scholarly journals Impaired Left Ventricular Longitudinal Function in Idiopathic Pulmonary Arterial Hypertension Children

2016 ◽  
Vol 1 (2) ◽  
pp. 146-152 ◽  
Author(s):  
Iolanda Muntean ◽  
Carmen Șuteu ◽  
Rodica Togănel
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Longitudinal Strain ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
Systolic Strain ◽  
Pulmonary Arterial ◽  
Dyssynchrony Index

Abstract Background: Pulmonary arterial hypertension is associated with right ventricular dilation and failure. As a result, left ventricular geometry is affected by shifting of the interventricular septum towards the left ventricle. Aim of the study: The aim of the study was to assess the effect of chronic right ventricular pressure overload on left ventricular longitudinal function and synchronicity in idiopathic pulmonary arterial hypertension children, using speckle-tracking echocardiography. Material and methods: We prospectively evaluated 13 children (5 with idiopathic pulmonary arterial hypertension and 8 sex- and age-matched controls) using conventional and speckle-tracking echocardiography and clinical status (WHO functional class). Left ventricular longitudinal strain curve was generated for 17 segments and global left ventricular longitudinal peak systolic strain was calculated. Dyssynchrony index of the left ventricle was determined calculating the standard deviation of time to peak-systolic strain for 12 left ventricular, 6 basal and 6 midventricular segments, from short axis views. Results: Strain imaging showed significantly decreased global left ventricular longitudinal strain and increased dyssynchrony index in idiopathic pulmonary arterial hypertension patients as compared with controls (−16.80 ± 2.94 vs. −21.50 ± 1.60, p = 0.003, and 53.80 ± 16.72 vs. 22.25 ± 6.18, p=0.0001, respectively). There was a significant correlation between left ventricular longitudinal strain, dyssynchrony index and right ventricular fractional area changes (r = −0.66, p = 0.013, and r = −0.72, p = 0.005, respectively), right ventricular myocardial performance index (r = 0.86, p = 0.0001, and r = 0.93, p = 0.000, respectively), and LV eccentricity index (r = 0.82, p=0.001, and r = 0.93, p = 0.000, respectively) in the study population as a whole. Conclusions: Left ventricular longitudinal systolic strain and synchronicity are impaired in idiopathic pulmonary arterial hypertension children with normal left ventricular ejection fraction.

scholarly journals Impact of right ventricular dyssynchrony on prognosis of patients with idiopathic pulmonary arterial hypertension

2019 ◽  
Vol 9 (4) ◽  
pp. 204589401988360
Author(s):  
Xiao-Ling Cheng ◽  
Bing-Yang Liu ◽  
Wei-Chun Wu ◽  
Wen Li ◽  
Li Huang ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Speckle Tracking ◽  
Speckle Tracking Echocardiography ◽  
Idiopathic Pulmonary Arterial Hypertension ◽  
World Health ◽  
Peak Strain ◽  
Ventricular Dyssynchrony ◽  
Pulmonary Arterial

Idiopathic pulmonary arterial hypertension is a progressive disease with high mortality with an increasing burden of right ventricular. Right ventricular dyssynchrony was observed in idiopathic pulmonary arterial hypertension, but the association with mortality is unclear. This study aimed to investigate the impact of right ventricular dyssynchrony on the survival of idiopathic pulmonary arterial hypertension. A total of 116 patients with idiopathic pulmonary arterial hypertension were enrolled in this study. All these patients underwent comprehensive clinical evaluation. Right ventricular dyssynchrony was assessed by two-dimensional speckle-tracking echocardiography. The time to peak strain (Tpeak) of right ventricular segments were obtained. Right ventricular dyssynchrony was quantified by the standard deviation of the heart rate-corrected Tpeak of right ventricular four segments. All patients were followed up and the primary endpoint was all cause of death. Results found patients with significant right ventricular dyssynchrony present with advanced World Health Organization functional class, worse hemodynamic status and right ventricular function. Right ventricular dyssynchrony was an independent predictive factor for the survival of idiopathic pulmonary arterial hypertension. Kaplan–Meier survival curves showed patients with right ventricular dyssynchrony had worse prognosis. In conclusion, right ventricular dyssynchrony analyzed by speckle-tracking echocardiography provided added value to hemodynamic and echocardiographic parameters in evaluating the survival of patients with idiopathic pulmonary arterial hypertension.

Right ventricular longitudinal strain with CMR can more accurately estimate right ventricular functional reserve in rats with pulmonary arterial hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Sato ◽  
Y Someya ◽  
Y Takahashi ◽  
K Kumasaka ◽  
W Sato ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Longitudinal Strain ◽  
Weight Ratio ◽  
Contractile Properties ◽  
Funding Source ◽  
Functional Reserve ◽  
Pulmonary Arterial ◽  
Cmr Imaging

Abstract Background Right ventricular (RV) function is an important prognostic factor in patients with pulmonary arterial hypertension (PAH). Recently, CMR has become an attractive modality for follow up and providing prognosis in the patients, and strain has been used as a newer parameter to assess contractile properties of ventricle. It has not yet been established, however, whether RV strain with CMR can estimate RV functional reserve in the patients with PAH. Purpose We focused on CMR imaging of RV, investigating whether RV longitudinal strain can estimate RV functional reserve using a rat model with PAH. Method Rats were given a subcutaneous injection of 60 mg/kg monocrotaline (MCT-rats) or solvent (Ctr-rats). Four weeks after the injection, 25% of MCT-rats died due to RV failure. In the survivors of MCT- (n=19) and Ctr-rats (n=5), retrospective ECG-gated cine MR (16 phases/beat) was imaged with a 7T scanner. Subsequently, we measured RV pressure (RVP) via right internal jugular vein and dissected trabeculae (length = 1.45±0.07 mm, width = 334±27 μm, thickness = 114±6 μm) from RVs. We calculated weight ratio of RV free wall to left ventricle (LV) by RV/(LV+septum). Trabeculae were electrically stimulated with 2-s stimulus intervals, and force was measured using a silicon strain gauge (0.7 mM extracellular Ca2+, 24°C). To determine contractile properties of RV muscle, dF/dt was calculated. Using CMR imaging, we measured RV ejection fraction (RVEF) and RV longitudinal strain (RVLS). To modulate RVP, we intravenously injected 5 nmol endothelin-1 (ET-1) and again measured RVEF and RVLS. Results MCT-rats showed higher systolic RVP (62.5±16.6 vs. 25.9±1.86 mmHg, p<0.01) and higher weight ratio of RV (0.60±0.03 vs. 0.28±0.02, p<0.05). In CMR imaging, MCT-rats showed lower RVEF (36.1±11.2 vs. 64.8±8.4%, p<0.001) and lower RVLS (−18±9 vs. −30±1%, p<0.05). In trabeculae from RVs, MCT-rats showed lower developed force and lower dF/dt (p<0.01). Correlation between RVLS and dF/dt was higher (n=20, r=0.53, p<0.05) than that between RVEF and dF/dt (r=0.24). In addition, RVLS and dF/dt had already been decreased in 5 MCT-rats with relatively preserved RVEF (>50%), suggesting that RVLS decreases earlier than RVEF in MCT-rats. Ten minutes after the injection of ET-1, RVP was increased from 49.4±7.9 to 57.9±6.4 mmHg in MCT-rats (n=6). In MCT-rats with preserved RVEF and decreased RVLS, the increase in RVP chiefly decreased RVEF while it did not change RVLS and RVEF in Ctr-rats, meaning that RV functional reserve had been decreased in MCT-rats. In trabeculae, developed force and dF/dt were increased after the addition of 0.1 μM ET-1 in MCT- (n=11, p<0.01) and Ctr-rats (n=4, p<0.01). Conclusion These results suggest that in rats with PAH, RVLS obtained from CMR can estimate RV functional reserve earlier and more accurately than RVEF. Therefore, RV strain with CMR may become an important parameter to assess RV functional reserve in patients with PAH. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Grant-in-Aid for Young Scientists

Why septal motion is a marker of right ventricular failure in pulmonary arterial hypertension: mechanistic analysis using a computer model

2017 ◽  
Vol 312 (4) ◽  
pp. H691-H700 ◽  
Author(s):  
Georgina Palau-Caballero ◽  
John Walmsley ◽  
Vanessa Van Empel ◽  
Joost Lumens ◽  
Tammo Delhaas
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pressure Gradient ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Ventricular Relaxation ◽  
Pulmonary Arterial ◽  
Rv Function ◽  
Septal Motion

Rapid leftward septal motion (RLSM) during early left ventricular (LV) diastole is observed in patients with pulmonary arterial hypertension (PAH). RLSM exacerbates right ventricular (RV) systolic dysfunction and impairs LV filling. Increased RV wall tension caused by increased RV afterload has been suggested to cause interventricular relaxation dyssynchrony and RLSM in PAH. Simulations using the CircAdapt computational model were used to unravel the mechanism underlying RLSM by mechanistically linking myocardial tissue and pump function. Simulations of healthy circulation and mild, moderate, and severe PAH were performed. We also assessed the effects on RLSM when PAH coexists with RV or LV contractile dysfunction. Our results showed prolonged RV shortening in PAH causing interventricular relaxation dyssynchrony and RLSM. RLSM was observed in both moderate and severe PAH. A negative transseptal pressure gradient only occurred in severe PAH, demonstrating that negative pressure gradient does not entirely explain septal motion abnormalities. PAH coexisting with RV contractile dysfunction exacerbated both interventricular relaxation dyssynchrony and RLSM. LV contractile dysfunction reduced both interventricular relaxation dyssynchrony and RLSM. In conclusion, dyssynchrony in ventricular relaxation causes RLSM in PAH. Onset of RLSM in patients with PAH appears to indicate a worsening in RV function and hence can be used as a sign of RV failure. However, altered RLSM does not necessarily imply an altered RV afterload, but it can also indicate altered interplay of RV and LV contractile function. Reduction of RLSM can result from either improved RV function or a deterioration of LV function. NEW & NOTEWORTHY A novel approach describes the mechanism underlying abnormal septal dynamics in pulmonary arterial hypertension. Change in motion is not uniquely induced by altered right ventricular afterload, but also by altered ventricular relaxation dyssynchrony. Extension or change in motion is a marker reflecting interplay between right and left ventricular contractility.

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