J Cardiol 2005 Jun; 45（6）: 257 – 262

Successfully Treated Triple Valve
Infective Endocarditis : A Case
ReportKenichi SAKAKURA, MD
Norifumi

KUBO, MD

TakujiKATAYAMA, MD

Tomio

UMEMOTO, MD

SatoshiOOSAWA, MD＊

Seiichiro

MURATA, MD＊

Yoshitaka

SUGAWARA, MD

Hiroshi

FUNAYAMA, MD

Yousuke

TAKAGI, MD

Takanori

YASU, MD, FJCC

YoshioTSURUYA, MD

Takashi INO, MD＊
Muneyasu

SAITO, MD, FJCC

Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
A 45-year-old woman presented with triple valve infective endocarditis and ventricular septal defect.
There were vegetations on the tricuspid valve, pulmonary valve, and aortic valve. She had multiple complications such as nephrotic syndrome, severe anemia, congestive heart failure, and convulsion. Her generalcondition was extremely poor. Intensive medical therapy, such as blood transfusion, mechanical ventilation, and continuous venovenous hemofiltration, allowed her to tolerate surgery. Triple valve replacement
and ventricular septal defect closure was successfully performed without major complication. She wasambulatory at the time of discharge.
──────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2005 Jun ; 45（6）: 257−262

Key Words
Endocarditis infective

Tricuspid valve triple valve replacement

INTRODUCTION

CASE REPORTInfective endocarditis usually invades one or twovalves. We present a case of triple valve infective
endocarditis causing vegetations on the tricuspid,pulmonary, and aortic valves, associated with complications such as nephrotic syndrome, severe anemia, and congestive heart failure, which was treatedsuccessfully.

A 45-year-old woman became aware of leg andfacial edema in February 2003, and dyspnea onexertion in March 2003. Her medical history wasunremarkable except for a ventricular septal defect（VSD）first identified at the age of 26 years. She
had undergone no dental procedures. She wasadmitted to a local hospital because of congestive
heart failure. Although diuretics（furosemide and──────────────────────────────────────────────
自治医科大学附属大宮医療センター総合医学Ⅰ 循環器科，＊心臓血管外科 : 〒 330−8503 さいたま市大宮区天沼町 1−847
The Cardiovascular Division, The First Department of Integrated Medicine, ＊ Department of Cardiovascular Surgery, Omiya MedicalCenter, Jichi Medical School, Saitama
Address for correspondence : KUBO N, MD, The Cardiovascular Division, The First Department of Integrated Medicine, Omiya
Medical Center, Jichi Medical School, Amanuma 1−847, Omiya, Saitama 330−8503 ; E-mail : kubonori@omiya.jichi.ac.jp
Manuscript received September 17, 2004 ; revised November 16, 2004 ; accepted November 16, 2004

257

258

Sakakura, Kubo, Katayama et al

Table 1 Laboratory data on admission
WBC

14,470/μl

RBC

198×104/μl

Cr2.13 mg/dl

T-Cho

169 mg/dl

5.6 g/dl

Na

139 mEq/l

Ht

17.1%

K

3.6 mEq/l

Plt

24.1×104/μl

Cl

105 mEq/l

T-P

5.7 g/dl

GLU113 mg/dl

ALB

2.1 g/dl

CRP

8.26 mg/dl

T-BIL

0.35 mg/dl

PT13.3 sec

GOT

17 IU/l

APTT47.6 sec

GPT10 IU/l

AT-3

LDH

352 IU/l

Fibrinogen

302 mg/dl

CPK34 IU/l

FDP

80.7μg/ml

BUN

47 mg/dl

Hb72%spironolactone）were administered, her medical
condition did not improve. Echocardiography
revealed a vegetation on the tricuspid valve. Shewas referred to our medical center on March 29,
2003.
The patient was 161 cm tall and weighed 69 kg.
Her blood pressure was 160/90 mmHg, heart rate
was 106 beats/min, and body temperature was37.3 °C. Her general status indicated severe systemic edema. Her palpebral conjunctiva was anemic. She had remarkable decay of the teeth. Agrade 4/6 pan-systolic murmur was audible at thesecond left sternal border and breath sounds werediminished. Her abdomen was severely distended.
A complete blood count revealed increased whiteblood cells and decreased hemoglobin concentration. Blood chemistry revealed hypoalbuminemia（albumin）, and renal dysfunction（blood urea nitrogen ; creatinine）（ Table 1）. Urinalysis revealed
proteinuria（ ＋＋＋）and occult blood（ ＋＋＋）.
Chest radiography showed cardiomegaly, pulmonary congestion, and bilateral massive pleuraleffusion（Fig. 1）.
Echocardiography demonstrated a VSD（perimembranous defect）and vegetations on the pulmonary and aortic valves as well as the tricuspidvalve（Fig. 2）. A large vegetation spanned the VSD
and the tricuspid valve. M-mode measurements
revealed that the left ventricular dimensions at enddiastole and endsystole were 62 and 47 mm, respectively. Doppler imaging revealed moderate aortic
regurgitation and moderate tricuspid regurgitation,
but the VSD jet was not clearly delineated. The
transtricuspid pressure gradient was 45 mmHg. The

Fig. 1 Chest radiograph on admission showing cardiomegaly, pulmonary congestion, and bilateralmassive pleural effusion

inferior vena cava was not dilated.
Our initial diagnosis was infective endocarditis,
nephrotic syndrome, anemia, and congestive heart
failure. Since her general status was too poor forsurgery, we began intensive medical therapy.
Antibiotics（penicillin G, 24 million units/day andgentamicine sulfate, 60 mg/day）were initiated for
infective endocarditis. Albumin concentrate andfurosemide were administered for severe edema
due to nephrotic syndrome. Blood transfusions
were also given for severe anemia. During theantibiotic therapy, blood cultures were examined
six times, but all failed to yield bacteria. As theinflammation progressed, other antibiotics（vancomysin and fulconazole）
were added.
She suddenly suffered convulsions on April 3,
2003. Following the convulsions, conjugate deviation to the left, anisocoria, and left hemiparesis
occurred. She was intubated and emergent brain
computed tomography was performed（ Fig. 3）.
Computed tomography found no signs of hemorrhage, or infarction. Her level of consciousness
improved and conjugate deviation, anisocoria, andhemiparesis disappeared. Magnetic resonanceimaging was performed 2 weeks later also excluded
infarction（Fig. 4）.
Although she recovered spontaneous respiration,
she was placed on a respirator for 6 days because ofhypoxia due to congestive heart failure. Largeamounts of albumin concentrate and furosemide
J Cardiol 2005 Jun; 45（6）: 257 – 262

Triple Valve Infective Endocarditis259

Fig. 2 Transthoracic echocardiograms demonstrating vegetations（arrows）
on the tricuspid valve（A）, aortic valve（B）, and pulmonary valve（C）

Fig. 3 Brain computed tomography scan just after convulsion showing no signs of infarction or hemorrhage

were administered intravenously, but her massive
edema could not be controlled. Continuous venovenous hemofiltration（CVVH）was initiated, andthe massive edema began to disappear. This aggressive medical therapy improved her general status
except for the infection. Levels of inflammatory
markers still continued to be high despite theadministration of many kinds of antibiotics such as
penicillin G, gentamicine sulfate, vancomycin, orfulconazole. C-reactive protein level above
J Cardiol 2005 Jun; 45（6）: 257 – 262

Fig. 4 T 2-weighted brain magnetic resonance image
showing no signs of infarction or hemorrhage

10 mg/dl persisted. We decided on surgery to control the infection.
Triple valve replacement and VSD closure wereperformed on April 18, 2003. The operative findings showed that each cusp of the tricuspid valve
was covered with vegetations（Fig. 5）. These tricuspid valve vegetations were connected with thevegetations around the VSD. The non-coronary
cusp of the aortic valve had a vegetation. The aorticvalve vegetation was not connected with the vegetations around the VSD. The right and anterior

260

Sakakura, Kubo, Katayama et alFig. 5 Intraoperative photograph of the tricuspid valve
severely damaged by large vegetations

cusps of the pulmonary valve also had vegetations.
There were no signs of infection around the valvular rings or myocardium. The VSD was closed witha pericardial patch. The aortic and pulmonary
valves were replaced with 21 mm mechanicalvalves and the tricuspid valve was replaced with a29 mm tissue valve.
Histopathological study found severe cellular
infiltration with neutrophils in all three valves, aswell as calcification. Culture of the vegetations
failed to yield any organism. Her general condition
began to improve with post-operative medical management. Complete atrioventricular block emerged
after the operation, so a permanent pacemaker wasimplanted on June 6, 2003. She was ambulatory at
the time of discharge.
DISCUSSION
This patient presented with triple valve infective
endocarditis complicated by nephrotic syndrome,anemia, congestive heart failure, and convulsions.
Combined medical and surgical therapy for infective endocarditis can decrease mortality in patientswith congestive heart failure, perivalvular invasive
disease and uncontrolled infection1）. However, herinitial general status was so poor that surgical therapy could not be tolerated（her body weight was
69 kg on admission and 40 kg on discharge）.
Hemodynamic status at the time of operation is themajor determinant of operative mortality. Thus, wefirst aimed to improve her general status withaggressive medical therapy for 20 days prior to surgical therapy.
CVVH was begun to treat her massive edema

because conservative treatment such as diuretics
and albumine concentrate did not ameliorate her
edematous condition. CVVH is a very usefulmodality for critically ill patients, especially withrenal failure2,3）. Although congestive heart failure isa controversial indication for CVVH, this procedure dramatically improved her edematous condition.
She did not receive a regular medical check up,
so any causality between endocarditis, nephrotic
syndrome and severe anemia is difficult to consider.
Before discharge, her creatinine level had normalized（ 0.65 mg/dl）, but proteinuria（ ＋＋＋）andhematuria（＋＋＋）were still present. The cause ofnephrotic syndrome was difficult to identify without renal biopsy. We suspected glomerulonephritis
because she had gross hematuria. The cause of thetransient increase of creatinine might be immunoreaction to infective endocarditis, or decrease of renal
blood flow due to hypoalbuminemia and congestive
heart failure.
Triple valve endocarditis is rare4−6）. Our patientwas critically ill due to multiple severe complications. However, we could improve her condition forsurgery with intensive medical treatment, especially with CVVH.
She suffered convulsion with focal symptom on
April 3, 2003. Her focal signs disappeared after
several hours. Computed tomography on the next
day and magnetic resonance imaging 2 weeks later
excluded brain infarction. This transient ischemic
attack might have been due to septic embolizationfrom endocarditis.
Transthoracic echocardiography is a highly specific and moderately sensitive modality for thediagnosis of infective endocarditis1,7,8）. Transthoracic echocardiography clearly demonstrated vegetations on the tricuspid, pulmonary, and aorticvalves. In our case, VSD might have played amajor role in these multiple vegetations（aortic, tricuspid, and pulmonary valves）. Congenital heartdisease is one of the major risk factors for infective
endocarditis9）, and there is an association between
infective endocarditis and congenital heartdiseases10,11）. Interestingly, triple valve（tricuspid,mitral, aortic）endocarditis was associated withVSD4）.
Since serial blood cultures were sterile, we could
not identify the primary causative organism.
Furthermore, we were unable to draw blood before
the administration of antibiotics. The histological
J Cardiol 2005 Jun; 45（6）: 257 – 262

Triple Valve Infective Endocarditis261

edema and severe anemia, we could not control theinfection in spite of multiple strong antibiotics. The
main purpose of surgery was infectious control,
which was accomplished without major complications. Complete atrioventricular block emerged
after the operation. The tricuspid valve was ravaged
by large vegetations and removal of these vegetations might have resulted in damage to the atrioventricular conduction system.
Even triple valve infective endocarditis withsevere complications can be treated successfully by
the replacement of all three valves.

study found severe cellular infiltration with neutrophils in all three valves, and calcification whichsuggested bacterial colonies. However, the histological study did not reveal whether these organisms were cocci or rods. Although we could notdetect the causative organism, her decayed teeth
were supposed to be the infection sources. Decayedteeth and dental procedures are classical incitantfactors, and current studies reveal that these factors
are still important in Japan12,13）.
Triple valve replacement and VSD closure wereperformed. Although we could manage her massive
要

約

三弁に及ぶ感染性心内膜炎の 1 例
坂倉建一

久保典史

片山卓志

梅本富士

大 澤村田聖一郎

菅原養厚

船 山大高木洋介

安鶴谷善夫

井野隆史

齋藤宗靖

暁隆 則

感染性心内膜炎は，通常，1 つもしくは 2 つの弁を病巣とするが，当センターに紹介された 45 歳の女性は 3 つの弁に病巣を持ち，さらに心室中隔欠損も伴っていた．三尖弁，肺動脈弁，大動脈弁にそれぞれ疣贅が認められた．症例はネフローゼ症候群，強度の貧血，うっ血性心不全，痙攣発作と多くの合併症を呈していた．当初は外科的手術が施行できる全身状態ではなかったが，輸血，人工呼吸管理，持続的静脈血液濾過などの集中的内科治療により全身状態の改善がみられたので，三弁同時置換および心室中隔欠損パッチ閉鎖術が計画された．この難手術は大きな合併症もなく，無事成功した．その後，症例は独歩で退院となった．

J Cardiol 2005 Jun; 45（6）: 257−262

References
1）Mylonakis E, Calderwood SB : Infective endocarditis inadults. N Engl J Med 2001 ; 345 : 1318−13302）Bellomo R, Farmer M, Boyce N : A prospective study ofcontinuous venovenous hemodiafiltration in critically illpatients with acute renal failure. J Intensive Care Med
1995 ; 10 : 187−192
3）Bent P, Tan HK, Bellomo R, Buckmaster J, Doolan L, Hart
G, Silvester W, Gutteridge G, Matalanis G, Raman J,Rosalion A, Buxton BF : Early and intensive continuous
hemofiltration for severe renal failure after cardiac surgery.
Ann Thorac Surg 2001 ; 71 : 832−837
4）Ohyama Y, Nihei T, Kimura K, Yakuwa H, Uchino K,Ishikawa T, Kuji N, Hayashi S, Watanabe Y, Ishii M,
Kondo J, Matsumoto A : A case of ventricular septal defectassociated with active infective endocarditis which wassuccessfully treated by triple valve replacement and ventricular septal defect patch closure. Kokyu To Junkan
1991 ; 39 : 1049−1053（in Jpn with Eng abstr ）5）Bortolotti U, Casarotto D, De Mozzi I, Gallucci V, Russo
R, Cevese PG : Acute bacterial endocarditis requiring

J Cardiol 2005 Jun; 45（6）: 257 – 262

emergency triple valve replacement and pace-maker
implant. J Cardiovasc Surg（Torino）1979 ; 20 : 587−590
6）Rippe JM, Curley F, Paraskos JA, Schoen FJ, Cohn LH,Alpert JS : Triple-valve endocarditis with unusual echocardiographic findings. Am Heart J 1984 ; 107 : 598−605
7）Bayer AS, Bolger AF, Taubert KA, Wilson W, SteckelbergJ, Karchmer AW, Levison M, Chambers HF, Dajani AS,Gewitz MH, Newburger JW, Gerber MA, Shulman ST,Pallasch TJ, Gage TW, Ferrieri P : Diagnosis and management of infective endocarditis and its complications.
Circulation 1998 ; 98 : 2936−29488）Prendergast BD : Diagnosis of infective endocarditis. BMJ
2002 ; 325 : 845−8469）Niwa K, Nakazawa M, Miyatake K, Tateno S, Yoshinaga
M ; Japanese Circulation Society（ JCS）Joint Working
Groups for Guidelines for Management of Infective
Endocarditis ; Japanese Society of Pediatric Cardiology andCardiac Surgery Joint Working Groups for Guidelines forProphylaxix, Diagnosis and Management of Infective
Endocarditis in Patients with Congenital Heart Disease :Survey of prophylaxis and management of infective endocarditis in patients with congenital heart disease : Japanese

262

Sakakura, Kubo, Katayama et al

nationwide survey. Circ J 2003 ; 67 : 585−591
10）Pekdemir H, Gokhan Cin V, Necdet Akkus M, Doven O :Cyanotic tetralogy of Fallot with its infective endocarditis
complication on the tricuspid and pulmonary. Circ J 2004 ;68 : 178−180
11）Watanabe Y, Taketani Y, Takei Y, Tanaka K, Watanabe Y :Complete heart block resulting from quadricuspid aorticvalve penicillin-resistant pneumococcal endocarditis : Acase report. Circ J 2003 ; 67 : 275−27612）Nakatani S, Mitsutake K, Hozumi T, Yoshikawa J,Akiyama M, Yoshida K, Ishizuka N, Nakamura K,Taniguchi Y, Yoshioka K, Kawazoe K, Akaishi M, NiwaK, Nakazawa M, Kitamura S, Miyatake K ; Committee on
Guideline for Prevention and Management of Infective
Endocarditis, Japanese Circulation Society : Current characteristics of infective endocarditis in Japan : An analysisof 848 cases in 2000 and 2001. Circ J 2003 ; 67 : 901−90513）Ako J, Ikari Y, Hatori M, Hara K, Ouchi Y : Changing
spectrum of infective endocarditis : Review of 194 episodes
over 20 years. Circ J 2003 ; 67 : 3−7J Cardiol 2005 Jun; 45（6）: 257 – 262