Early-diastolic left ventricular lengthening implies pulmonary hypertension-induced right ventricular decompensation

In chronic pulmonary hypertension (PH), right ventricular (RV) failure is associated with shortening of the RV free wall (RVFW) beyond pulmonary valve closure, temporarily paralleled by pronounced lengthening of the left ventricular free wall (LVFW). We hypothesized that this early-diastolic LVFW lengthening is caused by altered RVFW myofibre function and may therefore serve as a non-invasive measure of PH-induced RV (dys)function. In 22 idiopathic pulmonary arterial hypertension (IPAH) patients, five chronic thrombo-embolic PH (CTEPH) patients, and six healthy subjects, ventricular volumes and circumferential strains were obtained using magnetic resonance imaging. RV ejection fraction (RVEF) and stroke volume index (RVSVI) were smaller in IPAH and CTEPH patients than in normals (RVEF: 32 12 and 23 19 vs. 59 14, respectively, both P 0.01; RVSVI: 32 9 and 23 9 vs. 47 6 mL/m(2), both P 0.001). LV early-diastolic strain index (LVEDSI), defined as LVFW strain in the period between LVFW and RVFW peak shortening normalized for total systolic LVFW shortening, was larger in IPAH and CTEPH patients (0.52 0.33 and 0.55 0.40, both P 0.01) than in normals (0.03 0.03). LVEDSI correlated negatively with RVEF (R 0.74, P 0.0001) and RVSVI (R 0.69, P 0.0001). Three multi-scale computer simulations of PH (all with mean pulmonary artery pressure 55 mmHg) with complete, incomplete, and no structural adaptation of ventricular walls to local myofibre load showed that LVEDSI increased with deficiency of cardiac adaptation to PH (0.01, 0.52, and 0.84, respectively). Early-diastolic LV lengthening reflects inadequate structural adaptation of the RVFW to increased myofibre load and is therefore a useful, non-invasive, and easily obtainable predictor of PH-induced RV dysfunction.