Aortic regurgitation caused by rupture of a well-balanced fibrous strand suspending a degenerative tricuspid aortic valve

Nakajima, Masahiro; Tsuchiya, K; Naito, Yoshiro; Hibino, Narutoshi; Inoue, Hidenori

doi:10.1067/mtc.2002.124296

Cited by 17 publications

(25 citation statements)

References 3 publications

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“…4 It appears that there is a higher incidence in Japan of aortic valve regurgitation associated with anomalous fibrous cords than in the North America and European populations. 3,5 The aortic valve is affected by fenestration slightly more frequently than the pulmonary valve, but each valve is involved in more than half the subjects. With widening of the annular ring, there is a definite increase in the severity and frequency of fenestration in both of the semilunar valves.…”

Section: Discussionmentioning

confidence: 99%

Pathogenetic Significance of Myxomatous Degeneration in Fenestration-Related Massive Aortic Regurgitation

Akiyama

Hirota

Taniyasu

et al. 2004

Circ J

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enestration of the aortic valve is not an uncommon malformation, and appears as an oval hole immediately below the free edge of the cusp near its commissural attachment. Fenestration of the aortic cusp is not considered to have any pathological significance, and is rarely associated with aortic regurgitation, but we are operating on an increasing number of cases of massive aortic regurgitation in which large fenestrations play an important role in the pathogenesis of regurgitation. We present 6 cases in which the clinicopathological findings were analyzed. Methods PatientsDuring the past 9 years at Iwaki Kyoritsu General Hospital, more than 200 aortic valves have been replaced because of aortic regurgitation caused by idiopathic annular dilatation, infected endocarditis, rheumatic valvular disease or congenital bicuspid valve. Of these patients, 6 cases with large aortic valve fenestrations (Fig 1), which played an important role in producing massive aortic regurgitation, were evaluated from the clinical and pathological viewpoints. None of them showed systemic connective tissue disease or annuloaortic ectasia. The interval since onset was defined as the time span to surgical treatment from the appearance of new aortic regurgitant murmur, the Circulation Journal Vol.68, May 2004first experience of cardiac symptoms or echocardiographic detection of aortic regurgitation. Left ventricular hypertrophy was defined electrocardiographically by the QRS voltage criteria including RI + SIII ≥2.5 mV, R in aVf >2.0 mV, S in V1 ≥2.4 mV, R in V5 or V6 >2.6 mV, and R in V5 or V6 + S in V1 >3.5 mV. The aortic annular diameter (AAD), left ventricular diastolic dimension (LVDd), and left ventricular systolic dimension (LVDs) were measured by 2-dimensional echocardiography in the parasternal long-axis view. The severity of the aortic regurgitation was graded as trivial (I), mild (II), moderate (III) or severe (IV) using color flow mapping in the apical view of transthorac-

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Section: Discussionmentioning

confidence: 99%

Pathogenetic Significance of Myxomatous Degeneration in Fenestration-Related Massive Aortic Regurgitation

Akiyama

Hirota

Taniyasu

et al. 2004

Circ J

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“…4) In the present case, fibrous strands supported the aortic valve and maintained coaptation of the valve (Figure 3). Poorly controlled hypertension may have led to mechanical stress on the fibrous strands, and continuous tension to this supportive tissue may have gradually weakened the strand, resulting in AR due to cord rupture.…”

Section: Discussionmentioning

confidence: 94%

“…1) These reports have mostly been from Japan and other Asian countries 1,3,4) suggesting that some form of heredity involvement may exist with regard to fibrous strand formation. 4) In the present case, fibrous strands supported the aortic valve and maintained coaptation of the valve (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, an enlarged aortic annulus > 30 mm in diameter is often observed with echocardiography. 4) Transthoracic echocardiography and transesophageal echocardiography are reported to be useful for the detection of fibrous strand rupture. 1) In the absence of any other obvious cause, physicians must consider the possibility of a fenestrated aortic valve in patients with chronic AR or sudden deterioration of regurgitation.…”

Section: Discussionmentioning

confidence: 99%

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Aortic Regurgitation Due to Fibrous Strand Rupture in the Fenestrated Left Coronary Cusp of the Tricuspid Aortic Valve

et al. 2014

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SummaryFenestration-related massive aortic regurgitation is rare. The underlying mechanism is reported to be rupture of the fenestrated fibrous strand, and most ruptured cords have been reported in the bicuspid valve or in the right coronary cusp of the tricuspid aortic valve. We encountered a rare case of acute aortic regurgitation due to fibrous strand rupture in the fenestrated left coronary cusp. Preoperative echocardiography detected left coronary cusp prolapse, and operative findings revealed rupture of a fibrous strand in the left coronary cusp. For cases such as this, preoperative echocardiography would be useful for appropriate diagnosis. (Int Heart J 2014; 55: 550-551) Key words: Aortic valve regurgitation F enestration in the aortic valve is not uncommon and is often observed in normal subjects. In this type of aortic valve, the fibrous strand, which is said to be an embryonic remnant during semilunar cusp formation, is a supportive tissue that maintains aortic valve coaptation. Fibrous strand rupture causes acute aortic regurgitation (AR) and has been reported to occur in the congenital bicuspid valve or in the right coronary cusp of the tricuspid valves.1) Here we report the case of a patient with a fenestrated tricuspid aortic valve with a fibrous strand. The patient had a history of hypertension and suffered from acute AR due to fibrous strand rupture in the left coronary cusp. Case ReportA 76-year-old man underwent aortic valve replacement with a bioprosthetic valve (23 mm) for acute AR. He had a history of hypertension, and his blood pressure was poorly controlled despite medication. Chest X-rays revealed gradual worsening of cardiomegaly since the initiation of medication therapy at 66 years of age. He had no history of rheumatic heart valve disease.At the age of 75 years, moderate AR was identified with echocardiography. However, he did not have any definite symptoms at that time, and medication therapy was continued instead of surgical treatment. Dyspnea on exertion became gradually more severe, and he was transferred to our hospital due to acute heart failure. His blood pressure was 220/96 mmHg and the control of blood pressure was very poor. His body temperature was 36.7°C, and no inflammatory response was observed. Auscultation revealed a diastolic murmur (Levine III/VI) at the right second intercostal sternal border. Chest X-rays revealed cardiomegaly (cardiothoracic ratio = 65%) and pulmonary edema. His electrocardiogram showed a strain T pattern (concentric hypertrophy) in V5 and V6. Serum brain natriuretic peptide (BNP) was extremely high at 426 pg/mL. Echocardiography showed a dilated left ventricular chamber (left ventricular diastolic dimension: 57 mm) with fair contraction (ejection fraction = 50%). The aortic valve was tricuspid; however, fenestrated cusps with fibrous strands were detected in the right coronary cusp and noncoronary cusp. The left coronary cusp was prolapsed and had dropped into the left ventricular chamber. A ruptured fibrous strand was attached to the left co...

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“…[1][2][3] One case reported a severe aortic regurgitation resulting from a congenital downward displacement of anterior aortic annulus on a bicuspid valve with fibrous strands. 4 To our knowledge, our case is the first to describe this mechanism of aortic regurgitation due to the tenting of a tricuspid aortic valve by chordae attached to a dilated aortic root, without annular dilatation or chordae rupture, and without any congenital heart defect ( Figure 4).…”

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confidence: 99%

A Severe Restrictive Aortic Regurgitation Resulting From Valve Tenting by Unusual Aortic Chordae Tendineae Strands

et al. 2012

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W e report a case of a 74-year-old man who presented with progressive dyspnea and hypertension (200/ 63 mm Hg) without any chest pain. He had a history of chronic hypertension and heart murmur several years ago. Physical examination revealed a diastolic murmur with an acute pulmonary edema that required admission in the intensive care unit. The ECG results were normal. There was no fever and no inflammatory syndrome; hemocultures were sterile. Transthoracic echocardiography ( Figure 1, online-only Data Supplement Movies I and II) showed a severe aortic regurgitation on a mildly thickened valve with a mild dilatation of the aortic root (Valsalva aortic diameterϭ46 mm; 25 mm/m 2 ) with a normal annulus diameter (22 mm) and suspected intra-aortic mobile linear echoes.Transesophageal echocardiography (Figure 2, online-only Data Supplement Movies III through VI) showed a tricuspid aortic valve with a large coaptation defect resulting in a massive aortic regurgitation with a mild dilatation of the aortic root and a normal annulus. Several linear mobile echoes looking like chordae tendineae strands were connecting the Valsalva aortic root to the sigmoid cusps, without any

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Aortic regurgitation caused by rupture of a well-balanced fibrous strand suspending a degenerative tricuspid aortic valve

Abstract: Figure 1. Resected aortic valve showing six fibrous strands, with one strand ruptured (black arrow).

Cited by 17 publications

References 3 publications

Pathogenetic Significance of Myxomatous Degeneration in Fenestration-Related Massive Aortic Regurgitation

Pathogenetic Significance of Myxomatous Degeneration in Fenestration-Related Massive Aortic Regurgitation

Aortic Regurgitation Due to Fibrous Strand Rupture in the Fenestrated Left Coronary Cusp of the Tricuspid Aortic Valve

A Severe Restrictive Aortic Regurgitation Resulting From Valve Tenting by Unusual Aortic Chordae Tendineae Strands

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