Welcome to the exciting world of the right ventricle (2024)

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Right ventricular (RV) assessment has been a long time endeavour but difficult for many reasons, anatomic physiologic and imaging. Recently, new approaches have allowed better understanding of the how-to for RV evaluation providing new insights in a number of conditions.^1,2 Right ventricle failure and severe tricuspid regurgitation (TR) have been associated with outcomes following therapy.³ The latest published data demonstrate that worsening RV function and its ratio to pulmonary pressure are common and significantly associated with an increased risk of heart failure (HF) hospitalizations and cardiovascular death in patients with heart failure with preserved EF.⁴

Challenges

Anatomy

Right ventricle is triangular in shape, normally one-third of the size and has one-sixth of the mass of the left ventricle (LV). Furthermore, the curvature of the ventricular septum places the RV outflow tract antero-cephalad to that of the LV resulting in a characteristic ‘cross-over’ relationship between RV and LV outflows.⁴ Musculature of the subpulmonary infundibulum raises the pulmonary valve above the ventricular septum to position the pulmonary valve as the most superiorly situated of the cardiac valves.¹ The pulmonary valve marks the superior margin of the right ventricle while the tricuspid valve marks its right margin (Figure 1).

With regard to the myocardium,¹ this is a complex three-dimensional network of myofibres in a multiple helical arrangement: contraction of these bundles deforms the ventricle and generates ejection, whereas the relaxation aids diastole; moreover, knowing the myofibre orientation helps to understand the pattern of RV contraction in the three-dimensional space. Three main mechanisms contribute to RV pump function: (i) shortening of the longitudinal axis with traction of the tricuspid annulus towards the apex; (ii) inward (radial) movement of the RV-free wall, which is often referred as the ‘bellows effect’; and (iii) bulging of the interventricular septum into the RV during the left ventricular contraction and stretching of the free wall over the septum (causing shortening in the anteroposterior direction).

Physiology

Furthermore, the physiology of the RV is very different from the left. It is a highly trabeculated cavity (septoparietal trabeculation and moderator band) with low-pressure circulation. Acute changes in afterload lead to major changes in RV pressure–volume relationships, and a notable decline in its performance. In terms of myocardial fibres, the normal RV contracts by three separate mechanisms: longitudinal fibres, movement of the free wall towards the septum, and traction on the free wall at the points of attachment to the LV, secondary to LV contraction and LV–RV continuity of the superficial fibres. Interventricular interaction is responsible for RV dilatation and at a later stage impairment, in these patients with LV dysfunction or mitral/aortic valve pathology.

A very important component of RV physiology is RV–pulmonary artery (PA) coupling. A chronically increased RV preload (caused by fluid accumulation) and an increased RV afterload (caused by increased pulmonary vascular resistance and pulmonary venous pressures) result in progressive rightward displacements of both the end-diastolic pressure–volume relationship and the end-systolic pressure–volume relationship. When RV contractility can no longer compensate for the increase in afterload, there is RV–PA uncoupling.^5,6

Imaging of the right ventricle

The echocardiographer needs to follow a more lateral approach close to the axilla to get an on-axis view of the RV. Echocardiography is technically easier if the RV is dilated but still, when studies employed 3D echocardiography and cardiac magnetic resonance (CMR) to compare the two modalities, it was evident that in a dilated RV, the apex may get foreshortened which leads to an underestimation of volumes and ejection fraction in patients with dilated RV when compared to normal.⁷

Echocardiography is the first line modality for RV assessment, starting with a 2D transthoracic exam. Right ventricle qualitative assessment is based on dilatation, hypertrophy, and contractility. Right ventricle quantitative assessment is based on a multiple number of indices, which are either diagnostic for raised pulmonary pressures or prognostic for adverse cardiovascular outcomes. Tricuspid annular plane systolic excursion was one of the first echocardiographic indices described in large clinical trials for HF as well as those for transcatheter interventions. However, it is volume dependent and in those patients with more than moderate TR, the index will be pseudo-normalized. Indices such as RV outflow tract acceleration time and isovolumic relaxation time have been proved to be reflective of RV diastolic function in those patients with early signs of right ventricular decompensation. Pulmonary systolic notch from RV outflow tract has also been demonstrated to correlate well with the pulmonary vascular resistance from right heart catheterization.^5,6

A very important consideration in echocardiography is risk prognostication and stratification of patients.^5,6 The first line imaging of transthoracic echocardiography can separate a pressure vs. volume overloaded right ventricle, and to indirectly characterize pre vs. post vs. mixed pulmonary hypertension. When the right ventricle dilates, the septum shifts towards the LV due to pressure differences across the interventricular septum. This results in the characteristic D-shaped appearance of the LV.

3D Echo underestimates volume, and thus the emergence of computed tomography and CMR analysis of RV gives a chance for true volumetric analysis of RV. Cardiac magnetic resonance is superior in characterizing RV outflow tract in congenital patients as well as identifying the whole of RV apex in dilated ventricles.^7,8

Right ventricle-free wall and global longitudinal strain have been proved to be prognostic in pre-capillary pulmonary hypertensive patients but also in heart failure and cardio-oncology patients. Boczar et al. used echocardiographic methods to follow patients with breast cancer treated with anthracycline-based chemotherapy and revealed significant worsening of RV longitudinal strain 3 months after therapy initiation.^9,10 Lastly, RV contractile reserve has a great potential via exercise stress echocardiography and may be able to be an accurate parameter in the prediction of afterload mismatch post-interventional therapies.⁶

The importance of right ventricular fibrosis

Fibrosis is not only a feature of the ventricular insertion points but also the RV-free wall in pulmonary hypertension (PH) and should be considered a significant component of adverse RV remodelling and a contributor to RV dysfunction in patients with PH. Development of higher resolution T1 mapping sequences and further optimization and standardization of T1 and extracellular volume (ECV) measurements of the RV-free wall have improved the scientific and clinical value of these methods. Increased T1 relaxation times and ECV in ventricular insertion regions and fibre disarray may also be early markers of septal involvement/displacement and deteriorating RV function in patients with PH.¹¹

Open heart surgery and right ventricle

Mechanisms of RVF include suboptimal myocardial protection during surgery, long cardiopulmonary bypass time, RV myocardial ischaemia or infarction, atrial arrhythmias or loss of atrioventricular synchrony, reperfusion lung injury with secondary PH, post-operative pulmonary micro- or macro-embolism, pre-existing pulmonary vascular disease, protamine-induced PH, and others. TRI-SCORE was developed to predict operative mortality risk for tricuspid surgery. It includes clinical (age ≥ 70 years, NYHA functional class III–IV, right-sided heart failure signs, daily dose of furosemide ≥ 125 mg), biomarkers (glomerular filtration rate < 30 mL/min, elevated total bilirubin), and echocardiographic parameters (LV ejection fraction < 60%, moderate/severe RV dysfunction). The TRI-SCORE provides excellent risk assessment independently of TR mechanism and aetiology.⁶ It delineates patients at low-risk, best suited for surgery and those at high surgical-risk and may be considered to define futility in TR treatment vs. those to involve in clinical trials.

Structural interventions: eliminating tricuspid regurgitation or benefit for the right ventricle

The growth in tricuspid structural interventions and the recent FDA approval of the first ever percutaneous tricuspid valve replacement opens up a new space for the right heart. It is now well known that patients with RV ejection fraction < 45% do not benefit from tricuspid edge to edge repair. Accurate RV assessment is pivotal for post-procedural outcomes as well as avoiding afterload mismatch. There is also a tendency for operators to favour tricuspid valve replacement in impaired RV which eliminates TR completely vs. edge to edge which demonstrated comparable results to surgical procedure.^5,6

As a take-home message, the introduction of methods that are truly volumetric and comprehensive, we have a chance to evaluate the independent role of RV remodelling vs. PH in affecting outcome of patients with a variety of disease by appropriate cohorts and clinical trials.

Declarations

Disclosure of Interest

All authors declare no disclosure of interest for this contribution.

References

Published by Oxford University Press on behalf of the European Society of Cardiology 2024.

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