Tricuspid valve regurgitation in patients with heart failure: does it matter?

Abstract

This editorial refers to ‘Impact of tricuspid regurgitation on survival in patients with chronic heart failure: unexpected findings of a long-term observational study’, by S. Neuhold et al., doi:10.1093/eurheartj/ehs465 Tricuspid regurgitation (TR) aetiologies are currently divided into primary and secondary TR. Intrinsic abnormalities of the tricuspid valve leading to significant TR (primary) are rare and are seen in ∼8–10% of patients with severe TR.1,2 In contrast, secondary TR is the most frequent form of TR requiring surgical intervention. Secondary TR occurs mainly from tricuspid annular dilatation and increased tricuspid leaflet tethering due to right ventricular (RV) enlargement, which is often secondary to left heart failure (HF) from myocardial or valvular causes.3,4 As for secondary mitral regurgitation, secondary TR begets TR. Indeed, TR itself leads to further RV dilation and dysfunction, right atrial enlargement, more tricuspid annular dilatation and tethering, and worsening TR. With increasing TR, the right ventricle dilates and eventually fails, causing increased RV diastolic pressure and, in an advanced situation, a shift of the interventricular septum toward the left ventricle. Such ventricular interdependence might reduce the left ventricular (LV) cavity size (pure compression), causing restricted LV filling and increased LV diastolic and pulmonary artery pressure.5 The resulting increase in left and right atrial pressures may promote atrial fibrillation and precipitate symptom onset ( Figure 1 ). Figure 1 Pathophysiology of tricuspid regurgitation (TR) secondary to left-sided heart valve disease (HVD) and cardiomyopathy. LA, left atrial, LV, left ventricular; RA, right atrial; RV, right ventricular. When present, symptoms are often those of associated diseases. In fact, even if severe, TR may be well tolerated for years. …