Page 179 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt

in pressures. In our study ΔPAP did not correlate with ΔEes or with ΔSVI. Since it is known that the increase in SV in PH patients during exercise is only minor [3, 5-9], the increase in CI during exercise is highly HR dependent. Our data showed significant relations between the increases in pulmonary artery pressures and ΔHR. This is in line with a recent study showing a strong relation between ΔmPAP and ΔHR during exercise in PAH patients *7+. Therefore, a large increase in pulmonary artery pressures during exercise seems not to indicate an intact contractile reserve, but rather a more preserved HR response. The ability to increase HR is a well-known predictor of survival [36, 37] and the better survival found by Grunig et al [16] in PH patients with a larger increase in pulmonary artery pressures during exercise could reflect a relatively intact HR response.
Clinical implications
Although a direct link between exercise capacity and RV contractile reserve was not investigated in this study, our findings suggest that a decreased exercise capacity in PH is not only the direct result of an increased pressure in the lung circulation, but also caused by intrinsic changes in RV contractility. Moreover, our study results imply that inotropic drugs may have little value in improving RV dysfunction in PH. Studies are warranted to identify interventions which could restore RV contractile reserve by reversing maladaptive remodeling.
Because the rest-to-exercise response in pulmonary artery pressures was not related to the rest-to- exercise response in Ees, but rather reflected an intact HR response, the rest-to-exercise response in pulmonary artery pressures should not be used as a surrogate measure of the exertional contractile reserve.
Limitations
For safety reasons, we exercised subjects only at submaximal workloads (40% of Wmax). In a sub- analysis hemodynamic data were compared at comparable submaximal workloads of 37W±12 in PH patients and 46W±5 in control subjects (p=0.096). Differences between PH patients and control subjects in rest-to-exercise responses of hemodynamics and load-independent measures of RV function were similar in direction and magnitude as in the data at 40% of Wmax (results not shown). From our results, we cannot determine whether the observed differences at submaximal exercise can be extrapolated to maximal exercise testing.
In the calculation of Ees, we used mPAP as a surrogate for RV end-systolic pressure (RVESP) based on a study of Chemla et al [38] who found that in normal subjects mPAP was closely related to
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