Author + information
- Published online March 4, 2019.
- Rebecca T. Hahn, MD∗ (, )@hahn_rt,
- Tammo Delhaas, MD, PhD,
- Paolo Denti, MD and
- Aaron B. Waxman, MD, PhD
- ↵∗Columbia University Medical Center, New York-Presbyterian Hospital, 177 Fort Washington Avenue, New York, New York 10032
The pathophysiology of functional tricuspid regurgitation (FTR) is tied to the morphology and function of the right ventricle (RV) that, in turn, is dependent on left ventricular (LV) size and function, as well as on the compliance of the pulmonary vasculature and the left atrium (LA). Understanding this complex relationship may allow a more physiological approach for the treatment of FTR. The following is a brief overview of some of the important aspects of this complex relationship.
The tricuspid valve (TV) anatomy includes the valve and annulus, as well as the tensor apparatus (papillary muscles and chordae) (1). The tricuspid annulus is dynamic, being larger during ventricular diastole and atrial systole which allows large flow volumes under low pressure, and with a smaller annular area during ventricular systole to enhance leaflet coaptation. The TV tensor apparatus maintains TV function. Two TV leaflets (septal and anterior) are connected to the intraventricular septum (via chordal attachment to the septal papillary muscle or directly to the septum), and 2 leaflets (anterior and posterior) are dependent on a large anterior papillary muscle attached to the anterolateral RV wall. FTR is associated with dilatation and flattening of the annulus and/or dilatation of the RV free wall with papillary muscle displacement and leaflet tethering, which results in failure of leaflet coaptation.
TV function is thus dependent on RV shape and function, and the latter is significantly affected by RV−LV interdependence. Interdependence is not only created by the continuity of the circulation, but also by anatomic features. The muscle layers of the RV are composed of longitudinal deep muscle fibers and circumferential superficial fibers that join the superficial fibers of the LV, which allows the LV to aid in RV ejection. The 2 ventricles also occupy a single pericardial space and share a common interventricular septum (IVS). The IVS forms the stable base against which the RV contracts (the bellows effect). Flattening or reversal of the normal IVS curvature seen in volume overload or pulmonary hypertension, or exaggerated curvature seen in ischemic or nonischemic cardiomyopathies, may thus contribute to FTR.
Finally, the RV shape and function is more sensitive than the LV to acute increases in afterload. RV forward flow depends on a low-impedance distensible pulmonary vascular system and highly compliant LA to pump the same stroke volume as the LV against a closed mitral valve while using approximately two-thirds less stroke work. Thus, pulmonary hypertension, either pre-capillary or post-capillary, will affect RV function and lead to adaptive, followed by maladaptive, remodeling (2). Standard echocardiographic measurements of RV size and function, and pulmonary artery (PA) pressure (3,4) are important in patients with FTR. Perhaps even more important are the measurements of the relationship of RV function to RV afterload, or RV−PA coupling. Although usually measured invasively using pressure−volume loops, a number of investigators have used echocardiographic measures of RV contractility and RV afterload to describe RV−PA coupling.
In summary, FTR is not just a disease of the valve, but it rather involves the complex relationship of the TV to the RV, left heart, and pulmonary vasculature (Figure 1).
Please note: Dr. Hahn is a speaker for Boston Scientific and Bayliss; is a speaker and consultant for Abbott Vascular, Edwards Lifesciences, Philips Healthcare, Siemens Healthineers; is a consultant for 3Mensio, Medtronic, Navigate; and is the Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored trials, for which she receives no direct industry compensation. Dr. Denti has been a consultant for 4Tech. Dr. Waxman serves on steering committees for clinical trials sponsored by United Therapeutics, Medtronic, Gossamer Bio, and Acceleron, but does not receive any direct compensation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2019 American College of Cardiology Foundation
- Tretter J.T.,
- Sarwark A.E.,
- Anderson R.H.,
- Spicer D.E.
- Gorter T.M.,
- van Veldhuisen D.J.,
- Bauersachs J.,
- et al.
- Lang R.M.,
- Badano L.P.,
- Mor-Avi V.,
- et al.
- Harjola V.P.,
- Mebazaa A.,
- Celutkiene J.,
- et al.