ReviewRight Ventricular Function in Left Ventricular Disease: Pathophysiology and Implications
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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