A Hidden Cause of Primary Tricuspid Regurgitation

Abstract

Tricuspid regurgitation (TR) is characterized by the backward flow of blood from the right ventricle to the right atrium during systole. It can be primary, involving intrinsic valve abnormalities, or secondary, due to deformation of the valve apparatus. This case is notable for severe TR following previously unreported chest trauma, emphasizing the importance of detailed medical history in diagnosing valvular conditions. A 62-year-old patient with right atrial and ventricular dilation was diagnosed with severe TR during a routine checkup. Echocardiography showed a prolapsed posterior tricuspid leaflet and annular dilation. Later, a prior chest trauma from a car accident was identified as the likely cause. This case highlights the need for a detailed history and echocardiography to assess TR severity, especially after chest trauma, to prevent right dysfunction and worsening outcomes.

INTRODUCTION

Tricuspid regurgitation (TR) is the backflow of blood from the right ventricle to the right atrium during systole. It can be primary, due to intrinsic structural abnormalities, or secondary, caused by deformation of the valve apparatus without leaflet changes,[1,2,3] often linked to right ventricular dilation. Diagnosis relies on echocardiography to assess severity.[4,5,6] This case highlights severe TR resulting from chest trauma, a rare cause typically associated with motor vehicle accidents (MVAs). Traumatic tricuspid valve (TV) rupture in MVAs occurs due to abrupt deceleration and increased right-sided cardiac pressures, often affecting the tendinous cords, anterior papillary muscle, or anterior leaflet.[7,8] Detailed history taking and echocardiography are critical for timely diagnosis and management of such injuries.[9]

CASE REPORT

A 62-year-old male presented for a routine cardiovascular checkup, denying any history of trauma, cardiovascular disease, or significant illnesses, but reporting palpitations and mild physical limitations consistent with New York Heart Association class II (mild limitations of physical activity). During the examination, signs of jugular venous distension and peripheral edema were noted, raising suspicion of a potential underlying cardiac condition.

An electrocardiogram revealed sinus rhythm with P-wave anomalies. Transthoracic echocardiography [Figure 1] showed significant dilation of the right atrium (61 ml/m²) and right ventricle, with normal left heart structures. The aortic and mitral valves were competent, but eccentric TR was directed toward the interatrial septum (IAS), accompanied by a structural anomaly in the posterior leaflet of the TV. Doppler signal analysis confirmed pathological TR, with regurgitation velocity >2.8 m/s, excluding the possibility of physiological TR.

Figure 1.

Transesophageal echocardiography images: (a) Mid-esophageal view showing grade 4+/4 tricuspid regurgitation with a jet directed toward the interatrial septum; (b) Mid-esophageal view showing tricuspid annular dilation; (c) Mid-esophageal view showing posterior leaflet prolapse of the tricuspid valve (TV); (d) Transgastric view showing the three leaflets of the TV and the origin of the regurgitant jet; (e) Mid-esophageal view showing grade 4+/4 tricuspid regurgitation with a jet directed toward the interatrial septum; (f) three-dimensional transgastric view showing the three leaflets of the TV

Despite the patient’s insistence on having no history of chest trauma, the severity of the TR and the abnormality of the posterior leaflet prompted further investigation. A transesophageal echocardiography (TEE) was performed to confirm these findings and exclude other degenerative or pathological changes in the valve structures. TEE confirmed severe TR (grade 4+/4) with significant prolapse of the posterior leaflet, causing malcoaptation and the formation of a regurgitant jet towards the IAS. In addition, significant annular dilation (50 mm) reinforced the suspicion of long-standing TR, contributing to right atrium dilation.

Quantification of the TR jet using vena contracta measurement (>7 mm) and the convergence zone area (13 mm) provided further evidence of the severity of the condition. The right ventricle remained functionally preserved (fractional area change >0.40, basal diameter 38 mm, mid diameter 30 mm), but the right atrium was markedly dilated. Mild left ventricular diastolic dysfunction was observed, with a transmitral E/E’ ratio <14. TEE ruled out other differential diagnoses, such as Ebstein’s anomaly, rheumatic disease, vegetations, or other structural abnormalities, the patient did not have a cardiac implantable electronic device. The morphofunctional examination excluded the presence of right ventricular atrialization (typical of Ebstein’s anomaly), leaflet thickening or commissural lesions (pathognomonic of rheumatic disease), as well as the presence of vegetations or lesions suggestive of an endocarditic process.

Given the extensive diagnostic workup, the etiology of the TR remained unclear, prompting coronary angiography to exclude ischemic heart disease. The coronary arteries showed no significant stenoses, confirming that ischemic heart disease was not contributing to the valvular dysfunction.

The patient was operated on via a median sternotomy under cardiopulmonary bypass at normothermia. The superior and inferior venae cavae and ascending aorta were cannulated in the usual fashion. Whole blood cardioplegia was administered through the aortic root or the coronary sinus every 20 min. An MC3 annuloplasty ring was implanted. This is the first TV annuloplasty ring anatomically designed to conform to the three-dimensional (3D) shape of the normal TV. This design aims to provide a more normal stress distribution to the leaflets. Since the prolapse involved the posterior leaflet, it was possible to correct it by plicating the corresponding annulus. If the prolapse had involved the anterior or septal leaflets, the “edge-to-edge” technique would have been indicated due to the impossibility of annular plication, compounded by the marked annular dilation. Six months postsurgery, follow-up echocardiography demonstrated complete resolution of the TR, with no residual stenosis or regurgitation. The right atrium returned to near-normal dimensions, and the patient reported marked improvement in signs, including resolution of peripheral edema and palpitations.

Despite these successful outcomes, the cause of the TR remained elusive. However, during subsequent discussions, the patient recalled having been in a car accident approximately a year prior, during which he had sustained chest trauma. Initially deemed unimportant and not reported, the overlap of the traumatic event on a TV with leaflets presumably already myxomatous resulted in a lesion of the posterior leaflet, leading to severe regurgitation. This case highlights the importance of detailed history taking, as the underlying etiology of this significant valvular dysfunction was only uncovered through inquiry into the patient’s past trauma.

DISCUSSION

This case is noteworthy due to the unique etiology of severe TR following previously unreported chest trauma. While TR is commonly secondary to right ventricular dilation or intrinsic valve disease, trauma-induced TR is rare and often overlooked without a detailed medical history. The importance of taking a comprehensive history cannot be overstated, especially in cases where the patient may not initially recall or recognize a relevant traumatic event. In this case, the overlap of the traumatic event on a TV with leaflets presumably already myxomatous resulted in a lesion of the posterior leaflet, leading to severe regurgitation.

The case also underscores the importance of a systematic, multiparametric approach to evaluating TR, and systematic echocardiographic evaluation to avoid underestimating TR severity, as recommended by guidelines.[4] Relying solely on qualitative assessments can lead to underestimation of the severity of the condition, potentially delaying appropriate interventions. Severe TR can cause a progressive cycle of right ventricular dilation, leaflet malcoaptation, and worsening regurgitation, ultimately affecting patient prognosis.[10,11,12] Many patients with chronic severe TR remain asymptomatic for extended periods. When symptoms such as peripheral edema, ascites, or hepatomegaly do appear, they often indicate a more advanced stage of the disease, with elevated right atrial pressure. Unilateral pulmonary edema could further complicate severe TR and should prompt investigation of potential pulmonary vein abnormalities or advanced right-sided heart pathology.[13] This case highlights how severe TR can be secondary to trauma, even when such trauma is initially unreported. Mitral regurgitation can result from MVAs, as trauma-induced papillary muscle rupture-particularly of the posteromedial muscle-causes acute valve dysfunction, similar to what occurs in TV injury.[14]

Timely surgical intervention, as demonstrated here, can lead to favorable outcomes, with complete resolution of regurgitation and restoration of normal heart function.

In conclusion, detailed echocardiographic analysis and a careful review of the patient’s history, particularly in cases where trauma may have gone unreported, are critical for diagnosing and managing TR. This case also emphasizes the importance of cardiovascular imaging after MVAs to assess heart valves for any damage. It further highlights the irreplaceable role of both two-dimensional and 3D transthoracic and transesophageal echocardiography in diagnosing valvular heart diseases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.