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Early-diastolic left ventricular lengthening implies pulmonary hypertension-induced right ventricular decompensation.
Cardiovasc Res. 2012 Nov 01; 96(2):286-95.CR

Abstract

AIMS

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.

METHODS AND RESULTS

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).

CONCLUSION

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.

Authors+Show Affiliations

Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, PO Box 616, Maastricht, 6200 MD, The Netherlands. joost.lumens@maastrichtuniversity.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22875469

Citation

Lumens, Joost, et al. "Early-diastolic Left Ventricular Lengthening Implies Pulmonary Hypertension-induced Right Ventricular Decompensation." Cardiovascular Research, vol. 96, no. 2, 2012, pp. 286-95.
Lumens J, Arts T, Marcus JT, et al. Early-diastolic left ventricular lengthening implies pulmonary hypertension-induced right ventricular decompensation. Cardiovasc Res. 2012;96(2):286-95.
Lumens, J., Arts, T., Marcus, J. T., Vonk-Noordegraaf, A., & Delhaas, T. (2012). Early-diastolic left ventricular lengthening implies pulmonary hypertension-induced right ventricular decompensation. Cardiovascular Research, 96(2), 286-95. https://doi.org/10.1093/cvr/cvs251
Lumens J, et al. Early-diastolic Left Ventricular Lengthening Implies Pulmonary Hypertension-induced Right Ventricular Decompensation. Cardiovasc Res. 2012 Nov 1;96(2):286-95. PubMed PMID: 22875469.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early-diastolic left ventricular lengthening implies pulmonary hypertension-induced right ventricular decompensation. AU - Lumens,Joost, AU - Arts,Theo, AU - Marcus,J Tim, AU - Vonk-Noordegraaf,Anton, AU - Delhaas,Tammo, Y1 - 2012/08/08/ PY - 2012/8/10/entrez PY - 2012/8/10/pubmed PY - 2013/3/21/medline SP - 286 EP - 95 JF - Cardiovascular research JO - Cardiovasc. Res. VL - 96 IS - 2 N2 - AIMS: 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. METHODS AND RESULTS: 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). CONCLUSION: 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. SN - 1755-3245 UR - https://www.unboundmedicine.com/medline/citation/22875469/Early_diastolic_left_ventricular_lengthening_implies_pulmonary_hypertension_induced_right_ventricular_decompensation_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1093/cvr/cvs251 DB - PRIME DP - Unbound Medicine ER -