Introduction: Tricuspid regurgitation is defined by the passage of an abnormal amount of blood from the right ventricle to the right atrium during ventricular systole. The etiology of tricuspid regurgitation is frequently functional (secondary to dilation tricuspid annulus and / or dysfunction of the right ventricle, or associated with mitral valvular damage). Less often the etiology of tricuspid regurgitation is organic by direct damage of the tricuspid valve and it can be congenital, (associated with congenital disorders or isolated congenital lesion) or tricuspid regurgitation acquired after infectious en-docarditis, rheumatic damage, post thoracic trauma. Mild physiological tricuspid regurgitation has an incre-ased prevalence in echocardiographic studies but most of them show slow progression.
Case presentation: We present the case of a 75-year-old female who was admitted for exertional dyspnea, fatigue, palpitations, progressively worsened symptoms in the past few months. From patient’s cardiac history: permanent atrial fibrillation, moderate mitral regurgi-tation, moderate tricuspid regurgitation. Transthoracic and transesophageal echocardiography confirmed se-vere tricuspid regurgitation with multiple regurgitation jets, severely dilated tricuspid annulus, excess valvular tissue of the leaflets, with coaptation deficiency of the leaflets secondary to chordae rupture with flail of the septal leaflet. Associates severe dilatated right cavities, without interatrial shunt, with indirect echocardiographic signs of pulmonary hypertension, but without di-lation of the pulmonary artery trunk and without dys-function of the right ventricle. It is described moderate mitral regurgitation secondary to dilation of mitral annulus and billowing-mitral changes. In this context, the criteria for surgical valve correction were evaluated. Cardiac catheterization was performed and ruled out the presence of precapillary pulmonary hypertension and identified mild postcapillary pulmonary hypertension. Coronary angiography did not revealed stenoses of epicardial coronary arteries, wi-thout other valvular disease with indication for surgi-cal correction. Tricuspid annuloplasty was considered, but because of the large defect of leaflet coaptation, the effectiveness of this technique was assumed to be ques-tionable. Surgery was performed with replacement of the tricuspid valve with tricuspid biological prosthesis. Postoperatively, the patient showed a favorable evolu-tion, with decrease of right cavities dimensions, with normal ultrasound parameters of the tricuspid pros-thesis, without immediate or late postoperative com-plications, improvement of the symptomatology on exertion.
Conclusions: We consider this case as a severe tricus-pid regurgitation, due to primary valvular damage, with an aspect suggestive for rupture valvular chordae of the tricuspid leaflets, probably in the context of thoracic or idiopathic trauma. The presence of vegetation or perfo-rations of the tricuspid valve was denied. A pre-existing tricuspid valve prolapse is possible, the ultrasound also showed associated mitral valve billowing, condition that may have favored chordae rupture in the context of low-intensity thoracic trauma (the patient had no history of major trauma). Despite echocardiographic criteria of precapillary pulmonary hypertension, this was denied by cardiac catheterization.