Page 178 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt
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The rest-to-exercise response in RV-arterial coupling
We found a significant increase in load (Ea) on the RV in PH patients and control subjects during exercise, while TPVR (= Ea ∙ HR), significantly decreased in PH patients and remained stable in control subjects. Most hemodynamic exercise studies measured load as PVR and showed a decrease or stable PVR during exercise in both PH patients and healthy controls [2, 31-34]. The difference between both measures of load is explained by the way in which they are calculated: PVR as pressure divided by CO, and Ea as pressure divided by SV. Despite the larger RV afterload in PH patients at rest, no differences in RV-arterial coupling between PH patients and control subjects were found, implying that RV-arterial coupling at rest was well maintained. It was shown in a large cohort of IPAH patients, that RV-arterial coupling at rest was maintained in stable PH patients and decreased in PH patients with a more progressive disease [15]. Another study showed a decrease in RV-arterial coupling at rest in PH patients compared to control subjects [35]. In this study, the calculation of Ees was simplified as end-systolic pressure divided by end-systolic volume (measured by MRI), assuming the volume at zero pressure (V0) is zero. However, it has been shown that V0 depends on RV dilatation and therefore that the assumption of V0=0 leads to an underestimation of Ees and RV-arterial coupling [21].
The insufficient response in RV contractility to the increase in load, resulted in a deterioration in RV- arterial coupling during exercise in PH patients, while in control subjects the exertional contractile reserve was sufficient to maintain RV-arterial coupling. Studies of the LV showed that at an Ees/Ea ratio of 1, ventricular stroke work is optimal [14], although maximal ventricular efficiency, defined as ventricular stroke work divided by myocardial oxygen consumption, is reached at an Ees/Ea ratio of 2 [13]. Theoretically, the decrease in RV-arterial coupling in PH patients suggests that the coupling is shifted to an optimal ventricular stroke work at the cost of ventricular efficiency, although this cannot be determined from the current data.
Comparison of ΔEes with the rest-to-exercise change in pulmonary artery pressures
A recent study in PH patients defined the contractile reserve as the increase in systolic pulmonary artery pressure (PAP) during exercise [16]. In this study, a larger increase in sPAP was associated with a better survival. The rationale for using ΔsPAP as a measure of contractile reserve was derived from the pressure-flow relation. The authors stated that a greater increase in pressure allows the ejection of a higher SV and that therefore, the contractile reserve can be described by the increase





























































































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