Aims Atrial functional tricuspid regurgitation (A-FTR) is a recently defined phenotype of functional tricuspid regurgitation (FTR) associated with persistent/permanent atrial fibrillation. Differently from the classical ventricular form of FTR (V-FTR), patients with A-FTR might present with severely dilated right atrium and tricuspid annulus (TA), and with preserved right ventricular (RV) size and systolic function. However, the geometry and function of the right ventricle, right atrium, and TA in patients with A-FTR and V-FTR remain to be systematically evaluated. Accordingly, we sought to: (i) study the geometry and function of the right ventricle, right atrium, and TA in A-FTR by two- and three-dimensional transthoracic echocardiography; and (ii) compare them with those found in V-FTR. Methods and results We prospectively analysed 113 (44 men, age 68 ± 18 years) FTR patients (A-FTR = 55 and V-FTR = 58) that were compared to two groups of age- and sex-matched controls to develop the respective Z-scores. Severity of FTR was similar in A-FTR and V-FTR patients. Z-scores of RV size were significantly larger, and those of RV function were significantly lower in V-FTR than in A-FTR (P < 0.001 for all). The right atrium was significantly enlarged in both A-FTR and V-FTR compared to controls (P < 0.001, Z-scores > 2), with similar right atrial (RA) maximum volume (RAVmax) between A-FTR and V-FTR (P = 0.2). Whereas, the RA minimum volumes (RAVmin) were significantly larger in A-FTR than in V-FTR (P = 0.001). Conclusion Despite similar degrees of FTR and RAVmax size, A-FTR patients show larger RAVmin and smaller TA areas than V-FTR patients. Conversely, V-FTR patients show dilated, more elliptic and dysfunctional right ventricle than A-FTR patients.

We describe 2 patients with Babesia infection who presented with fever and multiple splenic infarcts. There were no other conditions present that could potentially be causes of splenic infarction. Although retinal infarction has been described rarely in patients with babesiosis, splenic infarction has not been reported previously in association with this infection in humans.

Functional tricuspid regurgitation (FTR) is a strong and independent predictor of patient morbidity and mortality if left untreated. The development of transcatheter procedures to either repair or replace the tricuspid valve (TV) has fueled the interest in the pathophysiology, severity assessment, and clinical consequences of FTR. FTR has been considered to be secondary to tricuspid annulus (TA) dilation and leaflet tethering, associated to right ventricular (RV) dilation and/or dysfunction (the “classical”, ventricular form of FTR, V-FTR) for a long time. Atrial FTR (A-FTR) has recently emerged as a distinct pathophysiological entity. A-FTR typically occurs in patients with persistent/permanent atrial fibrillation, in whom an imbalance between the TA and leaflet areas results in leaflets malcoaptation, associated with the dilation and loss of the sphincter-like function of the TA, due to right atrium enlargement and dysfunction. According to its distinct pathophysiology, A-FTR poses different needs of clinical management, and the various interventional treatment options will likely have different outcomes than in V-FTR patients. This review aims to provide an insight into the anatomy of the TV, and the distinct pathophysiology of A-FTR, which are key concepts to understanding the objectives of therapy, the choice of transcatheter TV interventions, and to properly use pre-, intra-, and post-procedural imaging.