Page 169 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt

Introduction
Precapillary pulmonary hypertension (PH) is characterized by an increase in pulmonary vascular resistance (PVR), increasing the load on the right ventricle (RV). The RV’s ability to cope with the increased load is the most important determinant of survival in PH patients [1]. RV dysfunction tends to be more visible during exercise [2-5] and most PH patients experience exercise intolerance due to an inadequate increase in pulmonary blood flow during physical activity [2, 4]. In healthy individuals, increased demand of oxygen is met by a proportional increase in cardiac output (CO) caused by an increase in stroke volume (SV) and heart rate. In PH patients CO response is truncated during exercise due to a blunted maximal heart rate response together with an inability to increase stroke volume (SV) [3, 5-10]. It is unclear whether exercise intolerance and the impaired CO response to exercise in PH, coincide with a failure to increase RV contractility during exercise, i.e. an impaired exertional contractile reserve.
The only way to assess the exertional contractile reserve is by determining end-systolic elastance (Ees): a load-independent measure of contractility which can be derived either from a family of pressure volume loops or from the so called single beat method [11, 12]. As such, the exertional contractile reserve can be described as the rest-to-exercise response in Ees (ΔEes). Pressure-volume loop analysis also provides the opportunity to determine arterial elastance (Ea), a measure of RV afterload. The matching of Ees to Ea is known as RV-arterial coupling and its preservation is important in terms of ventricular efficiency [13, 14]. Since in PH, Ees is already considerably increased at rest [15], we hypothesized that PH patients are unable to further increase Ees during exercise. Therefore, the increase in Ea will lead to a deterioration of RV-arterial coupling during exercise.
The aim of this study was to investigate in PH patients and no PH controls, the effects of exercise on RV contractility (Ees), arterial elastance (Ea) and RV-A coupling (Ees/Ea). Additionally, the exertional contractile reserve was compared with a recently proposed surrogate measure, the rest-to-exercise change in pulmonary artery pressure (ΔPAP) [16]. The findings of this paper contribute to a better understanding of exercise intolerance and right heart failure in PH. Some of the results of this study has been previously reported in the form of an abstract [17].
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