Whether exercise limitation in chronic thromboembolic pulmonary vascular disease (CTEPVD) is predominantly caused by increased dead space ventilation or impaired cardiac reserve is still a matter of debate. Purpose: To determine the relative contribution of impaired right (RV) of left ventricular (LV) contractile reserve, abnormal pulmonary vascular reserve or increased dead space ventilation on exercise capacity. Methods: Fifty-three subjects [12 controls and 41 CTEPVD patients with (n=28) or

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... ithout (n=13) pulmonary hypertension at rest] underwent cardiopulmonary exercise testing and exercise cardiac magnetic resonance with simultaneous registration of invasive pulmonary and radial artery pressures. The relation between peak oxygen uptake (VO2peak) and ventilatory efficiency (Ve/VCO2), peak dead space ventilation (VD/VT), peak arteriovenous oxygen difference (dAVO2), pulmonary vascular reserve (mPAP/CO slope), contractile reserve, peak cardiac index (CIpeak) and demographics were determined using Pearson's correlation. LV and RV contractile reserve were defined as the peak-to-rest ratio of the end systolic pressure-volume relation (LVESPVR and RVESPVR respectively). Independent determinants of VO2peak in CTEPVD patients were identified using multiple regression analysis. Results: In CTEPVD patients VO2peak correlated strongly with RVESPVR, CIpeak and Ve/VCO2 (all p<0.001), moderately with mPAP/CO slope and VD/VT (both p<0.01) but not with age, LVESPVR or dAVO2 (table 1) . Similarly VO2peak correlated with RVESPVR and CIpeak (both p<0.01) in controls but as opposed to CTEPVD also a significant correlation with LVESPVR (p=0.026) was noted and VO2peak did not correlate with either Ve/VCO2, VD/VT or mPAP/CO (table 1). In CTEPVD patients multiple regression only retained RVESPVR and CIpeak as independent determinants of VO2peak [R 2 =0.58, F(2,38)=26.2, p<0.001].