A 38-year-old woman, from a disadvantaged socioeconomic background, presented to our medical centre with a history of progressively worsening dyspnoea over the past 3 years. Initially categorised as class I, her symptoms worsened to class IV, sporadic haemoptysis, voice alterations accompanied by evident signs of right heart failure including anasarca, distended neck veins, fatigue, palpitations, and intermittent chest discomfort.

Upon examination, she was severely emaciated and displayed tachypnoea, tachycardia, markedly elevated jugular venous pressure, anasarca, and heart murmurs indicative of severe valve abnormalities: a grade V/VI pansystolic murmur in mitral area with radiation to the axilla and back, a short interval between the second heart sound (S2) to opening snap, and a grade IV mid-diastolic murmur without presystolic accentuation.

She was diagnosed of RHD at the age of 20 years. She was recommended treatment involving medications and regular 3 weekly penicillin injections, though adherence was poor due to various constraints. She lost to follow-up.

She had three children and hailed from a socioeconomically disadvantaged environment with limited access to clean water and suboptimal hygiene practices.

Electrocardiography (ECG) showed atrial fibrillation with a rapid ventricular response, while chest X-ray (CXR) exhibited significant cardiomegaly, enlargement of both atria, left pleural effusion, and signs of moderate pulmonary venous hypertension (Fig. 1). Two-dimensional echocardiography (2D ECHO) revealed a spectrum of severe valvular abnormalities, including rheumatic heart disease (RHD), mixed mitral valve disease comprising severe mitral stenosis (MS) with peak and mean gradient of 18 and 11 mm Hg (Fig. 2) with mitral valve area of 0.5 cm2, severe eccentric mitral regurgitation (MR) (Video 01), severe eccentric tricuspid regurgitation (TR) secondary to organic tricuspid valve involvement (Video 02), moderate pulmonary artery hypertension (PAH) (right ventricular systolic pressure = 42 mm Hg + right atrial pressure), mild aortic regurgitation (AR) without aortic stenosis (AS) due to aortic valve involvement (Video 03), giant left atrial enlargement (dimensions of 13 X 10 cm, calculated area 98 cm2) (Fig. 3), giant right atrial enlargement (dimensions of 10.5 X 8 cm, calculated area 65 cm2) (Fig. 4), yet with preserved biventricular function, mild pericardial effusion, and no evidence of left atrial clot formation. Cardiac computerised tomography revealed the grossly enlarged right atrium and left atrium without the evidence of thrombus formation in cardiac chambers (Fig. 5).

Chest X-ray. A Chest X-ray shows cardiothoracic ratio of 0.88 and B chest X-ray demonstrating dilated right atrium (RA), dilated left atrium (LA), tracheal uplifting due to LA enlargement, and left pleural effusion

Two-dimensional echocardiographic assessment of severe mitral stenosis gradient and atrial fibrillation

Two-dimensional echocardiography shows giant left atrium with dimensions of 13.0 × 10.1 cms (A) and area of 98.1 cm2 (B)

Two-dimensional echocardiography shows giant right atrium with dimensions of 10.5 × 8.0 cms (A) and area of 65.3 cm2 (B)

Cardiac computerised tomographic image of giant right atrium with dimensions of 10.7 × 10.5 cms (A) and giant left atrium with dimensions of 14.8 × 13.9 cms (B)

Her treatment protocol commenced with diuretics, beta-blockers, and anticoagulants, followed by a planned surgical intervention involving mitral valve replacement, tricuspid valve repair, and reduction of the left atrial volume. The surgical procedure successfully implemented a 29-mm mechanical mitral valve replacement (St Jude Medical bi-leaflet valve), tricuspid valve repair with annuloplasty ring, and left atrial volume reduction. The procedural bypass time was 210 min, and cross clamp time was 130 min.

One month post-surgery, she exhibited remarkable symptomatic improvement, achieving New York Heart Association (NYHA) class I status, with normalised prosthetic valve function, minimal residual tricuspid regurgitation, absence of pulmonary artery hypertension, and restored biventricular function. She was continued on anticoagulants and penicillin prophylaxis.