Echocardiography-based Spectrum of Severe Tricuspid Regurgitation: The Frequency of Apparently Idiopathic Tricuspid Regurgitation

Mutlak, Diab; Lessick, Jonathan; Reisner, Shimon A.; Aronson, Doron; Dabbah, Salim; Agmon, Yoram

doi:10.1016/j.echo.2006.09.013

Cited by 154 publications

(110 citation statements)

References 5 publications

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“…Mild tricuspid regurgitation can be found in approximately 70 % of the general population [14]. Moderate-to-severe regurgitation is rarer and is frequently functional [36], is accompanied by pulmonary hypertension and is associated with a poor survival rate [37]. In our series, none of our patients had risk factors for developing tricuspid regurgitation (apart, theoretically, from cabergoline).…”

Section: Discussionmentioning

confidence: 53%

Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia

et al. 2016

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Since the 1990's cabergoline has been the treatment of choice in prolactinoma, as it permits rapid and effective hormonal and tumor control in most cases. Evidence of cardiac valvulopathy was demonstrated in Parkinson's disease patients treated with dopamine agonists. Retrospective studies in prolactinoma patients treated with cabergoline at lower doses did not show such an effect. However, few prospective data with long-term follow-up are available. The aim of this study was to assess the safety of cabergoline regarding cardiac valvular status during prospective follow-up in patients treated for prolactinoma or idiopathic hyperprolactinemia. We report here a series of 100 patients (71F; median age at diagnosis: 41.5 years) treated with cabergoline for endocrine diseases (prolactinoma n = 89, idiopathic hyperprolactinemia n = 11). All patients underwent complete transthoracic echocardiographic studies at baseline and during long-term prospective surveillance using the same equipment and performed by the same technicians. The median interval between baseline and last follow-up echocardiographic studies while on cabergoline was 62.5 months (interquartile range: 34.75-77.0). The median total duration of cabergoline treatment was 124.5 months (interquartile range: 80.75-188.75) and the median cumulative total dose of cabergoline was 277.8 mg (interquartile range :121.4-437.8 mg) at last follow-up. We found no clinically relevant alterations in cardiac valve function or valvular calcifications with cabergoline treatment. Our data suggest that findings from retrospective analyses are correct and that cabergoline is a safe chronic treatment at the doses used typically in endocrinology.

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Section: Discussionmentioning

confidence: 53%

Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia

et al. 2016

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“…Such changes affect the tricuspid valve through 2 mechanistic pathways. First, an enlarged systolic annulus accompanies the larger RV, 29 leading to decreased valve coverage of the annulus. 30 Second, RV enlargement and widening centrifugally displace RV walls and tricuspid papillary muscles attached to each wall 31 away from the tricuspid valve, causing increased tethering and tenting height and area, which, similar to functional mitral regurgitation, 32 yield decreased leaflet coaptation.…”

Section: Morphological Alterations Associated With Tr Changesmentioning

confidence: 99%

Pathophysiology of Tricuspid Regurgitation

et al. 2010

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Background-Respiratory dependence of tricuspid regurgitation (TR), a long-held concept suggested by murmur variation, remains unproven and of unclear mechanisms. PϽ0.0001), increased systolic annular diameter (Pϭ0.003), valve tenting height (PϽ0.0001) and area (PϽ0.0001), and reduced valvular-to-annular ratio (Pϭ0.006). Effective regurgitant orifice during inspiration was independently determined by inspiratory valvular-to-annular ratio (Pϭ0.026) and inspiratory change in right ventricular length-towidth ratio (Pϭ0.008) and valve tenting area (Pϭ0.015). Conclusions-TR is dynamic with almost universal respiratory changes of large magnitude and complex pathophysiology. Methods and Results-InDuring inspiration, a large increase in effective regurgitant orifice causes, despite a decline in regurgitant gradient, a notable increase in regurgitant volume. Effective regurgitant orifice changes are independently linked to inspiratory annular enlargement (decreased valvular coverage) and to inspiratory right ventricular shape widening with increased valvular tenting. These novel physiological insights into TR respiratory dependence underscore right-side heart plasticity and are important for clinical TR severity evaluation. (Circulation. 2010;122:1505-1513.)

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“…In two series of severe tricuspid regurgitation, over 85% of "idiopathic" annular dilatation patients had atrial fibrillation (1,38).…”

Section: Atrial Fibrillationmentioning

confidence: 98%

“…An understanding of non-functional tricuspid regurgitation mandates an appreciation of functional tricuspid regurgitation because the former may ultimately be worsened by some of the same forces that propel the latter (1,2).…”

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confidence: 99%

Non-functional tricuspid valve disease

Adler¹

2017

Ann. Cardiothorac. Surg.

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Only 75% of severe tricuspid regurgitation is classified as functional, or related primarily to pulmonary hypertension, right ventricular dysfunction, or a combination of both. Non-functional tricuspid regurgitation occurs when there is damage to the tricuspid leaflets, chordae, papillary muscles, or annulus, independent of right ventricular dysfunction or pulmonary hypertension. The entities that cause non-functional tricuspid regurgitation include rheumatic and myxomatous disease, acquired and genetic connective tissue disorders, endocarditis, sarcoid, pacing, RV biopsy, blunt trauma, radiation, carcinoid, ergot alkaloids, dopamine agonists, fenfluramine, cardiac tumors, atrial fibrillation, and congenital malformations. Over time, severe tricuspid regurgitation that is initially non-functional, can blend into functional tricuspid regurgitation, related to progressive right ventricular dysfunction. Symptoms and signs, including a falling right ventricular ejection fraction, cardiac cirrhosis, ascites, esophageal varices, and anasarca, may occur insidiously and late, but are associated with substantial morbidity and mortality. Attempted valve repair or replacement at late stages carries a high mortality. Crucial to following patients with severe non-functional tricuspid regurgitation is attention to echo quantification of the tricuspid regurgitation and right ventricular function, patient symptoms, and the physical examination. Keynote Lecture Series Review of non-functional tricuspid regurgitationMore than 75% of severe tricuspid regurgitation is classified as functional or related to pulmonary hypertension or right ventricular dysfunction or dilatation, rather than independent abnormalities of the tricuspid valve components: leaflets, annulus, chordal attachments, and papillary muscles. An understanding of non-functional tricuspid regurgitation mandates an appreciation of functional tricuspid regurgitation because the former may ultimately be worsened by some of the same forces that propel the latter (1,2).The anatomy of the tricuspid valve lends itself to functional impairment. Unlike the dense, separate, fibrous structure, with two fibrous trigones, that surrounds the mitral valve, the tricuspid annulus, with only a right fibrous trigone, blends into the right atrial fibro fatty structures and is more susceptible to dilate or not reduce appropriately in size during systole, with either right atrial or right ventricular dilatation. Only two papillary muscles, albeit with an additional posterior commissural chord, supply three leaflets. The chordal attachments to the anterior leaflet arise largely from the anterolateral papillary muscle, not both papillary muscles, and there is a reliance on attachments to the moderator band and free wall. The smallest leaflet, the septal leaflet, is relatively fixed. Right ventricular expansion can readily tether or restrict the anterior leaflet. The posterior leaflet can become restricted via an interesting mechanism: the posteroseptal portion of the valve is more apically ...

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Echocardiography-based Spectrum of Severe Tricuspid Regurgitation: The Frequency of Apparently Idiopathic Tricuspid Regurgitation

Cited by 154 publications

References 5 publications

Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia

Prospective, long-term study of the effect of cabergoline on valvular status in patients with prolactinoma and idiopathic hyperprolactinemia

Pathophysiology of Tricuspid Regurgitation

Non-functional tricuspid valve disease

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