Introduction: Right heart failure (RHF) is often treated superficially, many times being considered secondary form to left heart, although it can appear in multiple situations (pulmonary hypertension (PHT), pathology of tricuspid valve/right ventricle (RV)/pericardum) and having important prognostic value.
Methods: We present the case of a 76 years old pati-ent who presented at the emergency room for dyspnea at moderate-mild effort evolved in the last month to dyspnea at rest with orthopnea and bilateral leg swelling. From history and clinical examination we thought at an acute episode of decompensating predo-minat right-sided heart failure – anasarca syndrome. The electrocardiogram showed AF (permanent docu-mented atrial fibrillation) cu 75/min, with negative T waves in V1-V4 and DII, DII and aVF. The laboratory tests revealed a moderate increase in NT-proBNP level to 400 pg/ml. Transthoracic and then transesophage-al echocardiography indicated severe dilatation of the right-sided chambers, severe tricuspid regurgitation, with important coaptation defect of the cusps, throu-gh mixed mechanism – organic (congenital anomaly of the tricuspid valve with hypoplasia of posterior cusp) and functional (annular dilatation), Dilated coronary sinus, pericardial effusion circumferentially distributed in moderate amount, and a normal systolic global and segmental function of the left ventricle.
Results: Due to recent HF syndrome with indirect sign of PHT at echocardiography, we performed a compu-ted tomography of the lung with contrast that revealed chornic obstruction of right inferior lobar artery and then we confirmed it by perfusion lung scintigraphy SPECT. The next step was the cardiac catheterism that cofirmed mild PHT (systolic pressure of pulmonary artery 42 mmHg) with normal pulmonary capillary wedge pressure (14 mmHg), which excluded the im-plication of the left heart in the pathology, and the coronary arteries was permeable. A pulmonary eva-luation was done – walk test with desaturation up to 88%, restrictive ventilatory dysfunction with decrease of vital capacity to 55,8% and severe decrease of alve-olar-capillary difussion to 35,4%. The patient is also known with generalized sporadic psoriasis vulgaris, chronic thyroiditis with euthyroidism without other autoimmune disorders at the rheumatologic screening done to exclude another possible etiological compo-nent of PHT. The persistence of pericardial effusion af-ter the decongestion of the patient was considered to be in the context of severe tricusid valve pathology.
Conclusions: Heart failure remains a syndrome of which etiology must be carefully given. Our case report illustrated 2 mechanisms that conduce to RHF: the in-creased preload of RV – tricuspid regurgitation of mi-xed etiology – mainly congenital organic, associated with increased afterload of RV (mild postembolic PHT) of a patient which also has autoimmune comorbidities. Congenital tricuspid regurgitation is a rare disorder, less met as an isolated lesion and more frequenty in the context of a congenital heart disease.