Author + information
- Lee Fong Ling, MD and
- Thomas H. Marwick, MD, PhD, MPH⁎ ()
- ↵⁎Address for correspondence:
Dr. Thomas H. Marwick, Cleveland Clinic, Cardiovascular Medicine J1-5, Euclid Avenue, Cleveland, Ohio 44195
echocardiography is the usual initial test in dyspneic patients, but its application to right ventricular (RV) analysis is challenging. RV evaluation involves 3 steps, starting with quantification of afterload and pre-load. RV afterload is assessed by measurement of pulmonary artery systolic pressure (PASP) from tricuspid regurgitation (TR) velocity and right atrial pressure; pulmonary regurgitation velocity can also be used to assess pulmonary artery (PA) diastolic and mean PA pressure. Estimation of pulmonary vascular resistance (PVR) is useful if RV function is impaired. The second step is to assess the mechanism and severity of TR. For quantification of RV performance, we usually use 1 conventional (tricuspid annular plane systolic excursion [TAPSE], fractional area change [FAC], or right ventricular index of myocardial performance [RIMP]) and 1 novel method (pulsed wave or color Doppler tissue imaging systolic velocity [s'], or strain imaging). RV volumes may be measured using 3-dimensional echocardiography (Fig. 1, Table 1).
Case 1—RV dysfunction with increased PASP and PVR
When RV dysfunction occurs in the setting of left ventricular dysfunction and mitral regurgitation, it may be due to myocardial disease or pulmonary hypertension (PHT). The patient shown in Figure 2 has elevation of both PASP and PVR. There is severe TR with tricuspid annular dilatation (Fig. 3). Although RV parameters show that RV systolic function is impaired (Fig. 4), this is in the context of increased afterload and pre-load.
Case 2—preserved RV systolic function with increased PASP and normal PVR
In patients with right heart failure and severe tricuspid regurgitation, the latter may be secondary from PHT or a primary valvular abnormality. Despite mild elevation of PASP to 44 mm Hg (Fig. 5), PVR was normal (1.3 Wood units). There is severe TR with apical displacement of the septal leaflet and coaptation point (Fig. 6). The RV is volume loaded but RV systolic function is normal (Fig. 7).
Case 3—RV dysfunction with normal PASP and increased PVR
Reduced stroke volume caused by RV dysfunction may compromise the assessment of RV afterload. Increased PA resistance (Fig. 8) is not apparent from PASP because forward RV stroke volume is reduced by severe TR (Fig. 9) and RV dysfunction (Fig. 10).
Case 4—RV dysfunction with normal PASP and PVR
RV dysfunction due to intrinsic right heart disease requires a different management approach to that caused by PHT. In this instance, the PASP and PVR are normal (Fig. 11), and secondary TR (evident from lack of coaptation of the tricuspid valve leaflets and annular dilatation) is severe (Fig. 12). The RV is dilated and RV systolic function is impaired (Fig. 13).
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation