title: Morphologic and functional remodeling of the right ventricle in pulmonary hypertension by real time three dimensional echocardiography.
abstract: The aims of this study were to assess the right ventricle in different causes of pulmonary hypertension (PH) and to assess the changes of the tricuspid apparatus during this remodeling. The functional and morphologic changes of the right ventricle and the tricuspid apparatus in relation to different causes of PH remain elusive. A total of 141 consecutive patients were prospectively recruited, of whom 55 had pulmonary arterial hypertension (PAH), 32 had chronic thromboembolic disease (CTED), and 34 had PH secondary to mitral regurgitation (MR). Twenty age- and gender-matched healthy volunteers were also studied to serve as controls. Real-time 3-dimensional echocardiography was used to assess right ventricular (RV) volumes and tricuspid valve mobility. Overall, RV diastolic volumes were greater and RV ejection fractions lower in patients with PAH compared to those with CTED and MR (186.4 ± 48.8 vs 113.5 vs 109.4 ml, p < 0.001, and 33.2% vs 36.8% vs 66.8%, p < 0.001, respectively). Among the 3 PH groups, tricuspid valve mobility was most restricted in the CTED group and least restricted in the MR group. Tricuspid tenting volume was greater in the CTED and PAH groups than in the MR group (p < 0.01). Most patients with PAH (54.6%) had at least moderate tricuspid regurgitation, while in the CTED group, most (59.4%) had mild and only 37.5% had moderate tricuspid regurgitation (p < 0.01). Conversely, patients with MR (85%) had only mild tricuspid regurgitation. There was no correlation between RV systolic pressures and the RV ejection fraction or tenting volume. In conclusion, this study demonstrates that different causes of PH may lead to diverse RV remodeling, with the most adverse remodeling being in patients with PAH. In addition, changes of the tricuspid apparatus also differed, with the most adverse effects seen in patients with CTED.
authors.affiliation: Department of Cardiology, Hammersmith Hospital, Imperial College London NHS Trust, London, United Kingdom. jgrapsa@gmail.com
authors.forename: Julia
authors.initials: J
authors.lastname: Grapsa
authors.forename: J Simon R
authors.initials: JS
authors.lastname: Gibbs
authors.forename: David
authors.initials: D
authors.lastname: Dawson
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Watson
authors.forename: Ravi
authors.initials: R
authors.lastname: Patni
authors.forename: Thanos
authors.initials: T
authors.lastname: Athanasiou
authors.forename: Prakash P
authors.initials: PP
authors.lastname: Punjabi
authors.forename: Luke S G E
authors.initials: LS
authors.lastname: Howard
authors.forename: Petros
authors.initials: P
authors.lastname: Nihoyannopoulos
mesh_terms: D000328:Adult; D018450:Disease Progression; D019560:Echocardiography, Three-Dimensional / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology; D016278:Ventricular Function, Right / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*