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Right Ventricular Function in Left Ventricular Disease: Pathophysiology and Implications

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The functions of the left and right ventricles are intimately linked. The right ventricle (RV) has transverse muscle fibres in its free wall and also shares oblique fibres in the interventricular septum with the left ventricle (LV). The latter constitute a link between left and right ventricular contractile function such that LV contraction augments RV contraction – a phenomenon called systolic ventricular interaction. When RV afterload is increased (by raised pulmonary artery pressure) overall contractile performance becomes increasingly dependent on this systolic ventricular interaction because the oblique septal fibres are more mechanically efficient than the free wall transverse fibres in conditions of high RV afterload. When LV end diastolic pressure is increased by heart failure due to LV systolic dysfunction, pulmonary artery pressure becomes raised, imposing an increased afterload on the RV. In such patients global LV performance is reduced, consequently systolic ventricular interaction is reduced resulting in a reduction in RV contractile performance even if the RV is not directly involved in the disease process causing LV systolic dysfunction. Furthermore, as the left ventricle becomes progressively more spherical the septal fibres become less oblique, dramatically reducing their mechanical advantage and further impairing RV contractile function. This ultimately leads to clinical right ventricular failure. This in turn typically results in tricuspid regurgitation and a vicious cycle of right ventricular enlargement with further reduction in the oblique nature of the septal fibres. In addition to the systolic interaction of the LV on the RV, when the RV is enlarged and stretches the pericardium, pericardial and right ventricular diastolic pressures may become markedly increased and this can result in constraint to filling of the LV by the pericardium (pericardial constraint) and by the RV via the interventricular septum (diastolic ventricular interaction).

Section snippets

Causes of RV Impairment

RV dysfunction can occur as a consequence of various aetiologies. The RV may be involved as a part of a global disease involving both ventricles such as arrhythmogenic right ventricular cardiomyopathy or dilated cardiomyopathy (DCM). Alternatively the RV can become specifically impaired as a consequence of RV infarction, or right sided valvular disease. However, most commonly, right ventricular failure is a consequence of increased right ventricular afterload in the context of pulmonary

RV Afterload and RV Systolic Dysfunction

The left ventricle is a high pressure pump. Within limits it is able to respond to increased afterload by increasing its contractility [1]. In contrast, beyond foetal life the healthy RV is a pump operating at substantially lower pressures.

The fibre orientation of the RV is key to understanding the response of the RV to increased afterload.

The free wall of the RV comprises transverse fibres. The left ventricle is encircled by oblique fibres [2], (Fig. 1). The interventricular septum consists

The Vicious Cycle of RV Dysfunction

LV systolic dysfunction results ultimately in a globular LV shape with a gradual change in the orientation of the oblique septal fibres to a more transverse configuration. This has adverse consequences for both LV and RV systolic function, (Fig. 3). The combination of pulmonary hypertension and loss of the oblique orientation of the septal fibres frequently leads to progressive RV dilation and the development of clinical RV failure. The RV dilation in turn causes tricuspid regurgitation (TR).

Prognostic Impact of RVSD in LV Disease

Reduced RVEF is a strong prognostic predictor of death or urgent transplantation in HF patients. Ghio et al. studied 379 patients by right heart catheterisation with moderate to severe HF (due to IHD or DCM) and LVEF < 35%, followed up over median time of 17months. Both high mean PAP and low RVEF were found to be independent predictors of survival [13]. The worst survival prognosis was found in patients with combination of high mean PAP and low RVEF.

To date the largest data evaluating the

Diastolic Ventricular Interaction

Whilst the normal LV exerts a favourable systolic interaction on the RV, the enlarged RV with elevated RV diastolic pressure may exert an unfavourable diastolic interaction (diastolic ventricular interaction) on the LV which reduces LV diastolic filling despite an increased LVEDP. Distension of the surrounding pericardium also plays an important role in impeding LV diastolic filling (pericardial constraint). These phenomena have been well described in acute models of pulmonary hypertension [20]

Summary

RV systolic dysfunction frequently coexists with LV systolic dysfunction. Changes in the complex fibre orientation and systolic ventricular interaction can explain this chamber interdependence. RV systolic dysfunction is a potent prognostic marker of outcome in HF patients with LV systolic disease. RV dysfunction is also associated with reduced exercise capacity in this population. The latter can be partly explained by diastolic ventricular interaction which occurs in conditions associated with

Funding

KS is supported by a Medical Research Council grant. SS is supported by a British Heart Foundation grant.

Acknowledgements

We would like to thank our previous collaborators J.V. Tyberg, I. Belenkie and J.J. Atherton who have significantly contributed to the research field of right ventricular function in LV disease.

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