Intermittent mitral prosthetic dysfunction. what interferes the valve closure?

Abstract

Background

Prosthetic valve dysfunction due to entrapment of the subvalvular apparatus is a rare condition, particularly when occurring as a delayed postoperative complication. Spontaneous papillary muscle rupture in the absence of an ischemic event is also uncommon. The simultaneous presence of both conditions renders this case of intermittent symptomatic mitral regurgitation exceptional.

Case presentation

We present the case of a 72-year-old woman with a history of rheumatic heart disease and a mechanical mitral valve prosthesis. Although the initial postoperative course was uneventful, she developed rapidly progressive heart failure symptoms two years after surgery, secondary to newly onset severe mitral regurgitation. Transesophageal echocardiography was crucial in elucidating the underlying mechanism, revealing a ventricular mass intermittently interfering with the proper closure of the mechanical prosthesis. The main differential diagnoses regarding the origin of the mass included: remnants of the subvalvular apparatus, vegetation, thrombotic material and pannus formation. Given the clinical deterioration, surgical intervention was considered necessary despite the lack of precise knowledge regarding the nature of mass. Surgical exploration confirmed the rupture of the subvalvular apparatus involving the anterolateral papillary muscle as the underlying cause of the prosthetic dysfunction. Excision of the ruptured chordae tendineae and residual papillary muscle was performed with a favorable outcome and no complications.

Conclusions

This case illustrates a rare cause of late prosthetic mitral valve dysfunction: the entrapment of the subvalvular apparatus due to spontaneous rupture of the papillary muscle. Transesophageal echocardiography proved highly valuable in understanding the mechanism of dysfunction; however, surgical exploration ultimately established the definitive diagnosis and facilitated the correction of the issue.

Supplementary Information

The online version contains supplementary material available at 10.1186/s13019-025-03521-8.

Background

Mitral valve repair is the preferred surgical technique for treating mitral valve disease and is the most employed approach in clinical practice. However, in some cases, achieving an adequate repair is not feasible, requiring prosthetic valve replacement. In these cases, surgical techniques involving the preservation of the subvalvular apparatus are preferred to maintain the original architecture of the mitral complex, promote early recovery of ventricular function, prevent left ventricular remodeling, and enhance long-term survival [1].

Although the excellent durability of mechanical prostheses has been well-documented, these devices may be associated with certain complications. Known adverse events include thromboembolic events, anticoagulant-related bleeding, prosthetic endocarditis, paravalvular leaks, hemolytic phenomena and valve dysfunction due to extrinsic factors such as pannus formation [2, 3], thrombosis [4] or interference from remnants of the subvalvular apparatus. This last condition is more commonly observed intraoperatively during the disconnection from extracorporeal circulation and may lead to intermittent prosthetic dysfunction [5–7].

This article presents an unusual case of delayed intermittent dysfunction of a mitral prosthesis due to entrapment of the subvalvular apparatus, secondary to spontaneous rupture of the papillary muscle.

Case presentation

We present the case of a 72-year-old woman with dyslipidemia as her only cardiovascular risk factor. She was diagnosed with rheumatic mitral valve disease at the age of 61. The patient remained asymptomatic for 9 years; however, she was admitted for decompensated heart failure and atrial fibrillation, which were preceded by a progressive deterioration in her functional status over the preceding months. Transthoracic echocardiography showed preserved global systolic function and a double mitral lesion with severe stenosis and moderate regurgitation. Given the advanced state of the valve disease, surgical treatment was planned. Preoperative coronary angiography demonstrated no significant coronary lesions. Following clinical stabilization, the patient underwent mitral valve replacement using a 27 mm St. Jude mechanical prosthesis, preserving the posterior leaflet and subvalvular apparatus. The patient had a satisfactory postoperative course and continued follow-ups in cardiology outpatient clinics.

Two years later, the patient presented with worsening dyspnea on mild to moderate exertion, accompanied by lower limb edema. She did not report any chest pain, and no changes were observed on the EKG. High-sensitivity troponin I levels were normal. Transthoracic echocardiography revealed preserved ventricular systolic function but severe intermittent intraprosthetic mitral regurgitation. A three-dimensional transesophageal echocardiogram was performed, revealing a bileaflet prosthesis with incomplete closure of the anterior disc. This finding was attributed to the presence of a mobile mass located on the ventricular side, measuring 10 × 7 mm, exhibiting echogenicity comparable to that of myocardium. The mass intermittently interfered with the closure of the lateral portion of the mitral annulus (Figs. 1 and 2, Video 1). This resulted in intermittent severe intraprosthetic mitral regurgitation. The principal hypotheses regarding the origin of the mass included remnants of the subvalvular apparatus, vegetation, thrombotic material, and pannus formation. However, the patient did not exhibit any infectious symptoms or thromboembolic events and anticoagulation levels had been within the therapeutic range in the preceding months. Due to the symptoms and severity of the prosthetic dysfunction, surgical intervention was considered necessary, even in the absence of precise knowledge regarding the nature of the mass. Preoperative catheterization revealed no significant coronary lesions. Surgical exploration identified a rupture of the subvalvular apparatus at the anterolateral papillary muscle as the cause of the prosthetic dysfunction. Excision of the ruptured chordae tendineae and residual papillary muscle was performed through the aortic valve (transaortic procedure) to simplify access and reduce procedural time, thereby avoiding a repeat left atriotomy. This approach also allows for improved visualization of the ruptured chordae, enabling complete excision. Intraoperative transesophageal echocardiography confirmed normal prosthetic function. The patient experienced a satisfactory postoperative recovery without complications, along with a notable improvement in her functional class.

Fig. 1.

Three-dimensional transesophageal echocardiography from the Surgeon’s View (images at the top)

A: Prosthetic disc with incomplete closure due to interference of subvalvular tissue (arrow). B: Valve in the open position, with the mass visible in the background on the ventricular side of the prosthesis (arrow). C: Disc closed with no presence of mass. D: Continuous Doppler assessment of the mitral prosthesis showing intermittent mitral regurgitation flow

Fig. 2.

A: Severe prosthetic regurgitation due to incomplete disc closure. B: On the next beat, color Doppler demonstrates no regurgitation, only a jet from the prosthetic closure. C: Multi-Plane Imaging of the mitral valve showing rupture of the subvalvular apparatus (arrows)

Discussion and conclusions

Mitral prosthetic dysfunction due to entrapment of subvalvular tissue is a rare and poorly documented complication [5–7]. It most often occurs as an intraoperative complication during disconnection from extracorporeal circulation, typically resulting from a redundant subvalvular apparatus. This condition can be detected with intraoperative transesophageal echocardiography and corrected during the same surgical procedure. Less frequently, it is observed in the early postoperative period due to a residual subvalvular apparatus [8] or interference from surgical material, while its late presentation [5, 6], as seen in our case, is exceptional.

Additionally, spontaneous rupture of the papillary muscle outside the context of acute myocardial infarction, infective endocarditis, or thoracic trauma is very rare [9, 10]. In the present case, no definitive cause for the rupture could be identified. This condition is often fatal and refractory to medical therapy, necessitating urgent surgical intervention to restore hemodynamic stability and prevent further deterioration of the patient’s condition. In our case, the presence of a mechanical mitral prosthesis contributed to a more insidious clinical presentation with better hemodynamic tolerance, manifesting as progressive symptoms of heart failure consequent of intermittent severe mitral regurgitation. The three-dimensional transesophageal echocardiogram provided high-quality, detailed images, which were crucial in diagnosing the mechanism of the prosthetic dysfunction; however, surgical re-intervention was necessary to clarify its etiology and facilitated the correction of the issue.

Electronic supplementary material

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Author contributions

PP: writing of the original draft and preparation of the figures; RMM: writing of the original draft and preparation of the figures; MNM: writing-review & editing; FGC: writing-review & editing; JISI: writing-review & editing; VPD: writing-review & editing. All authors read and approved the final manuscript.

Funding

Not applicable.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent for publication has been obtained from the patient described in the case report, including accompanying images.

Competing interests

The authors declare no competing interests.