valve area, PASP, TAPSE/PASP, LV/RV size and function, and TR
6 months Clinical assessment and TTE; selective TEE Evaluate durability, recurrent MR, iatrogenic stenosis, TR trajectory, iASD persistence, health status, GDMT tolerance, PASP, TAPSE/PASP, and chamber remodeling
12 months Clinical assessment and TTE Establish 1-year valve, ventricular, pulmonary-pressure, and functional outcomes; reassess recurrent MR, gradient, TR, arrhythmia, and heart-failure trajectory
Annually, indefinitely Valve-center and heart-failure review with TTE at a Comprehensive Valve Center Evaluate MR recurrence, mitral stenosis, LV/RV function, PASP, TR, arrhythmia, renal function, anemia, hospitalization burden, and functional status. The 5-year regulatory horizon does not define a stopping point for guideline surveillance
Any new or worsening symptom Prompt clinical assessment and TTE, with TEE when device dysfunction is suspected Evaluate recurrent MR, device instability, leaflet injury, thrombus, mitral stenosis, endocarditis, worsening TR, pulmonary hypertension, or progression of cardiomyopathy

In patients with severe residual MR, the interval should be shortened; the ACC/AHA guideline recommends TTE every 3–6 months in severe MR, or more frequently as ventricular enlargement progresses.[3]

Echocardiographic assessment

Each study should record blood pressure, heart rate, rhythm, volume status, and relevant changes in treatment. Serial comparisons are most reliable when loading conditions are similar.[6]

Post-repair MR assessment requires an integrated, multiparametric approach because device artifact and multiple residual orifices limit native-valve PISA and effective-regurgitant-orifice methods.

  • Assess residual jets from multiple views, including their origin, number, direction, and relationship to the devices.
  • Exclude device-related thrombus and chordal entrapment, which MVARC lists among the specific post-procedural echocardiographic assessments after edge-to-edge repair.[5]
  • Report the mean transmitral gradient together with heart rate and rhythm.
  • Measure mitral valve area when technically feasible using planimetry on three-dimensional multiplanar reconstruction positioned at the leaflet tips. Measurement on a three-dimensional rendered en-face image is strongly discouraged because of slice thickness and parallax. Two-dimensional planimetry may overestimate area when oblique planes miss the leaflet tips, and pressure half-time should not be used in isolation in the double-orifice valve.[9]
  • Assess pulmonary-vein flow. Elimination of systolic flow reversal and conversion from diastolic- to systolic-dominant flow support effective MR reduction and lower left-atrial pressure.[5]
  • In sinus rhythm, conversion from E-dominant to A-dominant mitral inflow supports meaningful MR reduction. Across serial studies, rising mitral E velocity or velocity-time integral accompanied by falling LV outflow-tract velocity suggests recurrent MR; these findings are not reliable in isolation or during atrial fibrillation.[6]
  • Record LV and left-atrial volumes, PASP, RV size and function, TR grade, inferior vena cava findings, and TAPSE/PASP.
  • Escalate to three-dimensional transesophageal echocardiography (TEE) when TTE is suboptimal; when residual orifices, leaflet insertion, device stability, or the mechanism of MR cannot be adequately characterized; when infection or device thrombus is suspected; or when planning further intervention. CT or cardiac magnetic resonance is reserved for specific questions unresolved by echocardiography.[10]

Pressure half-time by TTE may retain limited supportive value. In a small comparative study, awake post-procedural TTE pressure-half-time–derived valve area agreed well with intraprocedural three-dimensional orifice-area measurement (concordance correlation coefficient 0.95), whereas intraprocedural TEE pressure half-time agreed poorly (0.46). This may reflect loading effects from general anesthesia and does not justify replacing three-dimensional planimetry or integrated assessment with pressure half-time alone.[11]

Elective TEE has additional yield after a suboptimal acute result. In a prospective registry, elective 6-month TEE identified severe MR in 13.3%, an elevated mean gradient in 18%, and new partial or complete single-leaflet device attachment in 7.8%. A mean gradient of at least 5 mm Hg and severe MR at 6 months were associated with death or heart-failure rehospitalization at 2 years.[12]

Iatrogenic mitral stenosis

MVARC defines exclusion of clinically significant post-repair mitral stenosis by both a mitral valve area of at least 1.5 cm² and a mean transmitral gradient below 5 mm Hg at rest.[5] The prognostic weight of this threshold differs by MR etiology. In a 279-patient three-dimensional TEE cohort, post-procedural mitral valve area of 1.5 cm² or less was independently associated with all-cause mortality in degenerative MR, whereas neither small mitral valve area nor transmitral gradient was associated with mortality in the functional-MR cohort.[13]

An elevated gradient should not be interpreted in isolation: it varies with heart rate, rhythm, stroke volume, residual MR, anemia, and loading conditions. Because moderate or greater residual MR augments diastolic transmitral flow, an elevated gradient in the presence of significant residual MR does not by itself establish iatrogenic stenosis, and effective reduction of the residual MR may paradoxically lower the gradient.[6]

Mitral valve area provides prognostic information independent of the gradient. In a three-dimensional TEE study, mitral valve area and mean gradient were discordant in 40% of patients; a post-procedural area of 1.94 cm² or less was associated with all-cause mortality or heart-failure hospitalization (HR 4.28; 95% CI 1.56–11.7) and a blunted fall in PASP.[14]

Baseline anatomy identifies patients who merit closer gradient surveillance. In a quantitative three-dimensional TEE analysis of 112 patients, the risk of an increased post-procedural gradient—defined as at least 5 mm Hg or aborted device implantation because of gradient—was 86%, 28%, and 14% for baseline mitral valve areas below 4.0 cm², 4.0–6.0 cm², and above 6.0 cm², respectively. Within the borderline 4.0–6.0 cm² group, a concurrent baseline gradient of at least 4 mm Hg or mitral annular calcification extending at least 6 mm into the leaflets raised risk from 12% to 53%.[15]

The ASE M-TEER imaging guideline regards a baseline gradient below 5 mm Hg at a heart rate of 60–80 beats/min and a mitral valve area of at least 4.0 cm² as desirable. An area below 3.5 cm² is often considered prohibitive, whereas 3.5–4.0 cm² may be feasible depending on body size, anticipated device number and location, and operator experience.[9] These parameters principally guide procedural planning but also identify patients who warrant closer post-procedural gradient surveillance.

Expected mitral-valve-area reduction is approximately 47% with a PASCAL P10, 52% with a MitraClip NT, and 57% with a MitraClip XTW device; device type should therefore be considered when interpreting the post-procedural area and gradient.[9] A simplified “50–40” rule estimates that post-procedural area is approximately 50% of baseline after one device and 40% of baseline after two devices; this performs comparably to more complex models for identifying patients likely to fall below 2 cm².[16]

Post-procedural transmitral gradient is independently associated with death or heart-failure hospitalization per 1 mm Hg increase (HR 1.10; 95% CI 1.02–1.17). Residual MR should be graded multiparametrically: moderate residual MR with a gradient below 5 mm Hg carried risk similar to mild-or-less MR with a low gradient, whereas greater-than-moderate residual MR remained independently associated with adverse outcomes.[17]

Gradient prognosis also varies by MR etiology. In another analysis, predischarge transmitral gradient in the highest quartile—approximately 7 mm Hg—was associated with 3-year death or heart-failure hospitalization in the overall cohort and in primary MR, but not in secondary MR. In HFrEF, the benefit of MR reduction may therefore offset the adverse effect of a mildly elevated gradient, although marked gradients still require integrated evaluation.[18]

Late stenosis is uncommon but possible, particularly in patients with progressive calcification or advanced renal disease. In the EVEREST II High Risk Study, 2 of 78 patients developed mitral stenosis through 5 years, including one requiring surgery.[19]

Atrial functional mitral regurgitation

AFMR constitutes a distinct surveillance phenotype. In the multicenter MITRA-TUNE registry, midterm MR recurrence was 11%. Post-procedural MR of at least 2+ (HR 5.40; 95% CI 1.37–21.27) and intercommissural annular diameter of at least 35 mm (HR 4.16; 95% CI 1.06–16.36) independently predicted death or heart-failure hospitalization.[20] AFMR surveillance should emphasize residual MR, annular dimensions, left-atrial remodeling, recurrent atrial arrhythmia, TR, and heart-failure trajectory. These observational data do not establish a separate universal imaging interval.

Recurrent mitral regurgitation and device failure

Recurrent MR and device failure may occur after an initially successful repair. In the 5,000-patient COAPT Post-Approval Study, MR was no greater than 2+ in 90.7% at 1 year and heart-failure hospitalization occurred in 18.9%.[21]

Single-leaflet device attachment (SLDA) occurs in approximately 1.9% of patients in pooled studies, declining from 2.8% in studies published through 2018 to 1.4% thereafter. It is often detected during implantation, before discharge, or at early follow-up.[22] Device failure is not confined to the periprocedural period: in the FILM registry, 39.5% of failures were diagnosed during follow-up; mechanisms included SLDA in 67.3%, leaflet injury in 31.9%, and device embolization in 0.8%.[23]

Leaflet tear or perforation should be distinguished from isolated SLDA because leaflet injury more often requires surgical replacement or results in death, whereas selected SLDA can be treated with an additional device. New dyspnea, rising diuretic requirement, an unexplained decline in KCCQ, a new murmur, pulmonary-vein systolic flow reversal, increasing PASP or TR, hemolytic anemia, or a rising transmitral gradient should prompt early TTE and usually TEE.

Detailed economic implications of repair durability are addressed in the cost-effectiveness microchapter.

Tricuspid regurgitation after M-TEER

Post-procedural TR is a specific surveillance target. In OCEAN-Mitral, baseline TR was not associated with outcome, whereas new TR was associated with cardiovascular death or heart-failure hospitalization (HR 1.83; 95% CI 1.39–2.40) and residual TR with HR 1.45 (95% CI 1.23–1.72). Normalization of TR was not associated with excess risk.[24]

In a multicenter European cohort, TR improved by at least one grade in 35%, worsened in 19%, and remained unchanged in 46% at early follow-up. TR of 2+ or less was independently associated with a 42% lower mortality risk, and optimal residual MR predicted subsequent TR improvement.[25]

New or worsening TR should prompt reassessment of residual MR, PASP, RV function, atrial fibrillation, and volume status, with referral for dedicated tricuspid evaluation when severe TR, progressive RV dysfunction, or persistent symptoms develop.

Heart-failure therapy, rehabilitation, and health status

M-TEER treats MR but does not replace HFrEF therapy. The ACC mitral-regurgitation pathway and contemporary HFrEF guidance emphasize continued optimization of GDMT and multidisciplinary management after intervention.[26][27]

At every early visit:

  • Reassess blood pressure, congestion, renal function, potassium, adherence, and adverse effects.
  • Initiate or uptitrate foundational HFrEF therapies as tolerated; document the reason when a medication class is absent.
  • Review diuretic requirement, interval hospitalization, arrhythmia, functional capacity, and applicable rhythm or device therapy.
  • Reassess residual MR after GDMT titration before assuming that early residual MR requires nonurgent reintervention, unless device failure or hemodynamic instability is present.

The survival value of optimal MR reduction appears stage-dependent. In a multicenter secondary-MR cohort, residual MR of 1+ or less was associated with lower 2-year mortality only among patients without LV dilatation and without RV dysfunction. Survival curves converged in patients with either advanced LV remodeling or RV dysfunction, although NYHA class improved across all subgroups. Failure to achieve MR of 1+ or less in advanced disease should therefore be weighed against procedural risk rather than treated as an automatic indication for additional intervention.[28]

In a multicenter cohort, 38% of patients underwent GDMT uptitration by 6 months after M-TEER, and uptitration was associated with improved survival and fewer heart-failure hospitalizations.[29] Triple therapy at discharge was associated with lower 2-year mortality and greater LV reverse remodeling in observational data.[30]

Progressive LV dilation with recurrent MR suggests cardiomyopathy-driven MR and should intensify remodeling-directed therapy. Recurrent MR without corresponding LV progression raises greater concern for device-related failure. Persistent significant MR on medical therapy should trigger renewed valve-team assessment rather than a conclusion of futility. In COAPT, 21.5% of control patients crossed over to M-TEER during follow-up, and crossover was associated with a lower subsequent risk of death or heart-failure hospitalization.[1]

A transportability analysis applying COAPT to 15,275 STS/ACC TVT Registry patients estimated 2-year absolute risk reductions of 17.0% for heart-failure hospitalization and 15.4% for all-cause mortality among 7,289 trial-eligible patients, similar to the trial estimates. These modeled results support the external validity of COAPT expectations in comparable contemporary practice but do not extend them to patients outside the trial phenotype.[31]

Serial health-status assessment complements imaging. KCCQ was measured in COAPT at baseline and 1, 6, 12, and 24 months; changes of 5, 10, and 20 points represent small, moderate, and large clinical changes. An unexplained decline of at least 5 points should prompt clinical evaluation and earlier imaging.[32]

Exercise training or regular physical activity is recommended for patients able to participate (Class 1, LOE A), and formal cardiac rehabilitation is reasonable to improve functional capacity, exercise tolerance, and health-related quality of life (Class 2a, LOE B-NR).[33]

Prognostic markers during follow-up

Natriuretic peptides complement imaging and health-status assessment. In a COAPT analysis of 572 patients, higher baseline BNP or NT-proBNP combined with prior heart-failure hospitalization identified progressively higher absolute risk, but M-TEER benefit was consistent across strata. Elevated natriuretic peptides therefore identify risk rather than absence of benefit. Serial values should be interpreted with volume status, renal function, rhythm, and clinical trajectory.[34]

Right-ventricular–pulmonary-artery coupling, expressed as TAPSE/PASP, should be calculated when measurements are reliable. Approximately two-thirds of patients with secondary MR improve TAPSE/PASP after successful M-TEER, and improvement is independently associated with lower mortality. Failure to improve should prompt reassessment of residual MR, transmitral gradient, TR, pulmonary pressures, and advanced biventricular disease.[35]

Intraprocedural hemodynamic findings can set surveillance intensity. A profile based on MR reduction of fewer than three grades, pulmonary-vein systolic velocity-time-integral increment of 8 cm or less, and residual mean left-atrial pressure above 15 mm Hg classified patients as optimal, mixed, or poor. Risk of death or heart-failure hospitalization increased by HR 1.75 per profile category; mixed or poor profiles support earlier clinical and echocardiographic reassessment.[36]

Other markers of advanced disease and competing risk include severe LV dysfunction, PASP above 50 mm Hg, RV systolic dysfunction, chronic kidney disease, moderate-to-severe TR, and previous cardiac surgery. These findings should intensify multidisciplinary follow-up and goals-of-care discussions but should not be treated individually as validated futility criteria.[37]

Advanced disease, refractory symptoms, repeated hospitalization, worsening frailty, or inability to tolerate GDMT should prompt formal reassessment of prognosis, treatment goals, and need for supportive or palliative-care involvement.[33]

Comorbidity surveillance

Frailty modifies prognosis and the appropriate follow-up posture rather than technical procedural success. In OCEAN-Mitral, acute success and post-procedural MR were similar across Clinical Frailty Scale categories, but 2-year mortality increased stepwise from 15.5% in CFS 1–3 to 48.8% in CFS of at least 7.[38] Frailty should inform rehabilitation intensity, discharge support, prognosis, and goals of care; frailty alone does not mandate more frequent valve imaging.

Renal function and electrolytes should be checked before discharge, during early GDMT titration, and whenever congestion, hypotension, diuretic dose, or renin–angiotensin–aldosterone-system therapy changes. Acute kidney injury occurs in approximately 15% after M-TEER and is associated with worse outcomes and subsequent renal deterioration, particularly when significant residual MR persists.[39]

Anemia should prompt evaluation for bleeding, renal disease, nutritional deficiency, iron deficiency, and—when a significant residual or interdevice jet is present—mechanical hemolysis. Clinically significant hemolysis after M-TEER is rare and is generally associated with residual MR; targeted testing includes hemoglobin, lactate dehydrogenase, haptoglobin, bilirubin, reticulocyte count, and a peripheral smear. Transfusion-dependent or severely symptomatic mechanical hemolysis should prompt heart-team reassessment even when the associated regurgitant lesion is less than severe.[40]

Iron studies should be obtained when anemia, persistent symptoms, or recurrent hospitalization develops. Heart-failure iron deficiency is defined as ferritin below 100 μg/L, or ferritin 100–300 μg/L with transferrin saturation below 20%. Intravenous iron is reasonable to improve functional status and quality of life; evidence for mortality benefit remains absent.[26]

Antithrombotic therapy and stroke surveillance

No completed randomized trial has established an optimal post-M-TEER antithrombotic regimen. Current practice is based on device-trial protocols, expert reviews, and observational data.

  • In patients without an indication for long-term oral anticoagulation, expert reviews describe aspirin plus clopidogrel for approximately 1–6 months followed by aspirin monotherapy, with duration individualized according to thrombotic and bleeding risk. Di Biase et al. specify aspirin alone through 12 months after the DAPT period. These are expert proposals without a formal class or level of evidence for M-TEER.[41][42]
  • In patients with an independent indication for oral anticoagulation, long-term oral anticoagulation without routinely adding antiplatelet therapy is considered feasible unless a separate indication exists, such as recent coronary stenting; this is expert opinion rather than randomized evidence.[42]
  • In the COAPT protocol, intravenous heparin was administered after transseptal crossing to maintain an activated clotting time above 250 seconds throughout the procedure, and clopidogrel 75 mg daily and/or aspirin 81 mg daily was required for at least 6 months in the absence of concomitant oral anticoagulation. This is trial-protocol practice rather than a graded recommendation.[43]

Randomized evidence is pending. STAR-TEER is enrolling 1,912 patients stratified by oral-anticoagulation indication: rivaroxaban monotherapy versus rivaroxaban plus clopidogrel in the oral-anticoagulation cohort, and aspirin monotherapy versus aspirin plus clopidogrel in the non-anticoagulated cohort, with bleeding through 12 months as the primary outcome.[44]

In a propensity-matched analysis of 900 patients per group, single and dual antiplatelet therapy produced similar 1-year ischemic stroke rates (2.7% versus 2.3%; HR 1.15; 95% CI 0.64–2.06) and gastrointestinal bleeding rates (3.6% versus 4.0%; HR 0.89; 95% CI 0.55–1.43). These observational data may support earlier de-escalation in patients at high bleeding risk but do not replace randomized evidence.[45]

Cerebrovascular events are uncommon but occur predominantly after discharge. In a pooled cohort of 2,238 patients, stroke occurred in 1.47% over a median of 14 months. Atrial fibrillation, renal dysfunction, and higher thromboembolic risk identified higher-risk patients.[46] Follow-up should verify anticoagulant adherence, renal dose appropriateness, bleeding, falls, interval neurologic symptoms, and changes in rhythm.

Atrial fibrillation during follow-up

Atrial fibrillation should be reassessed at each visit for ventricular-rate control, anticoagulation appropriateness, symptom burden, heart-failure contribution, and recurrent atrial tachyarrhythmia.

Pharmacologic rhythm control should not be adopted reflexively. In a multicenter observational cohort of 542 patients, 3-year survival was lower with rhythm control than rate control, and amiodarone—used for most rhythm-control treatment—was independently associated with mortality. These findings are vulnerable to confounding by indication and do not establish that rate control is superior, but they support careful review of ongoing amiodarone exposure.[47]

Catheter ablation after M-TEER is feasible. In a small propensity-matched series, pulmonary-vein isolation was performed without periprocedural device interference, and arrhythmia-free survival was similar to controls. Left-atrial tachycardia accounted for a greater proportion of recurrences after prior repair, which should be considered when a post-M-TEER patient develops a new regular atrial arrhythmia.[48]

Iatrogenic atrial septal defect

Persistent iASD is common after transseptal M-TEER: at 6 months, approximately 27% are detected by TTE and nearly 50% by TEE. Proposed procedural predictors include larger catheter size, longer procedure duration, extensive sheath movement, high left-atrial pressure, and LV hypertrophy.[9]

In a systematic review of 10 studies, predictors of persistence included pre-procedural atrial fibrillation (OR 1.40), residual MR greater than 2+ (OR 2.36), residual TR greater than mild (OR 1.52), and prolonged fluoroscopy time. Persistent iASD was associated with right-atrial and right-ventricular enlargement and heart-failure rehospitalization (OR 2.71; P=0.003).[49]

Counterbalancing evidence suggests that an incidentally persistent defect may be benign in some patients. In a 53-patient TEE cohort, persistent iASD at 6 months occurred in 62% and was associated with larger RV end-diastolic diameter but not with differences in NYHA improvement, TAPSE, RV systolic pressure, 2-year rehospitalization, or mortality.[50]

ASE expert consensus favors case-by-case closure when there is right-to-left or bidirectional shunting, hypoxemia, pulmonary hypertension, new RV dysfunction or severe TR plausibly related to the shunt, or a large defect; routine closure is not supported. Defects greater than 1.0 cm are generally considered for closure, although this should be decided case by case.[9]

MITHRAS randomized 80 patients with an iASD and relevant left-to-right shunting (Qp:Qs ≥1.3) 30 days after M-TEER. Closure did not significantly improve clinical outcome compared with conservative management, but the trial was underpowered. Death or heart-failure hospitalization at 12 months occurred in 43% of patients with a relevant iASD versus 17% in a comparative cohort without one. Because the two randomized MITHRAS groups tracked closely together and both diverged from the no-iASD cohort, the defect likely functions primarily as a surrogate marker of more advanced disease rather than a direct cause of worse outcome. The practical implication is closer clinical surveillance, not routine closure.[51]

Urgent closure is occasionally required. In a Japanese nationwide series, approximately 1% of MitraClip recipients underwent transcatheter iASD closure, 73% within 24 hours, usually for hypoxemia caused by right-to-left shunting or right-heart failure with a significant left-to-right shunt.[52]

Infective endocarditis prevention and recognition

The 2020 ACC/AHA guideline states that antibiotic prophylaxis is reasonable before dental procedures involving manipulation of gingival tissue, the periapical region, or perforation of oral mucosa in patients with prosthetic material used for cardiac valve repair, explicitly including clips (Class 2a, LOE C-LD). It states that prophylaxis is not recommended for nondental procedures such as TEE, esophagogastroduodenoscopy, colonoscopy, or cystoscopy in the absence of active infection (Class 3: No Benefit, LOE B-NR).[3]

The 2023 ESC guideline is concordant. It strengthened prophylaxis before invasive dental procedures for its established high-risk categories from Class IIa to Class I and separately states that prophylaxis should be considered in patients after transcatheter mitral or tricuspid valve repair (Class IIa, LOE C). The Class I upgrade therefore does not apply specifically to M-TEER recipients.[53]

The AHA no longer recommends clindamycin for dental prophylaxis because of its adverse-effect profile. Detailed prophylactic regimens are addressed in Infective endocarditis prophylaxis.[54]

M-TEER-associated endocarditis is rare but carries high mortality. In a systematic review of 26 cases, median onset was 5 months, Staphylococcus aureus caused 46%, and in-hospital mortality was 50%.[55] Unexplained fever or bacteremia warrants prompt blood cultures and a low threshold for TEE.

Reintervention

Recurrent at least moderate-to-severe MR, severe MR, progressive symptoms, repeated heart-failure hospitalization, device instability, significant leaflet injury, symptomatic iatrogenic mitral stenosis, or transfusion-dependent mechanical hemolysis should prompt TEE and referral to a high-volume multidisciplinary mitral center.

In COAPT, the 4-year cumulative incidence of repeat mitral intervention was 3.90% at a median of 182 days; 9 of 10 procedures were repeat TEER and 8 of 10 were successful. Larger annular diameter, fewer implanted devices, and MR of at least 3+ at discharge identified patients more likely to require reintervention.[56]

Detailed anatomic selection and choice among repeat transcatheter or surgical strategies belong in the procedural-therapy assessment. Reintervention should be considered before advanced TR, RV failure, end-organ dysfunction, or frailty makes meaningful recovery unlikely.

References

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  2. ↑ Bonow RO, O'Gara PT, Adams DH; et al. (2020). "2019 AATS/ACC/SCAI/STS Expert Consensus Systems of Care Document: Operator and Institutional Recommendations and Requirements for Transcatheter Mitral Valve Intervention". Journal of the American College of Cardiology. 76 (1): 96–117. doi:10.1016/j.jacc.2019.12.002.
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  6. ↑ 6.0 6.1 6.2 6.3 Zoghbi WA, Asch FM, Bruce C; et al. (2019). "Guidelines for the Evaluation of Valvular Regurgitation After Percutaneous Valve Repair or Replacement". Journal of the American Society of Echocardiography. 32 (4): 431–475. doi:10.1016/j.echo.2019.01.003.
  7. ↑ Doherty JU, Kort S, Mehran R, Schoenhagen P, Soman P (2017). "ACC/AATS/AHA/ASE/ASNC/HRS/SCAI/SCCT/SCMR/STS 2017 Appropriate Use Criteria for Multimodality Imaging in Valvular Heart Disease". Journal of the American College of Cardiology. 70 (13): 1647–1672. doi:10.1016/j.jacc.2017.07.732.
  8. ↑ Marin-Cuartas M, Kang J, Noack T; et al. (2025). "Surgical Mitral Valve Repair vs Replacement After Failed Mitral Transcatheter Edge-to-Edge Repair: The CUTTING-EDGE Registry". JACC: Cardiovascular Interventions. 18 (7): 912–923. doi:10.1016/j.jcin.2025.02.008.
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  11. ↑ Kumar R, Dasani SS, Fields KG; et al. (2026). "Three-Dimensional Echocardiographic Approach to Mitral Valve After Transcatheter Edge-to-Edge Repair". Anesthesia and Analgesia. 142 (1): 85–92. doi:10.1213/ANE.0000000000007756.
  12. ↑ Bartkowiak J, Kassar M, Brülisauer SJ; et al. (2024). "Findings From Transoesophageal Echocardiographic Follow-Up After Mitral Transcatheter Edge-to-Edge Repair". EuroIntervention. 20 (20): e1298–e1308. doi:10.4244/EIJ-D-24-00297.
  13. ↑ Kagawa S, Hasegawa H, Kuwajima K; et al. (2024). "Long-Term Impact of Small Mitral Valve Orifice Area After Transcatheter Edge-to-Edge Mitral Valve Repair on Clinical Outcome: A Three-Dimensional Echocardiography Study". Journal of the American Society of Echocardiography. 37 (3): 328–337. doi:10.1016/j.echo.2023.11.007.
  14. ↑ Utsunomiya H, Itabashi Y, Kobayashi S; et al. (2017). "Effect of Percutaneous Edge-to-Edge Repair on Mitral Valve Area and Its Association With Pulmonary Hypertension and Outcomes". The American Journal of Cardiology. 120 (4): 662–669. doi:10.1016/j.amjcard.2017.05.036.
  15. ↑ Oguz D, Padang R, Rashedi N; et al. (2021). "Risk for Increased Mean Diastolic Gradient After Transcatheter Edge-to-Edge Mitral Valve Repair: A Quantitative Three-Dimensional Transesophageal Echocardiographic Analysis". Journal of the American Society of Echocardiography. 34 (6): 595–603.e2. doi:10.1016/j.echo.2021.01.018. PMID 33524491 Check |pmid= value (help).
  16. ↑ Alexandrino FB, Sandhu S, Oguz D; et al. (2023). "Estimating Mitral Valve Area Post-Transcatheter Edge-to-Edge Repair: As Simple as 50-40". JACC: Cardiovascular Interventions. 16 (23): 2948–2950. doi:10.1016/j.jcin.2023.10.006.
  17. ↑ Tsunamoto H, Yamamoto M, Kagase A; et al. (2025). "Using Transmitral Pressure Gradients and Residual Mitral Regurgitation to Optimize Outcome After Transcatheter Edge-to-Edge Repair". Journal of the American College of Cardiology. 86 (19): 1684–1700. doi:10.1016/j.jacc.2025.07.041.
  18. ↑ Sammour YM, Bou Chaaya RG, Hatab T; et al. (2024). "Impact of Residual Transmitral Mean Pressure Gradient on Outcomes After Mitral Transcatheter Edge-to-Edge Repair". JACC: Advances. 3 (10): 101227. doi:10.1016/j.jacadv.2024.101227.
  19. ↑ Kar S, Feldman T, Qasim A; et al. (2019). "Five-Year Outcomes of Transcatheter Reduction of Significant Mitral Regurgitation in High-Surgical-Risk Patients". Heart. 105 (21): 1622–1628. doi:10.1136/heartjnl-2017-312605.
  20. ↑ Popolo Rubbio A, Testa L, Grasso C; et al. (2022). "Transcatheter Edge-to-Edge Mitral Valve Repair in Atrial Functional Mitral Regurgitation: Insights From the Multi-Center MITRA-TUNE Registry". International Journal of Cardiology. 349: 39–45. doi:10.1016/j.ijcard.2021.11.027.
  21. ↑ Goel K, Lindenfeld J, Makkar R; et al. (2023). "Transcatheter Edge-to-Edge Repair in 5,000 Patients With Secondary Mitral Regurgitation: COAPT Post-Approval Study". Journal of the American College of Cardiology. 82 (13): 1281–1297. doi:10.1016/j.jacc.2023.07.015.
  22. ↑ Bhatia K, Gupta S, Carter K; et al. (2024). "Single-Leaflet Device Attachment After Mitral Transcatheter Edge-to-Edge Repair: Systematic Review and Meta-Analysis". JACC: Cardiovascular Interventions. 17 (21): 2571–2574. doi:10.1016/j.jcin.2024.08.008.
  23. ↑ Mangieri A, Melillo F, Montalto C; et al. (2022). "Management and Outcome of Failed Percutaneous Edge-to-Edge Mitral Valve Plasty: Insight From an International Registry". JACC: Cardiovascular Interventions. 15 (4): 411–422. doi:10.1016/j.jcin.2021.11.040.
  24. ↑ Matsumoto S, Ohno Y, Noda S; et al. (2025). "Tricuspid Regurgitation and Outcomes in Mitral Valve Transcatheter Edge-to-Edge Repair". European Heart Journal. 46 (15): 1415–1427. doi:10.1093/eurheartj/ehae924.
  25. ↑ Adamo M, Pagnesi M, Ghizzoni G; et al. (2022). "Evolution of Tricuspid Regurgitation After Transcatheter Edge-to-Edge Mitral Valve Repair for Secondary Mitral Regurgitation and Its Impact on Mortality". European Journal of Heart Failure. 24 (11): 2175–2184. doi:10.1002/ejhf.2637.
  26. ↑ 26.0 26.1 Maddox TM, Januzzi JL, Allen LA; et al. (2024). "2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction". Journal of the American College of Cardiology. 83 (15): 1444–1488. doi:10.1016/j.jacc.2023.12.024.
  27. ↑ Bonow RO, O'Gara PT, Adams DH; et al. (2020). "2020 Focused Update of the 2017 ACC Expert Consensus Decision Pathway on the Management of Mitral Regurgitation". Journal of the American College of Cardiology. 75 (17): 2236–2270. doi:10.1016/j.jacc.2020.02.005.
  28. ↑ Higuchi S, Orban M, Stolz L; et al. (2021). "Impact of Residual Mitral Regurgitation on Survival After Transcatheter Edge-to-Edge Repair for Secondary Mitral Regurgitation". JACC: Cardiovascular Interventions. 14 (11): 1243–1253. doi:10.1016/j.jcin.2021.03.050.
  29. ↑ Adamo M, Tomasoni D, Stolz L; et al. (2023). "Impact of Transcatheter Edge-to-Edge Mitral Valve Repair on Guideline-Directed Medical Therapy Uptitration". JACC: Cardiovascular Interventions. 16 (8): 896–905. doi:10.1016/j.jcin.2023.01.362.
  30. ↑ Tanaka T, Kavsur R, Spieker M; et al. (2022). "Guideline-Directed Medical Therapy After Transcatheter Edge-to-Edge Mitral Valve Repair". Heart. 108 (21): 1722–1728. doi:10.1136/heartjnl-2022-320826.
  31. ↑ Lalani C, Butala N, Dong H; et al. (2026). "Estimating the Effects of MTEER in U.S. Practice: A Transportability Analysis of the COAPT Trial". Journal of the American College of Cardiology. doi:10.1016/j.jacc.2026.04.025.
  32. ↑ Arnold SV, Chinnakondepalli KM, Spertus JA; et al. (2019). "Health Status After Transcatheter Mitral-Valve Repair in Heart Failure and Secondary Mitral Regurgitation: COAPT Trial". Journal of the American College of Cardiology. 73 (17): 2123–2132. doi:10.1016/j.jacc.2019.02.010.
  33. ↑ 33.0 33.1 Heidenreich PA, Bozkurt B, Aguilar D; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure". Journal of the American College of Cardiology. 79 (17): e263–e421. doi:10.1016/j.jacc.2021.12.012.
  34. ↑ Goel SS, Guha A, Lindenfeld J; et al. (2025). "Impact of Natriuretic Peptide and Prior Hospitalization in Patients With Severe Mitral Regurgitation: COAPT Trial". Circulation: Cardiovascular Interventions: e015192. doi:10.1161/CIRCINTERVENTIONS.125.015192.
  35. ↑ Adamo M, Inciardi RM, Tomasoni D; et al. (2022). "Changes in Right Ventricular-to-Pulmonary Artery Coupling After Transcatheter Edge-to-Edge Repair in Secondary Mitral Regurgitation". JACC: Cardiovascular Imaging. 15 (12): 2038–2047. doi:10.1016/j.jcmg.2022.08.012.
  36. ↑ Zaid S, Wessly P, Hatab T; et al. (2024). "Intraprocedural Doppler and Invasive Hemodynamic Profiling Predict Clinical Outcomes After Mitral TEER". JACC: Cardiovascular Imaging. 17 (4): 454–456. doi:10.1016/j.jcmg.2023.10.013.
  37. ↑ Ben-Shoshan J, Overtchook P, Buithieu J; et al. (2020). "Predictors of Outcomes Following Transcatheter Edge-to-Edge Mitral Valve Repair". JACC: Cardiovascular Interventions. 13 (15): 1733–1748. doi:10.1016/j.jcin.2020.03.025.
  38. ↑ Tokuda T, Yamamoto M, Kagase A; et al. (2024). "Clinical Impact of Baseline Frailty Status and Residual Mitral Regurgitation After Transcatheter Edge-to-Edge Repair: Insights From the OCEAN-Mitral Registry". Journal of the American Heart Association. 13 (21): e035109. doi:10.1161/JAHA.124.035109.
  39. ↑ Armijo G, Estevez-Loureiro R, Carrasco-Chinchilla F; et al. (2020). "Acute Kidney Injury After Percutaneous Edge-to-Edge Mitral Repair". Journal of the American College of Cardiology. 76 (21): 2463–2473. doi:10.1016/j.jacc.2020.09.582.
  40. ↑ Cannata A, Cantoni S, Sciortino A, Bruschi G, Russo CF (2021). "Mechanical Hemolysis Complicating Transcatheter Interventions for Valvular Heart Disease: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 77 (18): 2323–2334. doi:10.1016/j.jacc.2021.03.295.
  41. ↑ Galli M, Gragnano F, Berteotti M; et al. (2024). "Antithrombotic Therapy in High Bleeding Risk, Part I: Percutaneous Cardiac Interventions". JACC: Cardiovascular Interventions. 17 (19): 2197–2215. doi:10.1016/j.jcin.2024.08.022.
  42. ↑ 42.0 42.1 Di Biase L, Lakkireddy DJ, Marazzato J; et al. (2024). "Antithrombotic Therapy for Patients Undergoing Cardiac Electrophysiological and Interventional Procedures: JACC State-of-the-Art Review". Journal of the American College of Cardiology. 83 (1): 82–108. doi:10.1016/j.jacc.2023.09.831.
  43. ↑ Vincent F, Redfors B, Kotinkaduwa LN; et al. (2023). "Cerebrovascular Events After Transcatheter Edge-to-Edge Repair and Guideline-Directed Medical Therapy in the COAPT Trial". JACC: Cardiovascular Interventions. 16 (12): 1448–1459. doi:10.1016/j.jcin.2023.03.023.
  44. ↑ Wang C, Liu Z, Li Z; et al. (2026). "Strategies for Antithrombotic Treatment Following Transcatheter Edge-to-Edge Repair in Patients With Severe Mitral Regurgitation: Rationale and Design of STAR-TEER Trial". American Heart Journal. 296: 107362. doi:10.1016/j.ahj.2026.107362.
  45. ↑ Jarrar Y, Alomari L, Otabor E; et al. (2025). "A Safer Bet for MitraClip: Choosing Between Single Antiplatelet Therapy and Dual Antiplatelet Therapy". International Journal of Cardiology. 437: 133476. doi:10.1016/j.ijcard.2025.133476. PMID 40490030 Check |pmid= value (help).
  46. ↑ Giordano A, Ferraro P, Finizio F; et al. (2024). "Incidence and Predictors of Cerebrovascular Accidents in Patients Who Underwent Transcatheter Mitral Valve Repair With MitraClip". The American Journal of Cardiology. 228: 24–33. doi:10.1016/j.amjcard.2024.07.037.
  47. ↑ Waechter C, Ausbuettel F, Chatzis G; et al. (2021). "Impact of Rhythm vs Rate Control in Atrial Fibrillation on the Long-Term Outcome of Patients Undergoing Transcatheter Edge-to-Edge Mitral Valve Repair". Journal of Clinical Medicine. 10 (21): 5044. doi:10.3390/jcm10215044.
  48. ↑ Rottner L, Lemes C, Dotz I; et al. (2019). "The Clip and the Tip: Lessons Learned From Ablation of Atrial Fibrillation in Patients Postpercutaneous Mitral Valve Repair". Journal of Cardiovascular Electrophysiology. 30 (8): 1207–1214. doi:10.1111/jce.13964.
  49. ↑ Lei D, Zhou C, Zhou J, Luo C, Zheng B (2025). "Iatrogenic Atrial Septal Defect Following Transcatheter Edge-to-Edge Mitral Valve Repair: A Systematic Review and Meta-Analysis". Medicine. 104 (52): e46486. doi:10.1097/MD.0000000000046486.
  50. ↑ Alachkar MN, Alnaimi A, Reith S; et al. (2021). "Incidence and Clinical Relevance of Persistent Iatrogenic Atrial Septal Defect After Percutaneous Mitral Valve Repair". Scientific Reports. 11 (1): 12700. doi:10.1038/s41598-021-92255-3.
  51. ↑ Lurz P, Unterhuber M, Rommel KP; et al. (2021). "Iatrogenic Atrial Septal Defects Following Transcatheter Mitral Valve Repair and Implications of Interventional Closure". JACC: Cardiovascular Interventions. 14 (24): 2685–2694. doi:10.1016/j.jcin.2021.09.023.
  52. ↑ Takaya Y, Akagi T, Hara H; et al. (2022). "Iatrogenic Atrial Septal Defect Requiring Transcatheter Closure Following Transcatheter Mitral Valve Repair". Circulation Journal. 86 (11): 1740–1744. doi:10.1253/circj.CJ-22-0048. PMID 35387922 Check |pmid= value (help).
  53. ↑ Dayer MJ, Quintero-Martinez JA, Thornhill MH; et al. (2024). "Recent Insights Into Native Valve Infective Endocarditis: JACC Focus Seminar 4/4". Journal of the American College of Cardiology. 83 (15): 1431–1443. doi:10.1016/j.jacc.2023.12.043.
  54. ↑ Wilson WR, Gewitz M, Lockhart PB; et al. (2021). "Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the American Heart Association". Circulation. 143 (20): e963–e978. doi:10.1161/CIR.0000000000000969.
  55. ↑ Bertolino L, Ramadan MS, Zampino R, Durante-Mangoni E (2023). "Infective Endocarditis Involving MitraClip Devices: A Systematic Literature Review". Infection. 51 (5): 1241–1248. doi:10.1007/s15010-023-02067-y.
  56. ↑ Shahim B, Cohen DJ, Asch FM; et al. (2024). "Repeat Mitral Valve Interventions After Transcatheter Edge-to-Edge Repair: The COAPT Trial". The American Journal of Cardiology. 223: 7–14. doi:10.1016/j.amjcard.2024.05.025.
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