Introduction: The aim of this study is to demonstrate unrecognized tricuspid regurgitation leading to heart failure. (1-4) We would like to point out the importance of the ultrasound examination of the heart in detecting severe tricuspid regurgitation.

Case report: 81-years-old patient was admitted to the hospital because of the first clinical manifestation of right ventricular failure. He had acute myocardial infarction in 2009. He hasn’t seen a doctor in 14 years. On admission, he had dyspnea and bradyarrhythmia and massive pretibial edema. NT-proBNP was over 12000 pg/ml. The therapy includes a diuretic, bronchodilator, ACE inhibitor and other necessary drugs. He already has atrial fibrillation, and he is already at oral anticoagulant therapy. 12-lead ECG: dextrogram, atrial fibrillation with ventricular response around 60/beats per minute, right bundle branch block. Echocardiography: aorta normal, left atrium enlarged (Figure 1), diastolic dysfunction, mitral regurgitation 3-4+ (EROA 0.3 cm² and RVol 56ml) (Figure 2); left ventricular ejection fraction 45%, inferior wall akinesis; right atrium and right ventricle are extremely enlarged with spontaneous echo contrast (Figure 3); tricuspid leaflets impaired coaptation; severe TR 4+ in two jets with SPDK=80mmHg (Figure 4); inferior vena cava greatly expanded (about 40mm); vena contracta 15mm.Roentgenogram of lungs and heart: bilateral pleural effusion. Abdominal ultrasound: signs of liver congestion, VCI diameter 42 mm; ascites fluid perihepatic and perisplenic. Therapy at hospital discharge: furosemide, spironolactone, direct oral anticoagulant therapy, ACE inhibitor with mandatory prophylaxis of bacterial endocarditis.

Conclusion: This case report indicates the importance of regular visits to the cardiologist, as well as the importance of timely diagnosis to prevent unwanted cardiac events.