Page 177 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt

Figure 3: Relation between the change in pulmonary artery pressure and the change in heart rate (Δ HR) from rest-to-exercise. There was a significant relation between the change in pulmonary artery pressure and the change in heart rate from rest-to- exercise (ΔsPAP and ΔHR r=0.579 R2=0.335 p=0.019; ΔmPAP and ΔHR r=0.788 R2=0.621 p<0.001).
The RV exertional contractile reserve (ΔEes)
In line with previous studies, RV contractility (Ees) measured at rest was larger in PH patients than in control subjects [15, 22]. Here we show that PH patients are unable to increase RV contractility during exercise and this suggests that RV contractility is already maximally increased at rest.
As far as we know, the rest-to-exercise response in a load-independent measure of RV contractility has never been studied in healthy subjects. In the left ventricle of healthy humans, the increase in load-independent measures of contractility during exercise [23-25] is largely due to an increase in beta-adrenergic stimulation [26]. The impaired rest-to-exercise response in RV contractility in PH patients could relate to the downregulation and desensitization of beta-adrenergic receptors which has been shown in PH rat models [27] and PH patients [28]. It has been suggested that the increased catecholamine levels at rest in PAH [29], may lead to an inability to increase catecholamine levels during exercise [30]. Interestingly, an impaired inotropic RV response was also observed in a recent study using different PH rat models treated with several inotropic agents [27]. The impaired exertional contractile reserve found in our study, add to the debate whether it is useful to treat PH patients with RV failure with inotropic agents [30]. While a degree of caution has to be taken into account regarding the extrapolation of our findings during submaximal exercise to a situation of RV failure, the usefulness of inotropic agents in PH patients with RV failure should be studied in a randomized controlled trial. Absence of a contractile reserve suggests that it may be more useful to treat RV failure with agents that reverse maladaptive RV remodeling.
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