Complete Atrioventricular Block Complicating Mitral Infective Endocarditis Caused by Streptococcus Agalactiae

Abstract

Patient: Male, 74

Final Diagnosis: Infective endocarditis

Symptoms: Apetite loss • fever

Medication: —

Clinical Procedure: Transesophageal echocardiography

Specialty: Cardiology

Objective:

Rare co-existance of disease or pathology

Background:

Infective endocarditis (IE) involving the mitral valve can but rarely lead to complete atrioventricular block (CAVB).

Case Report:

A 74-year-old man with a history of infective endocarditis caused by Streptococcus gordonii (S. gordonii) presented to our emergency room with fever and loss of appetite, which had lasted for 5 days. On admission, results of serologic tests pointed to severe infection. Electrocardiography showed normal sinus rhythm with first-degree atrioventricular block and incomplete right bundle branch block, and transthoracic echocardiography and transesophageal echocardiography revealed severe mitral regurgitation caused by posterior leaflet perforation and 2 vegetations (5 mm and 6 mm) on the tricuspid valve. The patient was initially treated with ceftriaxone and gentamycin because blood and cutaneous ulcer cultures yielded S. agalactiae. On hospital day 2, however, sudden CAVB requiring transvenous pacing occurred, and the patient’s heart failure and infection worsened. Although an emergent surgery is strongly recommended, even in patients with uncontrolled heart failure or infection, surgery was not performed because of the Child-Pugh class B liver cirrhosis. Despite intensive therapy, the patient’s condition further deteriorated, and he died on hospital day 16. On postmortem examination, a 2×1-cm vegetation was seen on the perforated posterior mitral leaflet, and the infection had extended to the interventricular septum. Histologic examination revealed extensive necrosis of the AV node.

Conclusions:

This rare case of CAVB resulting from S. agalactiae IE points to the fact that in monitoring patients with IE involving the mitral valve, clinicians should be aware of the potential for perivalvular extension of the infection, which can lead to fatal heart block.

Background

Infective endocarditis (IE) involving the mitral valve often leads to supraventricular arrhythmia [1]; rarely a life-threatening conduction abnormality such as atrioventricular block (AVB) arises [2,3]. Here, we describe a case of Streptococcus agalactiae (S. agalactiae) IE involving the mitral valve and resulting in complete AVB (CAVB).

Case Report

A 74-year-old man presented to our emergency room with fever and loss of appetite, both of which had lasted for 5 days. His medical history included coronary artery bypass grafting, alcoholic liver cirrhosis, hypertension, and chronic diabetic kidney disease. He also had a prior (1 year) episode of IE due to S. gordonii detected by MALDI-TOF. Vegetation (7 mm) on the posterior mitral leaflet without mitral regurgitation or perforation was observed by transthoracic echocardiography and abolished eventually with penicillin and gentamycin. On presentation, he appeared pale and unwell. His body temperature was 38.8°C, blood pressure was 118/70 mmHg, heart rate was 65 beats/min, respiratory rate was 22 breaths/min, and oxygen saturation (obtained by pulse oximetry) was 96% on room air. On cardiopulmonary auscultation, there was no gallop, but a grade II/VI pansystolic murmur at the apex and minimal bibasilar crackles were heard. A lower limb diabetic cutaneous ulcer and edema were noted.

The electrocardiogram showed no specific changes compared with that during prior hospitalization; normal sinus rhythm, first-degree AVB, incomplete right bundle branch block, and high voltage with ST-T abnormalities in the precordial leads, suggestive of left ventricular hypertrophy (Figure 1). Chest X-ray showed mild cardiomegaly with mild pulmonary edema. Laboratory tests revealed a leukocyte count of 10,300/mm³ (normal range, 4000–8000/mm³) a markedly elevated C-reactive protein level of 25.5 mg/dL (normal range, <0.2 mg/dL), and an elevated N-terminal pro-brain natriuretic peptide (NT-pro-BNP) concentration of 27,498 pg/mL (normal range, <125 pg/mL). Transthoracic echocardiography and transesophageal echocardiography revealed a perimitral abscess, severe mitral regurgitation caused by posterior mitral leaflet perforation, and 2 vegetations (5 mm and 6 mm) on the tricuspid valve (Figure 2A–2C). The patient was initially treated with ceftriaxone and gentamycin. Cultures of the blood and the cutaneous ulcer yielded S. agalactiae.

Figure 1.

Twelve-lead electrocardiogram obtained on admission.

Figure 2.

Transthoracic echocardiographic image (A) and transesophageal echocardiographic images (B, C) obtained on the day of admission (apical 4-chamber view). (A) and (B) A perimitral abscess and severe mitral regurgitation caused by posterior mitral leaflet perforation are apparent (arrows). (C) Two vegetations, one measuring 5 mm and the other measuring 6 mm, are evident on the tricuspid valve on the tricuspid valve.

On hospital day 2, however, sudden CAVB requiring transvenous pacing occurred (Figure 3), and the heart failure and infection worsened. Although emergency surgery was considered to control the infection and heart failure and to prevent thromboembolic events, surgery was not performed because of the Child-Pugh class B liver cirrhosis. Despite intensive therapy, the patient’s condition continued to deteriorate, and he died on hospital day 16.

Figure 3.

Electrocardiogram showing complete atrioventricular block obtained on hospital day 2.

On postmortem examination, a 2×1-cm vegetation was found on the perforated posterior mitral leaflet (Figure 4A) and 2 vegetations of 8 mm on the septal leaflet of the tricuspid valve (Figure 4B). Histologic examination of the AV node and His bundle revealed extensive necrosis with fibrosis and calcification (Figure 4C–4E).

Figure 4.

Macroscopic appearance of the left ventricle (A) and pathological features of atrioventricular (AV) node and His bundle (B–D) on postmortem examination. (A) A vegetation, 2×1 cm in size, is present at the perforated posterior mitral leaflet (arrow). The perforation site is indicated by a probe. (B) Two vegetations of 8 mm in size are present at the septal leaflet of the tricuspid valve (arrow; another vegetation is hidden behind the septal leaflet in this view.) Serial cross sections including the AV node and His bundle. The area encompassing the AV node and His bundle is replaced by a whitish area with the hyperemic border. (C) Histologic examination of the (^*) area revealed extensive necrosis with fibrosis and calcification of the AV node. No nodal structure is seen. (E) Histologic examination of the (^**) area revealed only a vague His bundle structure (arrowhead) that was surrounded by fibrosis with calcification and necrosis.

Discussion

This case of fatal CAVB was characterized by bilateral IE with mitral and tricuspid valves involvement caused by S. agalactiae, by mitral abscess affecting the AV node, and by late Streptococcal reinfection by a different species.

Although IE due to S. agalactiae occurs infrequently, its incidence has increased to 3% over recent years [4]. When S. agalactiae IE occurs, the patient is likely to be of advanced age or to have a chronic debilitating disease, such as diabetes. Mitral valve involvement is frequently observed, and multiple valve involvement occurs in 22% of cases (vs. 15% of all cases of endocarditis overall) [4,5]. Typically, the endocarditis progresses rapidly and leads to acutely decompensated heart failure resulting from severe valve destruction. Although surgery is frequently performed, mortality remains high at 41–47% [5,6].

IE in the bilateral location is rare and reported to be 15–25% of multivalvular IE [7]. Bilateral IE usually occurs in patients with intracardiac devices [8] or congenital heart disease [9], or intravenous drug users [10]. However, the patient did not have these backgrounds. Furthermore, postmortem examination revealed no atrial or ventricular septal perforation and histologic examination revealed mitral abscess showed no tricuspid involvement. Given that, bilateral cardiac involvement in this case might be caused by hematogenous metastasis.

Conduction abnormalities develop in 4–10% of IE patients. Such abnormalities are most likely in patients with aortic valve IE and occur only rarely in patients with mitral valve infection; only a few such cases have been reported [2,3,11,12]. This is because although the AV node lies adjacent to the mitral valve, the His-Purkinje system is anatomically closer to the aortic valve [12]. In cases of conduction abnormality associated with infective endocarditis, anatomical destruction by an abscess or perivalvular extension of the infection should be considered [3]. Surgery is strongly recommended, even in patients with uncontrolled heart failure or infection [13], but a conduction abnormality that persists even after antibiotic therapy portends a poor prognosis [14]. Furthermore, 41% post-cardiac surgery mortality has been reported for patients with class B cirrhosis, and a Child-Pugh score >7 points has been shown to predict postoperative mortality with 86% sensitivity and 92% specificity [15]. Thus, although involvement of the interventricular septum in the perimitral abscess caused AV node necrosis in our case and led to AVB, the patient was not considered a candidate for surgery because of the Child-Pugh class B cirrhosis (Child-Pugh score 8).

The risk of reinfection defined as a repeat episode of IE has been reported to be 6% [16]. Repeat infective endocarditis due to a different species occurs less frequently. Further studies are warranted for risk stratification and management of repeat endocardial infection.

Conclusions

We encountered a rare case of fatal CAVB resulting from S. agalactiae IE. In monitoring IE, clinicians should be aware of the possibility of perivalvular extension of the infection and that such extension can lead to fatal heart block. In such case, surgical treatment is strongly indicated because medical treatment alone is insufficient.