J Cardiol 2006 Dec; 48（6）: 315 – 323

Severe Tricuspid Regurgitation in
the Aged: Atrial Remodeling Associated With Long-Standing Atrial
Fibrillation
NaohitoYAMASAKI, MD

Fumiaki

KONDO, MD＊

Toru

KUBO, MD

Makoto OKAWA, MD
Yoshihisa

MATSUMURA, MD, FJCC

Hiroaki KITAOKA, MD, FJCC
Toshikazu
TakashiYABE, MDFURUNO, MD＊

Yoshinori DOI, MD, FJCC
Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
Objectives. Severe idiopathic tricuspid regurgitation（TR）occurs in the aged, but the mechanism of TR isunclear and there is little information on atrial abnormalities associated with this condition. This study retrospectively analyzed patients with severe functional TR presenting with common clinical features suggesting a distinct syndrome.
Methods. Eleven patients with severe functional TR were identified by reviewing the records of 16,235
consecutive patients. All patients had undergone clinical evaluation including echocardiography, electrocardiography and laboratory data.
Results. The median age of patients with severe functional TR was 78 years. All had a long-standing
history of atrial fibrillation（median duration, 23 years）. Clinical features are characterized by severe functional TR due to annular dilation, markedly dilated right atrium, episodes of right-sided heart failure,absent or diminished fibrillation waves on electrocardiogram, bradycardia probably due to partial atrial
standstill, and decreased atrial natriuretic peptide secretion. During long-term follow up, right atrial size
progressively increased in association with worsening TR.
Conclusions. Severe functional TR occurs with long-standing atrial fibrillation and causes right-sided
heart failure. The TR is caused by tricuspid valve systolic coaptation loss due to tricuspid annular dilation
associated with atrial dilation. This condition is associated with atrial abnormalities, such as atrial standstill
and impaired atrial natriuretic peptide secretion. We propose that atrial remodeling associated with atrial
fibrillation is central to the occurrence of the syndrome.
─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2006 Dec ; 48
（6）
: 315−323

Key Words
Tricuspid regurgitation
Atrial function remodeling

Atrial fibrillation

INTRODUCTION
Tricuspid regurgitation（TR）mainly occurs sec-

Elderly

ondary to left-sided heart disease and secondary
pulmonary hypertension in adults, but can also
occur as a primary valvular lesion. For example,──────────────────────────────────────────────
高知大学医学部 老年病科・循環器科 : 〒 783−8505 高知県南国市岡豊町小蓮 ; ＊幡多けんみん病院 循環器科，高知Department of Medicine and Geriatrics, Kochi Medical School, Kochi ; ＊ Section of Cardiology, Hata Prefectural Hospital, Kochi
Address for correspondence : DOI Y, MD, FJCC, Department of Medicine and Geriatrics, Kochi Medical School, Kohasu, Oko-cho,Nankoku, Kochi 783−8505 ; E-mail : ydoi@med.kochi-u.ac.jp
Manuscript received June 23, 2006 ; revised September 3, 2006 ; accepted September 22, 2006

315

316

Yamasaki, Kondo, Kubo et alelderly patients with severe idiopathic TR havebeen reported with structurally normal tricuspid
valves and severe TR caused by annular
dilation.1−3）However, the mechanism of annular
dilation is unclear and there is little information on
atrial abnormalities in these patients. In this report,
we retrospectively investigated elderly patientswith common clinical features suggesting a distinct
syndrome of severe functional TR. We suggest that
this syndrome is caused by atrial remodeling associated with long-standing atrial fibrillation（AF）.
SUBJECTS AND METHODSPatients
Eleven patients with severe idiopathic TR wereidentified by reviewing reports of 16,235 consecutive patients who had undergone echocardiography
at Kochi Medical School and Hata Prefectural
Hospital during a 5-year period between January
2000 and December 2005. Exclusion criteria wereas follows : Anatomically abnormal tricuspid
valves（rheumatic, infective endocarditis, Ebsteinanomaly, carcinoid heart disease, history of
trauma）; presence of significant pulmonary hypertension（TR pressure gradient ＞ 40 mmHg by cardiac echo）; severe organic left-sided valvular heartdisease or congenital heart disease ; left ventricularsystolic dysfunction ; previous history of cardiac
surgery ; and TR due to previously implanted permanent pacemaker or implantable cardioverterdefibrillator leads. All patients had undergone clinical evaluation including physical examination,
chest radiography, electrocardiography, laboratory
data and echocardiography.
The control group consisted of 10 subjects（5males and 5 females ; mean age : 78 ± 6 years）
without cardiovascular disease who had no abnomalities on echocardiography.
Echocardiography
Two-dimensional and Doppler echocardiograms
were obtained from all patients according to a standard protocol using a commercially available imaging system（Sequoia 512, Mountain View）. All
recordings were performed on S-VHS videotape foranalysis. Mitral regurgitation（MR）and TR wereidentified as a color mosaic systolic jet. The maximum regurgitant jet area was planimetered in an
apical four-chamber view. The right atrial area andleft atrial area were measured on a still-frame
image at the same time. The severity of TR or MR

was determined by the ratio of the color Doppler jet
area to the right or left atrial area in mid-systole.
The degree of TR or MR was estimated as trace,
mild, moderate or severe defined as ratios of ＞ 0−10%, ＞ 10−20%, ＞ 20−40% and ＞ 40%, respectively.4）The right ventricular（RV）area was manually traced in the apical four-chamber view at enddiastole and end-systole. Right ventricular ejection
fraction was calculated as（RV end-diastolic areaRV end-systolic area）/RV end-diastolic area（%）.5）The tricuspid and mitral annuli were identified as
the hinge points of the leaflets defined by theirinsertion on the right or left ventricular wall. The
tricuspid annular diameter and mitral annular diameter were measured on a still image of the apicalfour-chamber view at the time of mid-systole. The
peak TR velocity was measured by continuouswave Doppler, and pulmonary artery systolic pressure was estimated by the modified Bernoulli
method in all patients.6）
Atrial and brain natriuretic peptides measurements
Blood was withdrawn from a forearm vein ineach patient after the patient had remained in thesupine position for at least 15 min. Immunoradiometric assay was performed to measure plasma human atrial natriuretic peptide（ANP）and brain
natriuretic peptide（BNP）levels（ShionoRIA kit ;Shionogi Co., Ltd）.
Data analysis
Data are expressed as the mean ± SD. The
unpaired Student s t-test was used to assess differences between the patient and control groups. A
value of p ＜ 0.05 was considered to be statisticallysignificant.
RESULTSClinical characteristics
Table 1 summarizes the clinical characteristicsof the 11 patients. All patients were elderly（agerange : 65−86 years ; median age : 78 years）andhad a long-standing history of AF（10−30 years ;median duration : 23 years）. Edema was the firstmanifestation in all patients. Auscultation detectedpansystolic murmur with tricuspid mid-diastolic
rumble. Hepatomegaly was observed in all patients.
Four patients（patients 1, 3, 4 and 8）presented withanasarca and required multiple hospitalizations fordecompensated right-sided heart failure. All
J Cardiol 2006 Dec; 48（6）: 315 – 323

Severe Tricuspid Regurgitation in the Elderly

Table 1

Clinical characteristics of 11 patients with idiopathic severe tricuspid regurgitation

Patient
No.

Age
（yr）

Sex

History of AF（yr）

Pacemaker
implantation

Chest radiography
CTR（%）

Pancytopenia

1

79

Male

30

−

75

＋

2

80

Female

20

＋

82

＋

3

79

Male

20

＋

73

＋

4

83

Female

30

＋

67

＋

5

68

Male

26

−

63

−

−

6

65

Male

10

58

−

7

81

Male

20

−

60

−

8

86

Male

20

−

67

＋

9

81

Male

25

＋

68

＋

10

74

Female

20

−

51

−

Female

30

−

69

＋

11

317

81

AF＝atrial fibrillation ; CTR＝cardiothoracic ratio.

A

B

C

Fig. 1 Echocardiograms
Apical four-chamber view of the heart in a representative patient（patient 1）revealing markedly dilated
right atrium and left atrium（A）. Color flow imaging shows severe tricuspid regurgitation（B）and moderate
mitral regurgitation（C）.
RV ＝ right ventricle ; RA ＝ right atrium ; LV ＝ left ventricle ; LA ＝ left atrium.

patients needed diuretic therapy to relieve symptoms of edema. Heart failure symptoms werealways right-side dominant, and no patient presented with pulmonary edema. Four patients required
permanent pacemaker implantation because of
symptomatic bradycardia. Chest radiography
showed marked cardiomegaly in all patients（Table1）. Seven patients had pancytopenia, andsplenomegaly secondary to congestive liver was
thought to be responsible for this pancytopenia.

J Cardiol 2006 Dec; 48（6）: 315 – 323

Echocardiography
All patients had markedly dilated right atrium
and severe TR（Fig. 1）. Although functional MR
was present in all patients, TR was always the predominant valvular lesion compared with MR. The
tricuspid valve and supporting structures were normal without prolapse, ruptured chord, flail segment,or any other disruption of the tricuspid apparatus.
However, the tricuspid annulus was markedly dilated, and associated with systolic coaptation loss
between septal and anterior tricuspid valve leaflet

318

Yamasaki, Kondo, Kubo et al

Fig. 2 Mechanism of severe tricuspid regurgitation
Apical four-chamber echocardiographic images in patient 2. A shows a markedly dilated tricuspid valve
annulus. In the magnified view（B）
, coaptation loss is evident and a systolic gap is present between the septal and anterior tricuspid valve leaflet tips. The color Doppler image（C）shows severe tricuspid regurgitation jet with prominent flow convergence.
TV ＝ tricuspid valve.

Table 2
Patient
No.

RA area
（cm2）

TAD
（mm）

LA area
（cm2）

MAD
（mm）

1

54

54

66

2

42

45

38

3

64

50

4

53

5

Echocardiographic data
MR
grade

RV area
（cm2）

RVEF
（%）

LVDd
（mm）

LVEF
（%）

TRΔP
（mmHg）

IVC size（mm）

56

Severe

21

73

57

53

31

38

37

Moderate

24

63

48

68

38

37

60

48

Moderate

22

41

55

71

24

38

46

51

53

Severe

11

31

58

62

32

36

46

44

40

40

Moderate

19

29

58

60

34

25

6

37

40

26

35

Trace

17

40

51

58

26

17

7

43

44

37

41

Mild

24

36

48

60

16

26

8

52

46

31

33

Mild

20

39

48

61

29

34

9

39

42

26

41

Mild

27

55

50

64

31

13

10

36

41

31

35

Trace

19

29

41

67

29

21

11

37

42

33

32

Mild

16

44

48

79

24

28

Control

14

28

15

31

Trace

10

43

48

63

19

10

RA＝right atrial ; TAD＝tricuspid annular diameter ; LA＝left atrial ; MAD＝mitral annular diameter ; MR＝mitral regurgitation ; RV
＝right ventricular ; LVDd＝left ventricular diastolic diameter ; R（L）VEF＝right（left）ventricular ejection fraction ; TRΔP＝tricuspid
regurgitation pressure gradient ; IVC＝inferior vena cava.

tips as shown in Fig. 2. A large systolic jet of TR
originated from the gap that was caused by theannular dilation.
Echocardiographic data are presented in Table 2.
Both atria were markedly dilated（right atrial area :45.7 ± 9.0 vs 14.2 ± 3.6 cm 2 , left atrial area :39.9 ± 14.0 vs 15.3 ± 5.8 cm2, patients vs controls,
both p ＜ 0.0001）with severe annular dilation（tricuspid annular diameter : 44.9 ± 4.1 vs 27.7 ±3.1 mm, mitral annular diameter : 41.0 ± 8.1 vs31.2 ± 3.4 mm, patients vs controls, both p ＜0.0001）. The right ventricle was significantly dilated（ RV end-diastolic area : 20.0 ± 4.4 vs 9.9 ±2.7 cm2, patients vs controls, p ＜ 0.0001）. RV systolic function assessed by right ventricular ejection
fraction was relatively preserved（right ventricularejection fraction : 43.6 ± 14.3%）. Regional RV
hypokinesia and segmental dilation of the RV suggesting arrhythmogenic right ventricular cardiomyopathy were not detected in any patient. The left
J Cardiol 2006 Dec; 48（6）: 315 – 323

Severe Tricuspid Regurgitation in the Elderly

319

B

A

C

Fig. 3 Electrocardiograms
Electrocardiogram of a representative patient（patient 4）with severe functional tricuspid regurgitation（A）.
Note the absence of fibrillation waves and junctional escape rhythm of 44 per minute. The previous electro. The
cardiogram recorded in 1988 showed atrial fibrillation with fine fibrillation waves in lead V（B）
2
height of the fibrillation waves progressively diminished and the waves were no longer visible in 2000
（C）.

Table 3

Plasma atrial and brain natriuretic peptide
concentration

Patient
No.

ANP（pg/ml）

BNP（pg/ml）

2

57.6

190

3

11.4

103

4

6.3

45

5

17.1

120

7

67.2

341

11

74.6

217

（Reference value）

<43.0

<18.4

ANP＝atrial natriuretic peptide ; BNP＝brain natriuretic
peptide.

ventricle was mildly dilated with preserved systolic
function（ ejection fraction : 63.9 ± 7.1 %）.
Significant pulmonary hypertension（TR pressure
gradient ＞ 40 mmHg）was not present in any
patient. All patients had markedly dilated inferior
vena cava（median : 28.5 ± 8.9 mm in diameter）
with loss of respiratory diameter change.
Electrocardiography
All patients had AF. Seven patients had slow AF（heart rate ＜ 60 beats/min）. Three patients were
initially treated with digitalis, which was later discontinued due to bradycardia. Six patients showed
flattened baseline without fibrillation waves. In
these patients, RR intervals were mostly regular,
suggesting partial atrial standstill with junctional
escape rhythm. Four patients had AF with diminJ Cardiol 2006 Dec; 48（6）: 315 – 323

ished fibrillation wave height（less than 1 mm）. A
representative electrocardiography is shown in Fig.
3−A. In all patients, the height of atrial fibrillation
waves progressively diminished during follow up（Figs. 3−B, C）.
Plasma atrial natriuretic peptide concentration
In six patients, both ANP and BNP plasma concentrations were measured at the same time. The
plasma ANP concentration was normal to slightly
elevated in the patients despite marked elevation ofplasma BNP concentration（Table 3）.
Long-term echocardiographic data
The progressive nature of TR severity was documented by serial echocardiograms（＞− 10 years）in
two patients（patients 1 and 4）. When first evaluated, both patients had AF rhythm and dilated rightatrium（right atrial areas of 25 and 36 cm2, respectively）. The severity of TR was moderate at most（TR jet areas of 6 and 8 cm2, respectively）. During
10years）,
rightatrialsize
long-term follow-up（＞−progressively increased in association with tricuspid valve annular dilation. As the tricuspid annular
diameter increased, regurgitation severity worsened, and TR finally became severe（TR jet areas of
54 and 42cm2, respectively）.
DISCUSSION
Severe functional TR was identified in 11 elderly
patients with common clinical features suggesting a
distinct syndrome characterized by occurrence in320

Yamasaki, Kondo, Kubo et al

the elderly with long-standing AF, severe functional TR due to annular dilation, giant right atrium,
signs of right-sided heart failure, absent or diminished fibrillation waves on electrocardiography,
bradycardia probably due to partial atrial standstill,and decreased ANP secretion.
Several previous reports of elderly patients withsevere functional TR 1−3）have not identified themechanism of such TR or explained the atrial
abnormalities associated with this syndrome. The
present study suggests that atrial remodeling associated with AF is central to the cause of this syndrome.
Mechanism of tricuspid regurgitation
The mechanism of severe TR in this syndrome isthought to be tricuspid valve systolic coaptation
loss due to tricuspid annular dilation associatedwith long-standing AF. The tricuspid annulus wasmarkedly dilated and the tricuspid valve leaflets
and their supporting structures were normal.
Although four of our patients had permanent pacemaker implantation due to bradycardia, severe TR
was present prior to the pacemaker implantation,
indicating that damage to the tricuspid valve by
pacemaker leads was not the main cause of TR.7）
Other causes of TR, such as rheumatic heart disease, infective endocarditis, Ebstein anomaly, carcinoid heart disease, traumatic chordal rupture, andpresence of significant pulmonary hypertension,
were excluded by echocardiography and carefulchart reviews.
We consider that atrial remodeling is central tothe progression of TR, based on the longitudinalfollow up data in two of our patients. In thesepatients, right atrial size progressively increased
over a period of 10 years in association with tricuspid annular dilation. As the tricuspid annular diameter increased, TR severity worsened due to progressive systolic coaptation loss. This observation
supports the causative relationship between atrial
remodeling and severe TR. The proposed pathophysiological mechanism is summarized in Fig. 4.
Long-standing AF causes progressive atrial remodeling and leads to atrial dilation. The dilated atrium
makes the tricuspid annulus larger and causes TR
due to systolic coaptation loss. The resulting TR
further dilates the atrium, resulting in progressive
annular dilation. Therefore, a vicious circle inwhich TR begets TR is established.
All of our patients had functional MR, but TR

Fig. 4 Proposed pathophysiological mechanism ofsevere tricuspid regurgitation development inpatients with long-standing atrial fibrillation
Long-standing atrial fibrillation causes chronic atrial
remodeling and leads to atrial dilation. The dilated atrium enlarges the tricuspid annulus and causes tricuspid
regurgitation due to coaptation loss. The resultant tricuspid regurgitation further dilates the atrium, resulting
in progressive annular dilation. Therefore, a vicious circle in which "tricuspid regurgitation begets tricuspid
regurgitation" is established. Marked stretching of theatria associated with increased pressure causes atrial
fibrosis.
TR ＝ tricuspid regurgitation. Other abbreviations as in
Tables 1, 3, Fig. 2.

was always the more predominant valvular lesion.
The cause of severe TR was not thought to be secondary to MR because no significant pulmonary
hypertension（TR pressure gradient ＞ 40 mmHg）
was present in any patient and no patient presented
with pulmonary congestion. The reason why TR
was more predominant can be explained by the
recent examinations of the impact of AF on the tricuspid and mitral valves which showed that annular
dilation and valvular regurgitation associated withAF are significantly greater in the tricuspid valve
than in the mitral valve4）and that isolated annular
dilation caused by AF does not usually cause significant MR.8）
Atrial remodeling associated with atrial fibrillation
AF is characterized by structural and functional
remodeling in the atrial myocardium. 9） Atrial
enlargement occurs as a consequence of AF.10）Our
patients had a long-standing history of AF, and atrial size progressively increased during follow up. In
addition, we found two atrial abnormalities in ourpatients that reflect the remodeling process, namely,
decreased ANP secretion and partial atrial standstill.
J Cardiol 2006 Dec; 48（6）: 315 – 323

Severe Tricuspid Regurgitation in the Elderly

Atrial natriuretic peptide
Our patients had impaired ANP secretion. ANP
is secreted mainly from the atria, whereas BNP issecreted mainly from the ventricles.11）The plasma
concentrations of ANP and BNP are elevated inproportion to the severity of congestive heart failure. In our patients, the plasma ANP concentration
was normal to slightly elevated despite marked elevation of the plasma BNP concentration.
Considering the presence of moderate to severe
heart failure and significantly increased BNP, ANP
secretion was thought to be impaired in ourpatients. In patients with heart failure, ANP issecreted from the ventricles in addition to theatria.12）This suggests that ANP production by theatria is more impaired than that predicted from themeasured ANP value in our patients.
Long-standing AF leads to reduced ANP production by the atria resulting from atrial structural
remodeling and eventually irreversible damage.13）
Plasma ANP concentration inversely correlateswith left atrial collagen volume fraction in patientswith AF.14）Therefore, the low ANP secretion in
our patients suggests high atrial collagen content
and significant atrial structural remodeling.
Atrial standstill
Atrial standstill is a rare disorder caused byinjury to the atrium. The diagnosis is established byconfirming both electrical silence and mechanicalsilence of the atria. The following criteria havebeen proposed for the diagnosis of atrial
standstill : 15）Absence of P wave on surface andintracardiac electrocardiograms ; absence of a wave
in the intracardiac pressure record ; regular rhythm ;and angiographic evidence of immobile atrium. A
partial form of atrial standstill has also been reported, which is defined as the absence of electricalactivity in a discrete area of the atrium.16）
In six of our patients, electrocardiography
showed bradycardia probably due to partial atrial
standstill. In these patients, the AF waves progressively diminished and finally became flattened in
all leads, suggesting electrical silence. Our echocardiographic investigation revealed absence of atrial
contraction（ mechanical silence）in the patients.
Furthermore, the RR intervals were mostly regularwith junctional escape rhythm. Taken together, theresults suggest that the bradycardia in our patientswas caused by partial atrial standstill.

J Cardiol 2006 Dec; 48（6）: 315 – 323

321

Moreover, a low plasma concentration of ANP
has been demonstrated in patients with atrial standstill.17）Attenuated increase in plasma ANP concentration to the increase in BNP concentration has
been suggested as a useful marker of atrial standstill.18）Our patients plasma ANP data are in agreement with this proposal.
Limitations
Our study has several limitations. First, the number of the patients was small and cases were collected retrospectively. Therefore, it is difficult toestimate the frequency of this clinical entity in theelderly with AF. Also, a moderate degree of functional TR is frequently observed in patients withlone AF and may be an early stage of this syndrome. A longitudinal follow up of a large group ofpatients with AF is necessary to characterize thepatients who present with and without this syndrome. Longer duration of AF, older age, andgenetic factors might be related to the occurrenceof this syndrome. Second, the echocardiograms
were reviewed retrospectively. Therefore, we could
not evaluate the severity of TR by quantitative
methods such as the PISA method19）or vena contracta width.20）In addition, only two-dimensional
echocardiography was available which has limitations in characterizing the complex three-dimensional structure of the tricuspid valve. Threedimensional imaging techniques may provide moreaccurate information for tricuspid valve geometry
such as tethering. Third, none of our patients underwent cardiac surgery to correct TR, so we could not
obtain any tissue samples. Histological data toshow the presence of atrial cardiomyopathy await
further study, although the low serum ANP level inour patients suggests fibrotic change of the atrium.
CONCLUSIONS
Severe functional TR occurs in the elderly withlong-standing AF and causes right-sided heart failure. This TR is caused by tricuspid valve systolic
coaptation loss due to tricuspid annular dilation.
This condition is associated with atrial abnormalities, such as atrial standstill and impaired ANP
secretion. We propose that atrial remodeling associated with AF is central to the occurrence of thissyndrome. This syndrome warrants further recognition.

322

Yamasaki, Kondo, Kubo et al

要約

高齢者における重症三尖弁閉鎖不全症: 長期持続する心房細動による心房リモデリングとの関連
山崎

目

直仁

近藤

史明

久 保

亨

大川

真理

松村

北岡

裕章

矢部

敏和

古野

貴志

土居

義典

敬久

的 : 高齢者において明らかな基礎疾患を有しない特発性の重症三尖弁閉鎖不全症が存在する

ことが報告されている．しかし，三尖弁閉鎖不全を生じる機序は明らかではなく，また本症での心房の異常について検討した報告は少ない．本研究では，特発性重症三尖弁閉鎖不全症患者の臨床的特徴を明らかにすることを目的とする.
方

法 : 心エコー図検査を施行した連続 16,235 例のうち，基礎疾患を有しない重症三尖弁閉鎖不全症の患者は 11 例存在した．これらの患者において，心エコー図，心電図，採血データなどの臨床データの検討を行った.
結果 : 患者の平均年齢は 78 歳で，11 例全例が長期（平均 23 年）持続する心房細動を有していた.

これらの患者は，1）弁輪拡大のため重症の三尖弁閉鎖不全症を有する，2）著明な右心房の拡大が認められる，3）右心不全を繰り返し生じる，4）心電図において心房細動波（f 波）が減高し消失している，5）部分的心房停止による徐脈が認められ，一部の患者では恒久的ペースメーカー植え込みを必要とする，6）心房性ナトリウム利尿ペプチドの分泌低下が認められる，といった共通の臨床的特徴を有しており，一つの症候群と考えられた．三尖弁閉鎖不全が重症化していく過程を長期間にわたり観察しえた症例では，心房細動に伴う三尖弁輪径の経時的な拡大に伴い，初期には軽度であった三尖弁逆流が重症化した.
結論 : 長期間持続する心房細動のために重症の三尖弁閉鎖不全を生じ，右心不全症状を呈する

高齢者の一群が存在する．三尖弁閉鎖不全の原因は，心房細動により三尖弁輪が拡大する結果生じる三尖弁の接合不全である．本症では心房の機能異常を伴っており，部分心房停止，心房性ナトリ
ウム利尿ペプチドの分泌不全が認められる.

長期間持続する心房細動に伴う心房のリモデリングが本症候群の発生に深く関係していると考えられる.

J Cardiol 2006 Dec; 48（6）: 315−323

References
1）Kasai A, Nishikawa H, Ono N, Unno M, Kakuta Y,
Hamada M, Nakano T : Clinical evaluation of severe idiopathic tricuspid regurgitation. J Cardiol 1990 ; 20 : 937−
944
（in Jpn with Eng abstr）
2）Iga K, Konishi T, Matsumura T, Miyamoto T, Kijima K,
Gen H : Markedly enlarged right atrium associated withphysical signs of tricuspid regurgitation : A cause of congestive heart failure in the elderly. Jpn Circ J 1994 ; 58 :683−6883）Girard SE, Nishimura RA, Warnes CA, Dearani JA, Puga
FJ : Idiopathic annular dilation : A rare cause of isolated
severe tricuspid regurgitation. J Heart Valve Dis 2000 ; 9 :283−2874）Zhou X, Otsuji Y, Yoshifuku S, Yuasa T, Zhang H,
Takasaki K, Matsukida K, Kisanuki A, Minagoe S, Tei C :Impact of atrial fibrillation on tricuspid and mitral annular
dilatation and valvular regurgitation. Circ J 2002 ; 66 :913−9165）Kaul S, Tei C, Hopkins JM, Shah PM : Assessment of rightventricular function using two-dimensional echocardiography. Am Heart J 1984 ; 107 : 526−531
6）Currie PJ, Seward JB, Chan KL, Fyfe DA, Hagler DJ, Mair
DD, Reeder GS, Nishimura RA, Tajik AJ : Continuous
wave Doppler determination of right ventricular pressure :A simultaneous Doppler-catheterization study in 127
patients. J Am Coll Cardiol 1985 ; 6 : 750−7567）Lin G, Nishimura RA, Connolly HM, Dearani JA, Sundt
TM Ⅲ, Hayes DL : Severe symptomatic tricuspid valve
regurgitation due to permanent pacemaker or implantablecardioverter-defibrillator leads. J Am Coll Cardiol 2005 ;45 : 1672−16758）Otsuji Y, Kumanohoso T, Yoshifuku S, Matsukida K,
Koriyama C, Kisanuki A, Minagoe S, Levine RA, Tei C :Isolated annular dilation does not usually cause importantfunctional mitral regurgitation : Comparison between
patients with lone atrial fibrillation and those with idiopathic or ischemic cardiomyopathy. J Am Coll Cardiol 2002 ;39 : 1651−16569）Allessie M, Ausma J, Schotten U : Electrical, contractile
and structural remodeling during atrial fibrillation.

J Cardiol 2006 Dec; 48（6）: 315 – 323

Severe Tricuspid Regurgitation in the Elderly

Cardiovasc Res 2002 ; 54 : 230−246
10）Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB,
Harrigan P, Hughes RA, Weyman AE : Atrial enlargement
as a consequence of atrial fibrillation : A prospective
echocardiographic study. Circulation 1990 ; 82 : 792−797
11）Yasue H, Yoshimura M, Sumida H, Kikuta K, Kugiyama
K, Jougasaki M, Ogawa H, Okumura K, Mukoyama M,
Nakao K : Localization and mechanism of secretion of Btype natriuretic peptide in comparison with those of A-typenatriuretic peptide in normal subjects and patients withheart failure. Circulation 1994 ; 90 : 195−203
12）Tsuchimochi H, Yazaki Y, Ohno H, Takanashi R, Takaku
F : Ventricular expression of atrial natriuretic peptide.
Lancet 1987 ; Ⅱ : 336−337
13）van den Berg MP, van Gelder IC, van Veldhuisen DJ :Depletion of atrial natriuretic peptide during longstanding
atrial fibrillation. Europace 2004 ; 6: 433−43714）Yoshihara F, Nishikimi T, Sasako Y, Hino J, Kobayashi J,
Minatoya K, Bando K, Kosakai Y, Horio T, Suga S,
Kawano Y, Matsuoka H, Yutani C, Matsuo H, Kitamura S,
Ohe T, Kangawa K : Plasma atrial natriuretic peptide concentration inversely correlates with left atrial collagen volume fraction in patients with atrial fibrillation : Plasma
ANP as a possible biochemical marker to predict the outcome of the maze procedure. J Am Coll Cardiol 2002 ; 39 :J Cardiol 2006 Dec; 48（6）: 315 – 323

323

288−29415）Bloomfield DA, Sinclair-Smith BC : Persistent atrial standstill. Am J Med 1965 ; 39 : 335−340
16）Levy S, Pouget B, Bemurat M, Lacaze JC, Clementy J,
Bricaud H : Partial atrial electrical standstill : Report ofthree cases and review of clinical and electrophysiologicalfeatures. Eur Heart J 1980 ; 1 : 107−11617）Seino Y, Shimai S, Ibuki C, Itoh K, Takano T, Hayakawa
H : Disturbed secretion of atrial natriuretic peptide inpatients with persistent atrial standstill : Endocrinologic
silence. J Am Coll Cardiol 1991 ; 18 : 459−463
18）Suguta M, Hara K, Nakano A, Amano A, Hasegawa A,
Kurabayashi M : Serum atrial natriuretic peptide concentration is a useful predictor of atrial standstill in patients withheart failure. Jpn Circ J 2000 ; 64 : 537−54019）Grossmann G, Stein M, Kochs M, Hoher M, Koenig W,
Hombach V, Giesler M : Comparison of the proximal flow
convergence method and the jet area method for the assessment of the severity of tricuspid regurgitation. Eur Heart J
1998 ; 19 : 652−65920）Tribouilloy CM, Enriquez-Sarano M, Bailey KR, Tajik AJ,
Seward JB : Quantification of tricuspid regurgitation bymeasuring the width of the vena contracta with Doppler
color flow imaging : A clinical study. J Am Coll Cardiol
2000 ; 36 : 472−478