Tricuspid valve regurgitation (TR) of moderate or high severity affects approximately 0.55% of the general population [1]. TR can be classified based on the underlying mechanisms as primary, secondary or isolated TR (iTR).

Primary tricuspid regurgitation can occur in the course of various conditions affecting valve apparatus such as infective endocarditis, congenital abnormalities, carcinoid heart disease [2], or injury/trauma and accounts for approximately 5% of TR cases. In some cases iatrogenic cause or pacemaker leads wires impinging on leaflets may cause severe tricuspid regurgitation.

On the other hand, the majority (approximately 90%) of TR are functional (also called secondary) [3] which means that they are caused by the dilation and remodelling of the right ventricle (RV) or right atrium and subsequent tricuspid annulus distention with anatomically normal leaflets and chords. This mostly happens due to right ventricle overload in the course of pulmonary hypertension (PH) of various origin. However, in some cases with normal leaflets and tricuspid apparatus, no pulmonary hypertension, an idiopathic tricuspid annulus dilatation may occur leading to isolated tricuspid regurgitation (iTR). It was given more attention in recent years, with novel therapeutic options, as previously TR was considered either rarely primary or ‘secondary’ to pulmonary hypertension [4].

TR velocity is the main echocardiographic marker used to screen patients for pulmonary hypertension (PH) and when it exceeds 3.4 m/s the patient is assigned a high probability of PH regardless of other echocardiographic signs of PH [5]. High PH probability can also be assigned to patients who have TR flow velocity of 2.9–3.4 and additional echocardiographic signs of PH including among the others right atrial and/or ventricular enlargement. Based on echocardiographic probability of PH the patient is referred for further diagnostic tests including right heart catheterization to make a diagnosis of PH or exclude this disease.

However, as emphasized by the guidelines [5], echocardiography can significantly underestimate pulmonary artery pressure in the presence of severe TR which can pose a clinical challenge to differentiate severe iTR from TR due to PH, especially in the presence of other signs of RV overload which may be similar in these two distinct diseases.

In our previous work we have shown that the surface electrocardiogram can differentiate patterns of RV hypertrophy or RV dilatation [6] therefore we hypothesized that ECG patterns can also be useful to differentiate between patients with iTR and TR secondary to PH. Accordingly, in the present study we aimed to assess the utility of ECG to distinguish patients with severe TR, isolated or secondary to PH and consequently the role of ECG in predicting PAH in patients with severe TR.