Acute posteromedial papillary muscle rupture secondary to aortic valve endocarditis: a case report.

Background: Acute papillary muscle (PM) rupture due to infective involvement has been recognized as a complication of infective endocarditis. However, there is very limited literature describing the rupture of the posteromedial PM in primary aortic valve endocarditis without aortic root abscess. This report highlights the aetiology of the PM rupture in the setting of primary aortic valve endocarditis and the importance of a multidisciplinary approach. Case summary: An 81-year-old man without any heart failure symptoms presented with fever and loss of vision in his left eye. Initial echocardiography revealed moderate aortic valve regurgitation due to a perforated right coronary cusp without aortic root abscess, and his blood cultures were positive for Group G Streptococci. During adequate antibiotic therapy, he developed acute severe mitral regurgitation secondary to posteromedial PM rupture. Following emergent aortic and mitral valve replacement using bioprosthetic valves, he made excellent progress on a 6-week course of intravenous antibiotics. Discussion: The echocardiography and the histological findings suggested that the main cause of PM rupture was most likely a metastatic focus of infection from the aortic valve via a regurgitant jet. Successful treatment of this fatal complication includes early diagnosis and prompt surgical intervention by a multidisciplinary approach.

Physicians should recognize the eccentric aortic regurgitant jets as a cause of the metastatic focus of infection on the left ventricular aspect in the aortic valve endocarditis.

We have demonstrated the key role of the ‘time-to-therapy’ concept using a multidisciplinary approach in the prompt management of infective endocarditis and related catastrophic complications.

Introduction

Medical management with antibiotics under strict clinical and echocardiographic observations is a good option for patients with infective endocarditis (IE) with well-tolerated severe valvular regurgitation. However, surgical treatment in the active phase despite adequate antibiotic treatment can strongly influence the outcome, if particularly when the infection spreads below the primary infected valve. Here, we report an unusual case of aortic valve endocarditis that developed acute posteromedial papillary muscle (PM) rupture during adequate antibiotic therapy.

Case presentation

An 81-year-old man with a history of hypertension was admitted to our hospital with a 4-day history of fever and rapid visual deterioration of the left eye. On presentation, his body temperature was 38.7°C and blood pressure was 132/49 mmHg, with a regular pulse rate of 60 beats/min, respiratory rate of 20 breaths/min, and oxygen saturation of 97% on room air. On physical examination, a grade 2 aortic diastolic murmur was noted. Funduscopic examination revealed a Roth spot in the left eye. His white blood cell count (normal range: 3800–8600 cells/mm3) and procalcitonin level (normal value: <0.5 ng/mL) were 17 720 cells/mm3 and 14.08 ng/mL, respectively. Transthoracic echocardiography (TTE) revealed mild mitral regurgitation (MR), moderate aortic regurgitation (AR) with a 347 ms of pressure half time, and no retrograde holodiastolic flow in the abdominal aorta (, Video 1, Supplementary material online, Video S1b–d). The left ventricular (LV) ejection fraction (LVEF) was 53% with diffuse global hypokinesis of the LV wall and mild LV dilation (LV diastolic dimension: 55 mm; LV systolic dimension: 38 mm). Transoesophageal echocardiography revealed 8 mm thickening and a perforation on the right coronary cusp (RCC) that caused moderate AR (, Video 2a, Supplementary material online, ). There was no evidence of an aortic root abscess, septal wall abscess that may cause a decreased heart rate regardless of the actual sepsis, or abnormal mitral apparatus. His vitreous and blood cultures were positive for Group G Streptococci that were sensitive to penicillin G. Aortic valve endocarditis complicated with endogenous endophthalmitis was diagnosed on the basis of the modified Duke criteria. Both the 2015 European Society of Cardiology (ESC) and 2015 American Heart Association/American College of Cardiology (AHA/ACC) guidelines recommend early surgery for patients with IE who present with symptoms or signs of heart failure (HF), persistent infection, and recurrent emboli. Early surgery, which is a class I level B recommendation according to both the guidelines, is recommended for patients with persistent bacteraemia or fever lasting for >7 days after the initiation of appropriate antimicrobial therapy., The management plan was discussed with a multidisciplinary care team, and the decision to perform surgery was made after the initiation of antibiotic therapy and relevant observations. Intravenous penicillin G was started based on the susceptibility study findings after empirical therapy. On Day 5, the blood cultures were negative for Streptococci, and the white blood cell count and procalcitonin level were decreased to 10 100 cells/mm3 and 1.80 ng/mL, respectively. No symptoms of HF were observed, and the vital signs other than low-grade fever were stable. Follow-up TTE demonstrated no remarkable changes from the initial findings. However, on Day 7, his condition suddenly deteriorated and he developed HF symptoms consistent with those of New York Heart Association functional class III. Follow-up TTE demonstrated a newly diagnosed severe MR with normal LV wall motion and 69% LVEF (, Video 3a, Supplementary material online, ), and electrocardiography revealed sinus tachycardia without ischaemic changes. The differential diagnosis for acute MR in patients with IE included destructive endocarditis extending to the mitral valve and coronary emboli.

Figure 1

Initial transthoracic echocardiography images. (A) The parasternal long-axis view of the diastole shows eccentric aortic regurgitation. The parasternal long-axis view of the systole shows mild mitral regurgitation. (B) The parasternal short-axis view of the diastole shows that the aortic regurgitation jets (red arrow) swirling along the basal posterior wall and reaching the P3 with normal mitral morphology. (C) Apical three-chamber view shows that aortic regurgitation jets impinge against the posteromedial papillary muscle.

Figure 2

Transoesophageal echocardiography images. Short-axis (A) and long-axis views (B) show moderate aortic regurgitation and a perforation on the right coronary cusp (yellow arrow). The eccentric aortic regurgitation jets reach the P2 (red arrow) (C). Mid-oesophageal four-chamber view (D) shows the intact A1 and P1 of the mitral leaflets. Mid-oesophageal commissural view (E) shows the intact posterior mitral leaflet and aortic regurgitation jets impinging on the P3 (red arrow).

Figure 3

Follow-up transthoracic echocardiography images just before surgery. Parasternal long-axis view (A) shows newly developed severe mitral regurgitation. Parasternal short-axis view (B) shows P3 prolapse (yellow arrow). Apical four-chamber view (C) shows a prolapsed leaflet with a mobile mass (red arrow).

The patient was immediately transferred to the operating room. Intraoperatively, vegetations were observed on the perforated RCC () without any evidence of aortic annulus infection. Close inspection of the mitral apparatus revealed complete rupture of the posteromedial PM head with presence of vegetations. No gross evidence of infection was found in the mitral leaflets (). After resecting the aortic valve leaflets, the anterior mitral leaflet and a part of the P2 and P3 scallops, debridement of all infected tissues were performed. Mitral valve replacement was completed with a 27-mm Epic bioprosthesis (St. Jude Medical Inc., St. Paul, MN, USA) followed by aortic valve replacement using a 23-mm Crown RPT bioprosthesis (Sorin Group, Burnaby, Canada). Although the postoperative course was complicated by persistent fever due to panophthalmitis requiring left ophthalmectomy on postoperative Day 17, the patient was discharged in a stable condition after completing antibiotic therapy. The culture of the resected PM was positive for Group G Streptococci. The histopathological examination of the PM indicated numerous neutrophilic leucocytes suggesting myocardial infection (). A postoperative follow-up after 3 years did not reveal any sign of a recurrent infection.

Figure 4

Macroscopic images of the specimens. (A) Fresh aortic valve specimen, (B) right coronary cusp in the aorta side view, and (C) formalin-fixed aortic valve specimen showing a perforation (arrow) and vegetation on the right coronary cusp. (D) Fresh specimen of the anterior mitral leaflet, (E) fresh specimens of the ruptured posteromedial papillary muscle (red arrow) and partial P2 (white arrow) and P3 (yellow arrow), and (F) formalin-fixed specimen demonstrating infective papillary muscle destruction and no evidence of infectious change on the mitral leaflets.

Figure 5

Histological images of the posteromedial papillary muscle. (A) Haematoxylin and eosin staining (original magnification ×40) and (B) haematoxylin and eosin staining (original magnification ×100) reveal the neutrophil infiltration in the papillary muscle, suggesting suppurative myocarditis.

Discussion

PM rupture is an unusual life-threatening complication in patients with IE, and only few reports have described this complication in aortic valve endocarditis settings. The clinical course of our patient was similar to those of three other cases occurring during adequate antibiotic management. However, the main difference was that our case involved endophthalmitis and that PM rupture occurred without the presence of aortic root abscesses. To the best of our knowledge, this is the only case of acute posteromedial PM rupture in the setting of primary aortic valve endocarditis without the presence of aortic root abscesses. The causes of PM rupture in aortic valve endocarditis may be caused by the direct invasion of the endocarditis into the aortic-mitral fibrous continuity, leading to a distraction of the mitral apparatus, coronary emboli, or metastatic foci of infection from the aortic valve via regurgitant jets. Initial echocardiography revealed a unique presentation of an eccentric AR jet via an RCC perforation impinged on the posteromedial PM that swirled in the LV impinging against P3 with a competent mitral valve with normal morphology. These characteristics and the discontinuous infected areas of the RCC and posteromedial PM strongly suggest that the possible pathogenic mechanisms underlying PM rupture are the translocation of infective organisms to the PM and mechanical damage by the AR jet via the RCC perforation.

Persistent fever during antibiotic therapy may be a critical sign of PM infection; however, early diagnosis is difficult via follow-up TTE. Multislice computed tomography scan is possibly superior to TTE in providing information regarding the extent of any perivalvular extension, and positron emission tomography/computed tomography may serve as an alternative diagnostic method for the detection of secondary infection sites. Taken together, identifying an optimal time for elective surgery in patients with IE requires new alternative diagnostic data and multidisciplinary approaches. This report highlighted the importance of these aspects in the management of IE to avoid any potential complications and improve the patient’s prognosis.

In conclusion, the rupture of the PM via AR jets due to the translocation of vegetations to the PM in an isolated aortic valve endocarditis is a potential complication. The adverse effects of AR jets with respect to LV aspects must be carefully considered, and the assessment of AR jets by initial echocardiography and strict follow-up examination for early diagnosis and prompt surgery with a multidisciplinary approach are imperative for the treatment of this rare complication.

Lead author biography

Akira Marumoto is a Physician-in-Chief of the Department of Cardiovascular Surgery, Japan Community Healthcare Organization Osaka Hospital, Osaka, Japan. He graduated from Tottori University School of Medicine, Tottori, Japan in 1997 and completed PhD programme of Tottori University School of Medicine in 2003. He completed the surgical training programme at the Department of Thoracic Surgery, Asan Medical Center, Seoul in 2007. He is a Board Surgeon of Japanese Association of Cardiovascular Surgery. He has a special interest in valvular heart disease and valve surgery.

Supplementary material

Supplementary material is available at European Heart Journal - Case Reports online.

Click here for additional data file.

Time	Events
Two days before admission	The patient began to experience left eye pain and worsening eyesight, and fever and general fatigue developed. Patient was taken to another hospital and was diagnosed as endogenous endophthalmitis and blood sample was sent for culture.
Day 0	The patient was admitted to our hospital without any signs or symptoms of heart failure. A funduscopic examination of the left eye revealed a Roth spot. Transthoracic echocardiography (TTE) revealed a perforation on the right coronary cusp of the aortic valve with moderate aortic regurgitation. A diagnosis of aortic valve endocarditis was made on the basis of the modified Duke criteria. Daptomycin was started as an empirical therapy.
Day 1	The blood cultures turned positive for streptococcus Group G that was sensitive for penicillin G. Antibiotic treatment was switched to penicillin G and gentamicin.
Day 4	No evidence of aortic root abscess was found, and the mitral leaflets were intact with mild mitral regurgitation (MR) in the transoesophageal echocardiography.
Day 5	Blood cultures returned negative.
Day 7	Patient’s condition suddenly deteriorated with symptoms of dyspnoea. Follow-up TTE demonstrated a newly severe MR with normal left ventricular wall motion. Emergent aortic and mitral valve replacement was completed successfully.
Day 34	Left ophthalmectomy was required because of left panophthalmitis.
Day 50	The patient completed 6 weeks of postoperative penicillin G.
Day 65	The patient made a full recovery from surgeries and was discharged home in a stable afebrile state.
3 years after discharge	The patient was regularly checked every year. There was no recurrence of infection.