INTRODUCTION

Trivial to mild tricuspid regurgitation is commonly seen in echocardiography of patients with a normal right heart. Causes of tricuspid regurgitation may be primary from an intrinsic valve defect such as rheumatic heart disease, Eibstein anomaly or prolapse from myxomatous valve changes. Tricuspid regurgitation is generally well tolerated and mostly asymptomatic. Symptoms of tricuspid regurgitation are predominantly related to right-sided heart failure such as ascites, edema and congestive hepatopathy. Tricuspid regurgitation when severe, may be considered for surgical replacement.

A 46-year-old female with no known comorbidities presented with 8 months duration of progressive bipedal edema. It was not accompanied by other signs of heart failure such as orthopnea, paroxysmal nocturnal dyspnea or exertional dyspnea. She initially sought consult with an internist and was given Furosemide on an as needed basis which helped relieve the edema. A month prior to admission, patient then noted persistence of edema despite daily intake of furosemide. At the time of admission, patient already had icteric sclerae, clear breath sounds, grade 4/6 systolic murmur loudest on 4^th ICS, augmented by inspiration, with presence of RV heave and bipedal edema. Her 12L ECG showed sinus rhythm, right ventricular hypertrophy with QT prolongation (Figure 1). A transthoracic echocardiogram was then done which revealed dilated right ventricle with RV base of 4.7cm, dilated right atrium with right atrial area of 26.5cm² and severe tricuspid regurgitation with DTI of 11cm/s, severe torrential regurgitation with vena contracta of 2.3cm (Figure 2). Right ventricular systolic function was normal with RV Fractional Area of Change (FAC) of 51.3% and TAPSE of 2cm. Cardiac MRI was done to investigate for other possible etiologies of the tricuspid regurgitation and to evaluate the right ventricular size and function. Cardiac MRI showed markedly dilated right ventricle with normal systolic function, enhancement of right ventricular insertion points which may be seen in right ventricular overload, dilated tricuspid valve annulus at 4cm and torrential tricuspid regurgitation with regurgitant volume of 77ml and regurgitant fraction of 75% (see Figure 3). Autoimmune work up was also done to rule out secondary causes of tricuspid regurgitation (see Table 1). Preoperative left and right heart catheterization was done which showed ventricularized c-v wave, attenuated x descent and rapid downstroke of y wave, elevated right sided pressures, pulmonary artery systolic pressure of 39.26mmHg, right ventricle pressure of 43/33mmHg and right atrial pressure of 43/32mmHg. Patient then underwent tricuspid valve replacement with a 29mm bioprosthetic valve. Intra-operatively, patient was noted to have dilated tricuspid valve annulus, retracted septal leaflet and part of anterior leaflet near anteroseptal commissure, chordae tendinae and leaflet were not thickened (see Figure 4). Final histopathology report showed myxomatous degeneration of valve leaflets. Post-operatively, patient developed increasing shortness of breath and orthopnea, with episodes of hypotension. A transthoracic echo was then done which revealed decompensation of the right ventricular systolic function with RV FAC now at 16% from previous of 49.3% but noted decrease in right atrial and ventricular size. Patient was then started on inotropic support with norepinephrine and milrinone. Adequate diuresis was also done with furosemide and spironolactone. Patient was then gradually weaned off from inotropes and maintained on oral diuresis with furosemide and spironolactone. Prior to discharge, a repeat 2D echo was done which showed slight improvement of right ventricular systolic function and presence of pericardial effusion. Colchicine was then added to home meds for the pericardial effusion.