Prognostic Significance of Ventricular Interdependence in Right Ventricular Pressure Overload: Reduction in Left Ventricular Systolic Strain Predicts Early Mortality in Pulmonary Arterial Hypertension

CHEST Journal ◽  
2011 ◽  
Vol 140 (4) ◽  
pp. 745A
Author(s):  
Evan Hardegree ◽  
Arun Sachdev ◽  
Hector Villarraga ◽  
Naser Ammash ◽  
Robert Frantz ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Prognostic Significance ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Early Mortality ◽  
Ventricular Pressure ◽  
Systolic Strain ◽  
Pulmonary Arterial

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.

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.

scholarly journals Icariin Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension via the Inhibition of TGF-β1/Smads Pathway in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yijia Xiang ◽  
Changhong Cai ◽  
Yonghui Wu ◽  
Lebing Yang ◽  
Shiyong Ye ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Western Blots ◽  
Pulmonary Arterial ◽  
The Right ◽  
Tgf Β1

Background. Pulmonary artery remodeling is important in the development of pulmonary artery hypertension. The TGF-β1/Smads signaling pathway is activated in pulmonary arterial hypertension (PAH) in rats. Icariin (ICA) suppresses the TGF-β1/Smad2 pathway in myocardial fibrosis in rats. Therefore, we investigated the role of icariin in PAH by inhibiting the TGF-β1/Smads pathway. Methods. Rats were randomly divided into control, monocrotaline (MCT), MCT + ICA-low, and MCT + ICA-high groups. MCT (60 mg/kg) was subcutaneously injected to induce PAH, and icariin (50 or 100 mg/kg.d) was orally administered for 2 weeks. At the end of the fourth week, right ventricular systolic pressure (RVSP) was obtained and the right ventricular hypertrophy index (RI) was determined as the ratio of the right ventricular weight to the left ventricular plus septal weight (RV/LV + S). Western blots were used to determine the expression of TGF-β1, Smad2/3, P-Smad2/3, and matrix metalloproteinase-2 (MMP2) in lung tissues. Results. Compared to the control group, RVSP and RI were increased in the MCT group (ρ < 0.05). Additionally, TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were obviously increased (ρ < 0.01). Compared to the MCT group, RVSP and RI were decreased in the MCT + ICA group (ρ < 0.05). TGF-β1, Smad2/3, P-Smad2/3, and MMP2 expressions were also inhibited in the icariin treatment groups (ρ < 0.05). Conclusions. Icariin may suppress MCT-induced PAH via the inhibition of the TGFβ1-Smad2/3 pathway.

Right Ventricular Pressure Waveform and Wave Reflection Analysis in Patients With Pulmonary Arterial Hypertension

CHEST Journal ◽  
2007 ◽  
Vol 132 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Mustafa Karamanoglu ◽  
Michael McGoon ◽  
Robert P. Frantz ◽  
Raymond L. Benza ◽  
Robert C. Bourge ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Wave Reflection ◽  
Ventricular Pressure ◽  
Pressure Waveform ◽  
Pulmonary Arterial

scholarly journals Organ-level right ventricular dysfunction with preserved Frank-Starling mechanism in a mouse model of pulmonary arterial hypertension

2018 ◽  
Vol 124 (5) ◽  
pp. 1244-1253 ◽  
Author(s):  
Zhijie Wang ◽  
Jitandrakumar R. Patel ◽  
David A. Schreier ◽  
Timothy A. Hacker ◽  
Richard L. Moss ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Multiple Time ◽  
Functional Changes ◽  
Pulmonary Arterial ◽  
Organ Level ◽  
Subcellular Level ◽  
Insight Into

Pulmonary arterial hypertension (PAH) is a rapidly fatal disease in which mortality is due to right ventricular (RV) failure. It is unclear whether RV dysfunction initiates at the organ level or the subcellular level or both. We hypothesized that chronic pressure overload-induced RV dysfunction begins at the organ level with preserved Frank-Starling mechanism in myocytes. To test this hypothesis, we induced PAH with Sugen + hypoxia (HySu) in mice and measured RV whole organ and subcellular functional changes by in vivo pressure-volume measurements and in vitro trabeculae length-tension measurements, respectively, at multiple time points for up to 56 days. We observed progressive changes in RV function at the organ level: in contrast to early PAH (14-day HySu), in late PAH (56-day HySu) ejection fraction and ventricular-vascular coupling were decreased. At the subcellular level, direct measurements of myofilament contraction showed that RV contractile force was similarly increased at any stage of PAH development. Moreover, cross-bridge kinetics were not changed and length dependence of force development (Frank-Starling relation) were not different from baseline in any PAH group. Histological examinations confirmed increased cardiomyocyte cross-sectional area and decreased von Willebrand factor expression in RVs with PAH. In summary, RV dysfunction developed at the organ level with preserved Frank-Starling mechanism in myofilaments, and these results provide novel insight into the development of RV dysfunction, which is critical to understanding the mechanisms of RV failure. NEW & NOTEWORTHY A multiscale investigation of pulmonary artery pressure overload in mice showed time-dependent organ-level right ventricular (RV) dysfunction with preserved Frank-Starling relations in myofilaments. Our findings provide novel insight into the development of RV dysfunction, which is critical to understanding mechanisms of RV failure.

scholarly journals Right Ventricular Dysfunction and Failure in Chronic Pressure Overload

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Marc A. Simon ◽  
Michael R. Pinsky
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Cause Of Death ◽  
Ventricular Dysfunction ◽  
Pressure Overload ◽  
Right Ventricular Dysfunction ◽  
Current Understanding ◽  
Diagnosis And Treatment ◽  
Pulmonary Arterial

Right ventricular (RV) dysfunction is the main cause of death in pulmonary arterial hypertension (PAH). Our understanding of the pathophysiology of RV dysfunction is limited but improving. Methods to better diagnose RV dysfunction earlier and treatments specifically designed to minimize or reverse the remodeling process are likely to improve outcomes. We review the current understanding of RV dysfunction in chronic pressure overload and introduce some novel insights based on recent investigations into pathophysiology, diagnosis, and treatment.

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