AIMS: Albeit right ventricular (RV) systolic function is a major determinant of outcomes in various cardiovascular diseases, the quantification remains challenging especially in pathologic loading conditions. In contrast to RV contraction, invasively derived RV contractility is load-independent and could represent the intrinsic potential of RV performance.

METHODS: RV contraction was quantified as ejection fraction (RV-EF) derived from cardiac magnetic resonance imaging prior to invasive hemodynamic characterisation, where RV contractility was derived as end-systolic elastance (RV-Ees) from pressure-volume loop analysis. Hemodynamic responses to handgrip-exercise induced after-load challenge were analysed in different RV loading conditions. In a subgroup of patients undergoing surgical or transcatheter RV load-modifying therapies, the prognostic value of baseline RV-Ees was determined.

RESULTS: A total of 108 patients were included in this analysis. Median patient age was 69 (range 11 to 87 years) in various RV loading conditions including healthy control patients (n=10), RV pressure overload (n=15), volume overload (n=14), pressure and volume overload (n=22) and no overt pressure and volume overload (n=47). Compared to control (median RV-Ees 0.52 mmHg/ml) RV contractility at rest was increased in RV pressure overload and (RV-Ees 0.90 mmHg/ml, p<0.001) and reduced in RV volume overload (RV-Ees 0.33 mmHg/ml, p=0.001). Physiologically, in healthy control contraction (RV-EF) and contractility (RV-Ees) showed a linear relationship. While contraction underestimated contractility in pressure overload, contraction overestimated contractility in volume overload. As a response to handgrip-exercise after-load challenge control cohort showed an increase of RV-Ees (ΔRV-Ees 0.19 mmHg/ml, p=0.009), while patients with RV pressure (ΔRV-Ees 0.07 mmHg/ml, p=0.314) and volume overload (ΔRV-Ees 0.02 mmHg/ml, p=0.385) failed to exhibit RV contractile reserve. In a sub-group of patients (n=30) who underwent load-modifying transcatheter interventions or surgical approaches, baseline RV contractility informed independently on the potential of the RV for RV-EF improvement (AUC 69%, sensitivity 93%, specificity 53%).

CONCLUSION: While RV contraction informs on ventricular performance at a given pre- and afterload, RV contractility represents the ability of the RV to adapt to loading conditions and the potential to recover after correction of pathological RV loading. Integration of RV contractility assessment into clinical practice bares the hope for optimisation of patient selection for novel interventional RV load-modifying therapies in future.


Figure 1: Pressure-volume loop derived right ventricular end-systolic elastance
Pressure-volume loops of control (green), pressure (red) and volume overload group (blue) illustrating the derived baseline ESPVR during pre-load reduction (A) and handgrip exercise challenge (B). While control patients demonstrated contractile reserve in exertion (steeper ESPVR), pressure and volume overloaded group failed to adapt to after-load challenge (ESPVR remains relatively unchanged).


Figure 2: Baseline contractility to predict alteration of right ventricular ejection fraction after load-modifying therapy 
Alterations of RV-EF after load-modifying therapies illustrated in respect to baseline RV-Ees (A). Receiver operating curve identified RV-Ees ≤0.45 mmHg as a proper cut-off to predict improvement of RV contraction >5% (B).