Left Atrial Plication for Left Ventricular Posterior Wall Bending With Atrial Functional Mitral Regurgitation

Abstract

Left ventricular basal posterior wall (LVbp) inward bending in patients with rheumatic mitral regurgitation and giant left atrium (LA) is a risk for low cardiac output after mitral valve (MV) surgery, which is dramatically improved by aggressive LA plication. However, the effects of LA plication on LVbp bending in patients with atrial functional mitral regurgitation (aFMR) and giant LA have not yet been reported. In 2 patients with LVbp bending, aFMR, and giant LA, MV replacement/repair with aggressive LA plication improved LVbp bending. However, compared to patient 1, in which MV replacement with posterior MV chordal preservation was followed by LA plication, improvements in LVbp bending was greater in patient 2, in which LA plication was followed by MV repair. These findings suggest that aggressive LA plication followed by MV repair has greater benefits (vs MV replacement with posterior MV chordal preservation before LA plication) on LVbp bending in patients with aFMR and giant LA.

Visual Summary

Visual Summary.

Different Consequences of LVbp Bending Between 2 Patients With aFMR and Giant LA After Aggressive Surgical LA Plication and MV Procedure

In patient 1, with aFMR, giant LA, and severe LVbp bending, only modest improvement in LVbp bending was seen after MV replacement with posterior MV chordal preservation followed by aggressive LA plication, despite a comparable degree of LA plication to patient 2. In contrast, patient 2, with aFMR, giant LA, and moderate LVbp bending, had a marked improvement in LVbp bending after aggressive LA plication followed by MV repair. aFMR = atrial functional mitral regurgitation; BSA = body surface area; LA = left atrium; LVbp = left ventricular basal posterior wall; MV = mitral valve.

There are 2 different phenotypes of atrial functional mitral regurgitation (aFMR). Type 1 aFMR has: 1) normal left ventricular (LV) morphology; 2) mitral valve (MV) annular dilatation due to mild to severe left atrial (LA) enlargement; 3) no MV organic lesion, tethering, or prolapse (type 1 mitral regurgitation [MR]); and 4) a central MR jet. Type 2 aFMR has: 1) LV basal posterior wall (LVbp) inward bending; 2) giant LA; 3) predominant posterior MV leaflet tethering (hamstring) with relative anterior MV prolapse; and 4) a posteriorly directed MR jet (Figures 1A and 1B).^1,2

Take-Home Messages

• •In 2 patients with LV basal posterior wall inward bending, atrial functional mitral regurgitation, and giant LA, MV replacement/repair with aggressive LA plication improved the LV basal posterior wall bending.
• •Performing LA plication before MV repair may promote greater beneficial influences on LV basal posterior wall bending.

Figure 1.

Preoperative and Postoperative Images of Patient 1

(A) Apical long-axis (LAX) view shows the LVbp inward bending (pink and black arrows) with giant LA, posterior MV leaflet tethering (hamstring) with relative anterior MV prolapse. (B) Posteriorly directed MR jet. (C1) Preoperative apical LAX view: The LV LAX diameter from the apex to the center of the MV annulus at end-diastole was 64 mm. The length from the LV wall outermost line, paralleling the LV LAX line, to the posterior MV annulus was measured as the LVbp bending length (B length); this was 36 mm preoperatively. (C2) Postoperatively, the LV LAX diameter elongated to 72 mm and the B length shortened to 28 mm, but considerable LVbp bending remained. (D1) Preoperative anatomical M-mode image: Setting a perpendicular line to the deformed LVbp (pink line) showed early systolic paradoxical motion of the LVbp (yellow arrow). (D2) Disappearance of LVbp paradoxical motion postoperatively. Ao = aorta; LA = left atrium; LV = left ventricle; LVbp = left ventricular basal posterior wall; MR = mitral regurgitation; MV = mitral valve.

Giant LA is considered to cause the characteristics of type 2 aFMR.² In patients with rheumatic MR, LVbp bending with giant LA could exaggerate LV dysfunction and heart failure (HF) after MV surgery, with low cardiac output syndrome and frequent in-hospital death.^3,4 Aggressive LA plication, reducing massive LA dilatation, is effective to attenuate or eliminate LVbp bending in these rheumatic patients, contributing to dramatically improved postoperative outcome with highly reduced incidences of low cardiac output, respiratory failure, and in-hospital death.⁴ However, the effect of LA plication on LVbp bending in patients with aFMR and giant LA has not been fully evaluated.

We have observed the beneficial effects of LA plication on LVbp bending in 2 patients with aFMR and giant LA, but with considerably different degrees of improvement, potentially related to procedural differences.

Patient 1

History of presentation

A 78-year-old woman with a 7-year history of chronic atrial fibrillation and HF recently developed worsening HF (NYHA functional class III) and was admitted to our hospital. She had grade 4/6 holosystolic murmur in the apex. Her blood pressure was 102/58 mm Hg, and her heart rate was 72 beats/min.

Investigations

Transthoracic echocardiography (TTE) showed increases in LV end-diastolic and end-systolic volumes of 112 and 56 mL/m², respectively, an ejection fraction of 50%, giant LA (LA volume: 357 mL/m²), LVbp bending, predominant posterior MV tethering, relative anterior MV prolapse, and severe posteriorly directed MR jet, expressing all features of type 2 aFMR (Figures 1A, 1B, and 1C1). The portion of LVbp bending showed paradoxical motion during early systole (Figures 1D1), suggesting ineffective contraction of the portion.³ She also had moderate to severe tricuspid valve regurgitation and enlarged right atrium.

Management (surgery)

Cardiac surgery was performed through median sternotomy; the right atrium was incised and MV surgery was performed via the transinteratrial septal approach. The anterior MV was mildly tethered, the posterior MV showed predominantly severe tethering, and both leaflets had thickening but without typical rheumatic or degenerative changes. The anterior MV with chordae were resected, the posterior MV with chordae were preserved, and MV replacement with a 31-mm Epic MV bioprosthetic valve (St Jude Medical) was performed. Then, the LA appendage was closed, and the LA wall between the level of the LA appendage and posterior MV annulus was sutured with the double-stitch technique. The LA was further plicated by suturing of the LA roof, and the incised interatrial septum was also sutured with enough margin, consistent with aggressive LA plication for giant LA. Tricuspid valve annuloplasty with a 36-mm Physio Tricuspid ring (Edwards Lifesciences) was performed, and the incised right atrial wall was sutured with enough margin as right atrial plication.

Outcome and follow-up

The postoperative clinical course was good except for the surgical need of removing pericardial hematoma 6 days postoperatively. The patient's HF improved to NYHA functional class II status. TTE 20 days after the surgery confirmed no MR, normal prosthetic valve function, reduced LV end-diastolic and end-systolic volumes of 105 and 65 mL/m², respectively, an ejection fraction of 38%, markedly reduced LA dilatation (LA volume: 107 mL/m²), and elimination of the paradoxical motion of LVbp, suggesting restored effective contraction (Figures 1C2 and 1D2). Although abnormal LVbp bending configuration improved, considerable bending remained (Figures 1C2).

We quantified the degree of LVbp bending as follows: 1) LV long-axis diameter, measured from the apex to the center of the MV annulus in the end-diastolic apical long-axis plane; and 2) LVbp bending length, measured as the distance from the LV wall outermost line, paralleling the LV long-axis line, to the posterior MV annulus (Figures 1C1 and 1C2). In this patient, the LV long-axis diameter was lengthened from 64 to 72 mm, and the LVbp bending length was shortened and improved from 36 to 28 mm (Figures 1C1 and 1C2).

Patient 2

History of presentation

A 70-year-old man had a history of chronic atrial fibrillation and hypertension for 16 years. He developed shortness of breath (NYHA functional class III) and cardiomegaly on chest x-ray performed 6 months prior to admission. He was referred to our hospital. He had grade 4/6 holosystolic murmur in the apex. His blood pressure was 128/67 mm Hg, and his heart rate was 67 beats/min.

Investigations

TTE showed increase in LV end-diastolic and end-systolic volumes of 87 and 38 mL/m², respectively, an ejection fraction of 55%, giant LA (LA volume: 257 mL/m²), predominant posterior MV tethering, relative anterior MV prolapse, moderate to severe posteriorly directed aFMR, and LVbp bending with paradoxical motion (Figures 2A, 2B, 2C1, and 2D1). He also had moderate tricuspid valve regurgitation.

Figure 2.

Preoperative and Postoperative Images of Patient 2

(A) The apical long-axis (LAX) view shows LVbp inward bending (pink, black, and white arrows) with giant LA and posterior MV leaflet tethering (hamstring) with relative anterior MV prolapse. (B) Posteriorly directed MR jet. (C1) Preoperative apical LAX view: The LV LAX diameter was 75 mm, and the LVbp bending length (B length) was 25 mm. (C2) Postoperatively, the LV LAX diameter elongated to 83 mm, and the B length shortened to 14 mm. (D1) Preoperative anatomical M-mode image (pink line) showing early systolic paradoxical motion of the LVbp (yellow arrow). (D2) Disappearance of LVbp paradoxical motion postoperatively. Abbreviations as in Figure 1.

Management (surgery)

Cardiac surgery was performed through median sternotomy; the right atrium was incised and MV surgery was performed via the transinteratrial septal approach. The posterior MV was short and tethered. The anterior MV was thickened and prolapsed, being consistent with relative anterior MV prolapse in aFMR with posterior MV hamstring but without typical rheumatic or degenerative changes. LA plication was performed initially, before MV surgery, using procedures similar to patient 1 with LA appendage closure and suturing of the LA wall between the level of the LA appendage and the posterior MV annulus. MV repair was then performed. Artificial chordae were implanted between the anterior papillary muscle and the prolapsed anterior MV with the anchor technique. MV annuloplasty with a 34-mm Physio Flex ring (Edwards Lifesciences) followed. After confirming absence of MR by water test, the LA was further plicated by suturing of the LA roof and incised interatrial septum. Tricuspid annuloplasty was performed with a 34-mm Physio Tricuspid ring (Edwards Lifesciences). The incised right atrial wall was also sutured with an intention to perform right atrial plication.

Outcome and follow-up

The patient's postoperative clinical course was good without any complications, and his HF improved to NYHA functional class II. TTE 7 days after surgery confirmed only trivial MR, reduced LV end-diastolic and end-systolic volumes of 69 and 40 mL/m², respectively, an ejection fraction of 43%, considerably reduced LA dilatation (LA volume: 121 mL/m²), lengthened LV long-axis diameter from 75 to 83 mm, and markedly improved LVbp bending, with bending length shortened from 25 to 14 mm. The paradoxical motion of the LVbp also disappeared after the surgery (Figure 2C1, 2C2, and 2D2).

Discussion

In both of our patients, LVbp bending improved after surgery with MV replacement/repair and aggressive LA plication. The preoperative configurations of the LVbp bending suggested that associated giant LA compresses the LVbp and posterior MV annulus inferiorly and anteriorly.² Kawazoe et al⁴ showed that in patients with rheumatic MV disease and giant LA, MV replacement with aggressive LA plication eliminated the LVbp bending, while isolated MV replacement had no influences on the bending. Therefore, it is reasonable to consider that LA plication in our 2 patients with aFMR and giant LA also attenuated the abnormal compression down on the LVbp, and the bending improved.

What was the reason for the lesser improvement in LVbp bending in patient 1 compared with patient 2? It is not easy to establish this reason, but we consider the following points. Patient 2, with greater improvements in LVbp bending, was male, and had less severe LV remodeling, less severe preoperative LVbp bending and LA remodeling, and underwent LA plication followed by MV repair. In contrast, patient 1 was female, and had more severe LV remodeling, more severe preoperative LVbp bending and LA remodeling, and underwent MV replacement with posterior MV chordal preservation followed by LA plication. The degree of LA plication was not less in patient 1 (patient 2 vs patient 1: reduction in LA volume, −136 vs −250 mL/m²; postoperative LA volume, 121 vs 107 mL/m²). All of these differences could have contributed to the variance in LVbp improvement between our 2 patients; in addition, we consider the following explanations.

The abnormal LVbp bending configurations before the surgery strongly suggested a deformed MV complex structure with an inferiorly and anteriorly shifted position of the posterior MV annulus due to compression from the giant LA. Patient 1 underwent initial MV replacement with posterior MV chordal preservation. This would freeze the deformed geometry of the posterior part of the MV complex, which may have been resistant to subsequent structural changes by the attenuated compression force derived from LA plication. In contrast, LA plication followed by MV repair in patient 2 would allow greater reverse remodeling of the deformed MV complex owing to the chance of LA plication to promote the reverse remodeling before the MV complex was influenced by MV procedures, and the inherent difference between a ring and a prosthesis.

The reason for the successful MV repair in patient 2 is also important. In both patients, MR appears related to MV malcoaptation with predominant posterior MV tethering and relative anterior MV prolapse, leading to an eccentric, posteriorly directed MR jet. Malcoaptation relates to MV complex deformity, including those of the MV annulus and papillary muscles, caused by LVbp inward bending owing to advanced LA remodeling. Aggressive LA plication seems to attenuate the MV complex deformity and realigns the leaflets for a better chance of successful MV repair. This would be consistent with the concept of the MV being like a marionette controlled by its tethering masters.⁶ Matsumori et al⁵ reported that performing LA plication before MV repair in patients with aFMR and giant LA resulted in a larger implanted MV ring size and more frequent disappearance of MR by water test before the MV procedure compared with isolated MV repair. These findings suggest that aggressive LA plication may attenuate the deformity of the MV complex structure and lengthen anteroposterior MV annulus diameter before the MV procedure. Their report is consistent with our insight, however further studies are needed to confirm these observations. Nevertheless, the current report is to our knowledge the first to demonstrate the beneficial effects of aggressive LA plication on preoperative LVbp inward bending in patients with aFMR and giant LA.

Kawazoe et al⁴ further reported highly favorable hemodynamic effects of concomitant aggressive LA plication, with dramatically reduced incidences of postoperative low cardiac output syndrome and in-hospital death in patients with rheumatic MR and giant LA. It is difficult to evaluate whether concomitant LA plication promoted beneficial influences on HF hemodynamics in our patients, given the lack of control patients with isolated MV surgery without LA plication. However, both of our patients had a good postoperative clinical course, with no low cardiac output syndrome, improved postoperative stroke volume (from 29 to 38 mL/m² in patient 1 and from 34 to 40 mL/m² in patient 2), disappearance of the preoperative paradoxical motion of the LVbp, suggesting restored effective contraction, and lengthened LV long-axis diameter. These results suggest that aggressive LA plication, reducing its compression down on the LVbp, may promote beneficial influences on LV pump function and HF hemodynamics beyond the observed elimination of MR and structural improvements. More studies are needed to confirm these findings.

Conclusions

Aggressive surgical LA plication in 2 patients with aFMR and giant LA resulted in improved LV basal posterior wall inward bending, but with considerably different degrees of improvement. The differences suggest that LA plication followed by MV repair has greater beneficial influences on LVbp bending, while MV replacement with posterior MV chordal preservation may freeze the abnormal geometry of the posterior part of the MV annulus and LV wall, attenuating the influence of subsequent LA plication on LVbp bending.

Funding Support and Author Disclosures

Dr Iwataki has received funding from the Japan Society of the Promotion of Science KAKENHI, Tokyo, Japan (grant number 25K15972), and Dr Levine is supported in part by the National Institutes of Health (R01HL173930), the American Heart Association (22TPA963793 and 24CSA1255237), and the Leducq Foundation (grant 22ARF02) for the Preventing Rheumatic Injury bioMarker Alliance. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.