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      Left ventricular diastolic dysfunction in pulmonary hypertension predicts functional capacity and clinical worsening: a tissue phase mapping study

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          Abstract

          Background The function of the right and left ventricles is intimately related through a shared septum and pericardium. Therefore, right ventricular (RV) disease in pulmonary hypertension (PH) can result in abnormal left ventricular (LV) myocardial mechanics. To assess this, we implemented novel cardiovascular magnetic resonance (CMR) tissue phase mapping (TPM) to assess radial, longitudinal and tangential LV myocardial velocities in patients with PH. Methods Respiratory self-gated TPM was performed using a rotating golden-angle spiral acquisition with retrospective cardiac gating. TPM of a mid ventricular slice was acquired in 40 PH patients and 20 age- and sex-matched healthy controls. Endocardial and epicardial LV borders were manually defined, and myocardial velocities calculated using in-house software. Patients without proximal CTEPH (chronic thromboembolic PH) and not receiving intravenous prostacyclin therapy (n = 34) were followed up until the primary outcome of disease progression (death, transplantation, or progression to intravenous therapy) or the end of the study. Physicians who determined disease progression were blinded to CMR data. Conventional ventricular volumetric indices and novel TPM metrics were analyzed for prediction of 6-min walk distance (6MWD) and disease progression. Results Peak longitudinal (p < 0.0001) and radial (p = 0.001) early diastolic (E) wave velocities were significantly lower in PH patients compared with healthy volunteers. Reversal of tangential E waves was observed in all patients and was highly discriminative for the presence of PH (p < 0.0001). The global radial E wave (β = 0.41, p = 0.017) and lateral wall radial systolic (S) wave velocities (β = 0.33, p = 0.028) were the only independent predictors of 6MWD in a model including RV ejection fraction (RVEF) and LV stroke volume. Over a median follow-up period of 20 months (IQR 7.9 months), 8 patients commenced intravenous therapy and 1 died. Global longitudinal E wave was the only independent predictor of clinical worsening (6.3× increased risk, p = 0.009) in a model including RVEF and septal curvature. Conclusions TPM metrics of LV diastolic function are significantly abnormal in PH. More importantly, abnormal LV E wave velocities are the only independent predictors of functional capacity and clinical worsening in a model that includes conventional metrics of biventricular function. Electronic supplementary material The online version of this article (doi:10.1186/s12968-015-0220-3) contains supplementary material, which is available to authorized users.

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          Most cited references36

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          Updated clinical classification of pulmonary hypertension.

          In 1998, a clinical classification of pulmonary hypertension (PH) was established, categorizing PH into groups which share similar pathological and hemodynamic characteristics and therapeutic approaches. During the 5th World Symposium held in Nice, France, in 2013, the consensus was reached to maintain the general scheme of previous clinical classifications. However, modifications and updates especially for Group 1 patients (pulmonary arterial hypertension [PAH]) were proposed. The main change was to withdraw persistent pulmonary hypertension of the newborn (PPHN) from Group 1 because this entity carries more differences than similarities with other PAH subgroups. In the current classification, PPHN is now designated number 1. Pulmonary hypertension associated with chronic hemolytic anemia has been moved from Group 1 PAH to Group 5, unclear/multifactorial mechanism. In addition, it was decided to add specific items related to pediatric pulmonary hypertension in order to create a comprehensive, common classification for both adults and children. Therefore, congenital or acquired left-heart inflow/outflow obstructive lesions and congenital cardiomyopathies have been added to Group 2, and segmental pulmonary hypertension has been added to Group 5. Last, there were no changes for Groups 2, 3, and 4. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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            Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT).

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              Prognostic value of right ventricular mass, volume, and function in idiopathic pulmonary arterial hypertension.

              This study investigated the relationship between right ventricular (RV) structure and function and survival in idiopathic pulmonary arterial hypertension (IPAH). In 64 patients, cardiac magnetic resonance, right heart catheterization, and the six-minute walk test (6MWT) were performed at baseline and after 1-year follow-up. RV structure and function were analysed as predictors of mortality. During a mean follow-up of 32 months, 19 patients died. A low stroke volume (SV), RV dilatation, and impaired left ventricular (LV) filling independently predicted mortality. In addition, a further decrease in SV, progressive RV dilatation, and further decrease in LV end-diastolic volume (LVEDV) at 1-year follow-up were the strongest predictors of mortality. According to Kaplan-Meier survival curves, survival was lower in patients with an inframedian SV index or= 84 mL/m(2), and an inframedian LVEDV
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                Author and article information

                Journal
                Journal of Cardiovascular Magnetic Resonance
                J Cardiovasc Magn Reson
                Springer Science and Business Media LLC
                1532-429X
                December 2015
                December 29 2015
                December 2015
                : 17
                : 1
                Article
                10.1186/s12968-015-0220-3
                9c470880-e5c4-4bbe-a901-e8c4bdc6bee5
                © 2015
                History

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