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. 2012 Jul;2(3):309-26.
doi: 10.4103/2045-8932.101407.

Right ventricular plasticity and functional imaging

Evan L Brittain  1 , Anna R Hemnes, Mary Keebler, Mark Lawson, Benjamin F Byrd 3rd, Tom Disalvo
Affiliations

Right ventricular plasticity and functional imaging

Evan L Brittain et al. Pulm Circ. 2012 Jul.

Abstract

Right ventricular (RV) function is a strong independent predictor of outcome in a number of distinct cardiopulmonary diseases. The RV has a remarkable ability to sustain damage and recover function which may be related to unique anatomic, physiologic, and genetic factors that differentiate it from the left ventricle. This capacity has been described in patients with RV myocardial infarction, pulmonary arterial hypertension, and chronic thromboembolic disease as well as post-lung transplant and post-left ventricular assist device implantation. Various echocardiographic and magnetic resonance imaging parameters of RV function contribute to the clinical assessment and predict outcomes in these patients; however, limitations remain with these techniques. Early diagnosis of RV function and better insight into the mechanisms of RV recovery could improve patient outcomes. Further refinement of established and emerging imaging techniques is necessary to aid subclinical diagnosis and inform treatment decisions.

Keywords: cardiac magnetic resonance imaging; echocardiography; pulmonary arterial hypertension; right ventricular failure; right ventricular function.

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Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Reproduced with permission from Voelkel et al.[1] RV dilation changes LV geometry decreasing LV preload and worsening diastolic function. If acute, RV dilation may contribute to pericardial constraint, limiting filling of both ventricles. IPAH = idiopathic pulmonary arterial hypertension; LV = left ventricle; RV = right ventricle.
Figure 2
Figure 2
Reproduced with permission from Mertens and Friedberg.[180] (A) %FAC, calculated from measures of the apical four-chamber view. The importance of longitudinal shortening can be appreciated in this image. (B) MPI, calculated by measuring the ejection time on the pulmonary artery tracing and the time between closure and opening of the tricuspid valve on the tricuspid inflow tracing. MPI = (TCOT - ET)/ET. In this patient, the MPI was normal after tetralogy of Fallot repair. (C) TAPSE. An M-mode echocardiogram through the tricuspid annulus is obtained and the excursion of the tricuspid annulus is measured as illustrated. This index enables assessment of longitudinal RV function. (D) Tissue Doppler velocities of the tricuspid annulus. Pulse tissue Doppler measurements can be used to calculate tissue velocities. Systolic velocities can be used as a parameter for systolic longitudinal RV function. (E) Longitudinal strain measurements of the right ventricle, made using speckle tracking technology. By convention, systolic longitudinal shortening is represented as a negative value and can be measured in six different segments. The mean values of these segments are used to trace a mean longitudinal strain curve (white dotted line). The value at end-systole is then measured. (F) Color tissue Doppler echocardiogram at the lateral tricuspid valve annulus and measurement of IVA. Aortic valve opening and closure are depicted by green lines for event timing. The timing of these events may be taken as that of pulmonary valve opening and closure. The slope of IVA is shown. Note that IVA occurs within the QRS complex and peaks before pulmonary valve opening in the isovolumic period. A’= late-diastolic tissue velocity; AVC = aortic valve closure; AVO = aortic valve opening; E’ = early-diastolic tissue velocity; ET = ejection time; %FAC = percentage fraction area change; IVA = isovolumic acceleration; MPI = myocardial performance index; S’ = systolic tissue velocity; TAPSE = tricuspid annular systolic plane excursion; TCOT = tricuspid valve closure-opening time.[179]
Figure 3
Figure 3
(A) RV enlargement and hypertrophy in patient with CTEPH. (B) Normal RV size 6 months after PTE in the same patient as in A. (C) Parasternal short-axis view demonstrating RV dilation and hypertrophy and displacement of septum. (D) Tricuspid regurgitation jet demonstrating severe PH in patient with PAH. (E) Peak systolic velocity of tricuspid annulus borderline depressed at 10 cm/s. (F) TAPSE in patient with PAH measured at 14 mm consistent with RV hypokinesis.
Figure 4
Figure 4
(A) Mild RV and RA dilation with RV hypertrophy and prominent hypertrophy of moderator band. (B) Severe RV and RA dilation with RVH and compression of left-sided chambers by septal deviation. (C) End-stage RV failure with marked RV and RA dilation and thinned out RV free wall. (D) Late gadolinium-enhanced short-axis image demonstrating fibrosis at the RV septal insertion point.
Figure 5
Figure 5
Reproduced with permission from Haddad et al.[181] A decrease in pulmonary arterial pressure in patients with PH may indicate low cardiac output and severe right ventricular failure. CO = cardiac output; MPAP = mean pulmonary artery pressure; PAP = pulmonary artery pressure; PCWP = pulmonary artery capillary wedge pressure; PVR = pulmonary vascular resistance.[180]
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