Severe continuous prosthetic mitral regurgitation from chordal rupture after valve-sparing replacement: a case report

Abstract

Background

After mitral valve replacement with preservation of the subvalvular apparatus, prosthetic dysfunction resulting from retained native structures is extremely rare. When it occurs, it may directly threaten the patient’s life. We report an unusual case of severe regurgitation resulting from preserved chordal rupture. The key distinction of this case is the presentation of late, severe continuous prosthetic regurgitation and reversibility.

Case presentation

A 54-year-old man had undergone double mechanical valve replacement for severe rheumatic mitral stenosis with mild regurgitation and concomitant aortic regurgitation three years earlier. During surgery, the posterior mitral leaflet and its entire subvalvular apparatus were preserved. Current transesophageal echocardiography revealed a mobile, cord-like structure between the lateral occluder and the prosthetic sewing ring, interfering with leaflet excursion and preventing full closure. This was accompanied by severe prosthetic mitral continuous regurgitation. Surgical findings revealed a ruptured chordae tendineae at the papillary muscle attachment, with the remnant preventing leaflet coaptation. Surgical excision of the ruptured chordal remnant successfully restored normal leaflet function, with complete resolution of the regurgitation confirmed on intraoperative transesophageal echocardiography.

Conclusions

When obstruction or regurgitation develops after valve replacement with subvalvular preservation, uncommon causes—such as residual subvalvular tissue or ruptured chordal entrapment—should be considered after excluding more common etiologies. This case illustrates the critical role of transesophageal echocardiography in the diagnosis of chordal entrapment after mitral valve replacement and potentially in preventing complications. The potential benefit of preserving the subvalvular apparatus warrants thoughtful deliberation. Surgical removal of the offending tissue or valve replacement remains the definitive treatment.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s13019-026-04656-y.

Background

Current evidence supports preserving the continuity of the mitral leaflets, chordae tendineae, and papillary muscles during mitral valve replacement to optimize ventricular function and maintain ventricular geometry. However, potential complications—such as left ventricular outflow tract obstruction and prosthetic valve dysfunction—should be anticipated.

Case presentation

A 54-year-old man presented with intermittent dizziness. He denied fever or other systemic symptoms, and inflammatory markers were unremarkable. Apart from atrial fibrillation, no comorbidities were identified. Three years earlier, he had undergone double mechanical valve replacement for severe rheumatic mitral stenosis with mild regurgitation and concomitant aortic regurgitation. During surgery, the posterior mitral leaflet and its entire subvalvular apparatus were preserved, and a 27-mm St. Jude Medical mechanical mitral prosthesis was implanted. Postoperative echocardiography showed satisfactory prosthetic function. The patient was discharged on regular warfarin anticoagulation with scheduled echocardiographic follow-ups, all of which had remained normal until presentation.

Current transthoracic echocardiography revealed a mobile, cord-like, isoechoic structure (~15 × 7 mm) on the left ventricular aspect of the lateral occluder of the mitral prosthesis. During systole, the strand moved toward the occluder; during diastole, it swung back into the left ventricular cavity (Fig. 1A, Video 1). Transesophageal echocardiography confirmed that the structure lay between the lateral occluder and the prosthetic sewing ring, interfering with leaflet excursion and preventing full closure (Fig. 1B, Video 2). This was accompanied by severe prosthetic mitral regurgitation (Fig. 1C, Video 4); Color Doppler imaging revealed a large central regurgitant jet originating from the site where the coaptation point of the valve leaflets was located close to the impacted structure. The jet was directed centrally into the left atrium, with an estimated vena contracta of 0.7 cm and an effective regurgitant orifice area (EROA) of 0.65 cm². Continuous-wave Doppler demonstrated a pan-systolic continuous regurgitant jet, indicating that the entrapment prevented leaflet closure throughout the entire systolic period. The mean transprosthetic gradient was 5 mmHg, and no paravalvular leak was noted.

Fig. 1.

A Transthoracic echocardiography (apical four-chamber view) revealed a cord-like, echogenic structure (red arrow) adjacent to the lateral prosthetic leaflet on the ventricular side. LA : Left atrium LV : Left ventricle. B Two-dimensional transesophageal echocardiography (midesophageal four-chamber view) showing a mass (18 mm × 9 mm) between the outer disc of the mechanical mitral valve prosthesis and the housing in the open position on the ventricular side. C Transesophageal echocardiography (midesophageal non-standard two -chamber view) with Color Doppler imaging demonstrating severe transvalvular mitral regurgitation

Alternative diagnoses were systematically considered and excluded: pannus (non-mobile, echodense mass, gradual onset), thrombus (irregular morphology, subtherapeutic anticoagulation absent), vegetation (no clinical or laboratory signs of infection). A key point is that the patient underwent subvalvular structure preservation during the initial surgery; therefore, the mobile structure was considered to be a ruptured chordal remnant. Mitral prosthetic valve regurgitation may result from residual chordae tendineae interfering with proper valve closure.

Preoperatively, two surgical strategies were considered: (1) exploration with simple excision of the offending tissue if the prosthesis was intact and functional, versus (2) complete valve replacement if the prosthesis was damaged, thrombosed, or if complete debridement was not feasible. The patient underwent reoperation via median sternotomy under cardiopulmonary bypass with antegrade cold blood cardioplegia. Cardiopulmonary bypass time was 78 min, with aortic cross-clamp time of 52 min. Intraoperative inspection revealed a fibrous cord (~ 18 × 7 mm) firmly entrapped between the lateral occluder and the prosthetic annulus. After careful dissection, the chordal remnant was completely excised. The prosthesis was then tested: leaflet mobility was normal, the sewing ring was intact, and no other abnormal tissue was found on or around the prosthesis. Intraoperative transesophageal echocardiography confirmed normal mobility of the leaflet and complete resolution of regurgitation. Thus, valve replacement was avoided, sparing the patient the additional risks of prosthesis explantation and reimplantation (Fig. 2B and C, Video 3).

Fig. 2.

A Surgically resected chordal tissue. B Postoperative two-dimensional transesophageal echocardiography (midesophageal two-chamber view) showing the prosthetic valve in the open position with no mass. C Postoperative color Doppler transesophageal echocardiography(midesophageal left ventricilar long-axis view) indicating physiological transvalvular mitral regurgitation without an abnormal jet

Histologic examination of the excised tissue confirmed chordal tissue with fibrous proliferation and collagenization

During the most recent follow-up (14 months after surgery), transthoracic echocardiography showed normal mechanical valve function with a mean gradient of 3 mmHg and no regurgitation. The left ventricular ejection fraction was preserved at 63% (compared to 56% pre-reoperation), indicating recovery of ventricular hemodynamics. The patient has not experienced any recurrence of dizziness. The previous intermittent dizziness was likely attributable to a reduction in forward cardiac output resulting from severe mitral regurgitation, which was exacerbated during physical activity.

Discussion

While preservation of the subvalvular apparatus ensures myocardial protection, improves postoperative ventricular function and reduces the risk of left ventricular rupture [1], these advantages must be balanced against potential complications. This case underscores a rare but serious long-term risk—chordal rupture and entrapment. Previous reports primarily describe intermittent dysfunction [4, 5]; our case highlights that continuous, severe regurgitation can also occur.The pathophysiological basis maybe lie in the specific anatomy: the ruptured chordal stump was lodged firmly between the lateral occluder and the prosthetic housing, preventing leaflet closure throughout systole. Unlike intermittent cases where the structure may be displaced during diastole, here the entrapment was fixed. We hypothesize that the large size (18 × 7 mm) and location at the hinge point created mechanical obstruction that could not be dislodged by normal hemodynamic forces.

Retaining the anterior leaflet may lead to left ventricular outflow tract obstruction [2], while redundant chordae or residual chordal stumps can interfere with prosthetic function. Mok et al. [3] reported two fatal cases in which retained chordal tissue became entrapped between the occluder and housing of a bileaflet mechanical valve, causing acute prosthetic obstruction. Gallet et al. [4] described severe intermittent regurgitation 6 days postoperatively in a patient with retained subvalvular structures that required resection.

Tan et al. [5] reported a case of declining ejection fraction and severe intermittent trans-prosthetic regurgitation after mitral valve replacement due to chordal remnants interfering with leaflet motion.

In our case, mechanism of late chordal rupture after surgery warrants discussion. First, progressive rheumatic involvement: rheumatic heart disease is characterized by ongoing inflammatory and fibrotic processes. Even after valve replacement, retained chordal remain susceptible to progressive collagen degeneration. Histology confirmed fibrous proliferation and collagenization. Second, chronic mechanical stress: the bileaflet mechanical valve creates altered flow patterns and shear stresses, potentially accelerating fatigue of retained chordal tissue. Third, delayed chordal degeneration: the three-year latency is consistent with the slow, progressive nature of rheumatic structural deterioration, rather than an acute perioperative event. So the potential benefit of preserving the subvalvular apparatus warrants thoughtful deliberation.

Rafael et al. [6] reported that the technique of complete chordal preservation can provide patients with rheumatic mitral valve disease with superior ventricular function protection, higher long-term survival rates, and improved clinical outcomes.Coutinho et al. [7] regarded preservation of the subvalvular apparatus during rheumatic mitral valve replacement does not have a significant impact on patients’ long-term survival rates.

Whether to preserve the subvalvular apparatus in mitral valve replacement surgery should be determined by an individualized assessment of the valve’s anatomical and pathological characteristics. Considerations: (1) the degree of pre-existing chordal pathology (thickening, fusion, calcification); (2) the presence of chordal redundancy or elongation; (3) the surgeon’s experience with chordal management techniques; and (4) the patient’s overall risk profile for reoperation. In patients with severely thickened, fused, or calcified chordae, complete resection may be safer than preservation. Conversely, in patients with relatively normal chordal architecture, the benefits of preservation likely outweigh the low risk of late complications.

Echocardiography is crucial for diagnosis and differential diagnosis. However, it is not clear if chordal entrapment can be predicted by intraoperative transesophageal echocardiography. After weaning from cardiopulmonary bypass, careful interrogation of the prosthesis should be performed to exclude any residual or retained chordal tissue that could interfere with leaflet motion. While it is not always possible to predict late chordal rupture, the presence of redundant, elongated, or tenuous chordae should prompt consideration of more aggressive debridement. Patients who undergo subvalvular preservation should have regular echocardiographic follow-up even after years of normal prosthetic function.

In terms of treatment, surgeons employ two primary strategies: some opt solely for debridement of the residual tissue, while others proceed with valve replacement. The choice between these approaches warrants careful discussion.

Conclusion

When obstruction or regurgitation develops after valve replacement with subvalvular preservation, uncommon causes—such as residual subvalvular tissue or ruptured chordal entrapment—should be considered after excluding more common etiologies. As demonstrated in this case, chordal rupture can occur as late as three years postoperatively and may cause continuous severe regurgitation. Importantly, simple surgical excision of the offending tissue can restore normal valve function without prosthesis replacement when the prosthesis is intact, underscoring the reversible nature of this complication.

This case illustrates the critical role of transesophageal echocardiography in the diagnosis of chordal entrapment after mitral valve replacement. Intraoperative transesophageal echocardiography plays a crucial role potentially in preventing complications. Given the progressive nature of rheumatic heart disease, the potential benefit of preserving the subvalvular apparatus warrants thoughtful deliberation. Surgical removal of the offending tissue or valve replacement remains the definitive treatment.

Supplementary Information

Below is the link to the electronic supplementary material.

Author contributions

HXW and JBY collect medical data. HXW writes the manuscript . YM guidance of final revision. All authors approved the final manuscript.

Funding

None.

Data availability

Not applicable.

Declarations

Ethics approval and consent to participate

Written informed consent was obtained from the patient for the publication of the case report and accompanying images in this manuscript. Theconsent form is held by the authors and is available for review.

Consent for publication

Yes.

Competing interests

The authors declare no competing interests.