scholarly journals 17β-Estradiol mediates superior adaptation of right ventricular function to acute strenuous exercise in female rats with severe pulmonary hypertension

2016 ◽  
Vol 311 (2) ◽  
pp. L375-L388 ◽  
Author(s):  
Tim Lahm ◽  
Andrea L. Frump ◽  
Marjorie E. Albrecht ◽  
Amanda J. Fisher ◽  
Todd G. Cook ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Aerobic Capacity ◽  
Acute Exercise ◽  
Female Rats ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Exercise Challenge ◽  
17Β Estradiol ◽  
Rv Function

17β-Estradiol (E2) exerts protective effects on right ventricular (RV) function in pulmonary arterial hypertension (PAH). Since acute exercise-induced increases in afterload may lead to RV dysfunction in PAH, we sought to determine whether E2 allows for superior RV adaptation after an acute exercise challenge. We studied echocardiographic, hemodynamic, structural, and biochemical markers of RV function in male and female rats with sugen/hypoxia (SuHx)-induced pulmonary hypertension, as well as in ovariectomized (OVX) SuHx females, with or without concomitant E2 repletion (75 μg·kg−1·day−1) immediately after 45 min of treadmill running at 75% of individually determined maximal aerobic capacity (75% aerobic capacity reserve). Compared with males, intact female rats exhibited higher stroke volume and cardiac indexes, a strong trend for better RV compliance, and less pronounced increases in indexed total pulmonary resistance. OVX abrogated favorable RV adaptations, whereas E2 repletion after OVX markedly improved RV function. E2's effects on pulmonary vascular remodeling were complex and less robust than its RV effects. Postexercise hemodynamics in females with endogenous or exogenous E2 were similar to hemodynamics in nonexercised controls, whereas OVX rats exhibited more severely altered postexercise hemodynamics. E2 mediated inhibitory effects on RV fibrosis and attenuated increases in RV collagen I/III ratio. Proapoptotic signaling, endothelial nitric oxide synthase phosphorylation, and autophagic flux markers were affected by E2 depletion and/or repletion. Markers of impaired autophagic flux correlated with endpoints of RV structure and function. Endogenous and exogenous E2 exerts protective effects on RV function measured immediately after an acute exercise challenge. Harnessing E2's mechanisms may lead to novel RV-directed therapies.

Abstract 19288: Pulmonary Hypertension and Sex Hormone Depletion Affect Lung and Right Ventricular Estrogen Receptor Expression

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Andrea Frump ◽  
Amanda Fisher ◽  
Anthony Cucci ◽  
Marjorie Albrecht ◽  
Kara Goss ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Receptor Expression ◽  
Female Rats ◽  
Sprague Dawley ◽  
Apoptotic Signaling ◽  
Ovx Rats ◽  
Rv Function ◽  
Er Expression

Introduction: Women with pulmonary arterial hypertension exhibit more preserved right ventricular (RV) function than men. The underlying mechanisms are unknown. We measured 17beta-estradiol (E2) levels and lung and RV expression of the two main estrogen receptors (ERalpha and -beta) in male and in intact or ovariectomized (OVX) female rats with Su5416/hypoxia (SuHx)-induced pulmonary hypertension (PH). Hypothesis: E2 is required for adaptation to increased RV afterload in females, and ER expression is inversely correlated with PH severity. Methods: Male and age-matched female Sprague-Dawley rats received Su5416 (20mg/kg), followed by 3 weeks of hypoxia (Patm=362 mmHg) and 4 weeks of room air. Selected females underwent OVX with or without concomitant E2 repletion (75 mcg/kg/d). RV hypertrophy (RV/[LV+S]), RV systolic pressure (RVSP), and PA muscularization were measured; complemented by echocardiographic assessment of RV function and measurement of exercise capacity (VO2max). In addition, we assessed RV pro-apoptotic signaling (bcl-2/bax; caspase-3 activity), serum E2 levels, and lung and RV ER expression by Western blot. N was 7-8/group. P<0.05 was considered significant. Results: While no sex differences were noted in RV/(LV+S), RVSP or PA remodeling, female SuHx rats exhibited more preserved cardiac indices (CI; p<0.05). OVX worsened SuHx-induced alterations in RV hypertrophy, RVSP and CI (p<0.05). In turn, E2 replacement in SuHx-OVX rats prevented SuHx-induced alterations in PH endpoints and RV function; this was accompanied by attenuated RV pro-apoptotic signaling. RV ERbeta decreased in OVX SuHx females, but was restored with E2 repletion (p<0.05). RV ERbeta correlated negatively with RVSP and RV/(LV+S), and positively with RV bcl-2/bax (p<0.05). Similarly, serum E2 levels correlated negatively with RVSP and RV/(LV+S) (p<0.05). While healthy females exhibited higher lung ERbeta than healthy males (p<0.05), no such differences were observed in SuHx-PH. Neither lung nor RV ERalpha was affected by PH or hormone depletion. Conclusions: E2 is required for female adaption to SuHx-PH, through a mechanism that may involve ERbeta-mediated RV cell viability signaling, thus allowing for better adaptation to increases in RV afterload.

Abstract P150: Estrogen Protects Against and Reverses Adverse Ventricular Remodeling in Pulmonary Hypertension-Induced Right Ventricular Failure

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Rangarajan D Nadadur ◽  
Soban Umar ◽  
Andrea Iorga ◽  
Humann Matori ◽  
Rod Partow-Navid ◽  
...  
Keyword(s):  
Gender Differences ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Right Ventricular Failure ◽  
Female Rats ◽  
Male Rats ◽  
Protective Effects ◽  
Ventricular Failure ◽  
Male And Female Rats

Pulmonary hypertension (PH) leads to right-ventricular failure (RVF). RVF is characterized by adverse RV remodeling including hypertrophy and changes in the cardiac Extracellular Matrix (ECM) such as fibrosis and re-expression of cardiac fetal genes. Among the potentially re-expressed genes are the novel ECM interacting proteins Osteopontin (OPN) and Osteocalcin (OCN). Gender differences found in experimental PH are attributed to protective effects of Estrogen (E2). We hypothesize that gender differences observed in experimental PH are partially due to the effects of E2 on the cardiac ECM, and that exogenous E2 may be able to reverse adverse RV remodeling. Male and female rats received single monocrotaline (MCT, 60mg/kg) injection. Some rats were given E2 (42.5μg/kg/day) from day 21–30. Saline treated rats were controls. Cardiopulmonary hemodynamics were serially monitored and RV pressures (RVP) were recorded terminally. RV fibrosis was assessed by trichrome staining. Gene expression was determined by RT PCR and plasma OPN by ELISA. All rats developed PH by day 21 and RVF by day 30. Male rats developed more severe PH-induced RVF than females (RVP=70 vs. 41.5±5 mmHg; RV/(LV+IVS)= 0.69±0.07 vs. 0.47±0.04; RVEF = 30.4±1.8 vs. 42.8±2% resp., all p<0.05). Males also revealed more severe RV fibrosis and greater re-expression of OPN (4.5 fold vs. females, p<0.05) and OCN (2-fold vs. females, p<0.05). Plasma OPN was also elevated in RVF males (1.00±0.11 in control to 1.47±0.18 pg/ml, p<0.05) but not RVF females (0.848±0.18 in control to 0.859±0.294 pg/ml, p=ns). Since females experienced less severe RV remodeling than males, MCT injected males were treated with exogenous E2 from day 21–30. Some E2 treated male rats were sacrificed at day 30, and some were kept an additional 12 days after E2-withdrawal (E2-W group). E2 reversed PH-induced RVF (RVP=38mmHg; RV/(LV+IVS) = 0.28±0.03; RVEF=61.5±0.8%, all p<0.05 vs. male RVF) and fibrosis. OPN and OCN were fully restored following E2 withdrawal by day 42. E2 therapy also restored circulating OPN levels (p<0.05 vs. RVF) showing that OPN has potential value as a plasma marker for PH-induced RV failure. These results suggest that E2 protects against adverse RV remodeling in females, and reverses adverse RV remodeling in males.

CMR markers for early right ventricular dysfunction in precapillary pulmonary hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Vos ◽  
T Leiner ◽  
A.P.J Van Dijk ◽  
F.J Meijboom ◽  
G.T Sieswerda ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Circumferential Strain ◽  
Peak Strain ◽  
Healthy Controls ◽  
Free Wall ◽  
Global Circumferential Strain ◽  
The Right ◽  
Rv Function

Abstract Introduction Precapillary pulmonary hypertension (pPH) causes right ventricular (RV) pressure overload inducing RV remodeling, often resulting in dysfunction and dilatation, heart failure, and ultimately death. The ability of the right ventricle to adequately adapt to increased pressure loading is key for patients' prognosis. RV ejection fraction (RVEF) by cardiac magnetic resonance (CMR) is related to outcome in pPH patients, but this global measurement is not ideal for detecting early changes in RV function. Strain analysis on CMR using feature tracking (FT) software provides a more detailed assessment, and might therefore detect early changes in RV function. Aim 1) To compare RV strain parameters in pPH patients and healthy controls, and 2) to compare strain parameters in a subgroup of pPH patients with preserved RVEF (pRVEF) and healthy controls. Methods In this prospective study, a CMR was performed in pPH patients and healthy controls. Using FT-software on standard cine images, the following RV strain parameters were analyzed: global, septal, and free wall longitudinal strain (GLS, sept-LS, free wall-LS), time to peak strain (TTP, as a % of the whole cardiac cycle), the fractional area change (FAC), global circumferential strain (GCS), global longitudinal and global circumferential strain rate (GLSR and GCSR, respectively). A pRVEF is defined as a RVEF &gt;50%. To compare RV strain parameters in pPH patients to healthy controls, the Mann-Whitney U test was used. Results 33 pPH-patients (55 [45–63] yrs; 10 (30%) male) and 22 healthy controls (40 [36–48] yrs; 15 (68%) male) were included. All RV strain parameters were significantly reduced in pPH patients compared to healthy controls (see table), except for GCS and GCSR. Most importantly, in pPH patients with pRVEF (n=8) GLS (−26.6% [−22.6 to −27.3] vs. −28.1% [−26.2 to −30.6], p=0.04), sept-LS (−21.2% [−19.8 to −23.2] vs. −26.0% [−24.0 to −27.9], p=0.005), and FAC (39% [35–44] vs. 44% [42–47], p=0.02) were still significantly impaired compared to healthy controls. The RV TTP was significantly increased in pPH patients compared to healthy controls (47% [44–57] vs. 40% [33–43], p≤0.001). Conclusions Several CMR-FT strain parameters of the right ventricle are impaired in pPH patients when compared to healthy controls. Moreover, even in pPH patients with a preserved RVEF multiple RV strain parameters (GLS, sept-LS, and FAC) remained significantly impaired, and TTP significantly prolonged, in comparison to healthy controls. This suggests that RV strain parameters may be used as an early marker of RV dysfunction in pPH patients. Funding Acknowledgement Type of funding source: None

scholarly journals Delineating the molecular and histological events that govern right ventricular recovery using a novel mouse model of pulmonary artery de-banding

2019 ◽  
Vol 116 (10) ◽  
pp. 1700-1709 ◽  
Author(s):  
Mario Boehm ◽  
Xuefei Tian ◽  
Yuqiang Mao ◽  
Kenzo Ichimura ◽  
Melanie J Dufva ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mouse Model ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Exercise Capacity ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Sequence Of Events ◽  
Reverse Remodelling ◽  
Rv Function

Abstract Aims The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement of pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model of gradual RV recovery from pressure overload and use it to delineate RV reverse-remodelling events. Methods and results Surgical pulmonary artery banding (PAB) around a 26-G needle induced RV dysfunction with increased RV pressures, reduced exercise capacity and caused liver congestion, hypertrophic, fibrotic, and vascular myocardial remodelling within 5 weeks of chronic RV pressure overload in mice. Gradual reduction of the afterload burden through PA band absorption (de-PAB)—after RV dysfunction and structural remodelling were established—initiated recovery of RV function (cardiac output and exercise capacity) along with rapid normalization in RV hypertrophy (RV/left ventricular + S and cardiomyocyte area) and RV pressures (right ventricular systolic pressure). RV fibrotic (collagen, elastic fibres, and vimentin+ fibroblasts) and vascular (capillary density) remodelling were equally reversible; however, reversal occurred at a later timepoint after de-PAB, when RV function was already completely restored. Microarray gene expression (ClariomS, Thermo Fisher Scientific, Waltham, MA, USA) along with gene ontology analyses in RV tissues revealed growth factors, immune modulators, and apoptosis mediators as major cellular components underlying functional RV recovery. Conclusion We established a novel gradual de-PAB mouse model and used it to demonstrate that established pulmonary hypertension-associated RV dysfunction is fully reversible. Mechanistically, we link functional RV improvement to hypertrophic normalization that precedes fibrotic and vascular reverse-remodelling events.

scholarly journals Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

2001 ◽  
Vol 91 (4) ◽  
pp. 1828-1835 ◽  
Author(s):  
Nicole Stupka ◽  
Peter M. Tiidus
Keyword(s):  
Muscle Damage ◽  
Ischemia Reperfusion Injury ◽  
Serum Insulin ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Female Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

The Influence of Pulmonary Hemodynamics on Right Ventricular Function in Pulmonary Hypertension

2013 ◽  
Author(s):  
Vitaly O. Kheyfets ◽  
Lourdes Rios ◽  
Triston Smith ◽  
Theodore Schroeder ◽  
Jeffrey Mueller ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Pulmonary Hypertension ◽  
Shear Stress ◽  
Right Ventricular ◽  
Pulmonary Arteries ◽  
Pulmonary Hemodynamics ◽  
Arterial Hemodynamics ◽  
Computational Fluid Dynamics Cfd ◽  
Pulmonary Arterial ◽  
Rv Function

Pulmonary arterial hypertension (PAH) is a degenerative disease that can lead to substantial morphometric remodeling of the pulmonary arteries. Previous studies have revealed coupling relationships between right ventricular (RV) function and pulmonary arterial hemodynamics. The objective of this study was to utilize computational fluid dynamics (CFD) to estimate spatially averaged Wall Shear Stress (WSS) for patients with PH and explore correlations between hemodynamics metrics and RV function.

Estradiol-induced attenuation of pulmonary hypertension is not associated with altered eNOS expression

2001 ◽  
Vol 280 (1) ◽  
pp. L88-L97 ◽  
Author(s):  
Thomas C. Resta ◽  
Nancy L. Kanagy ◽  
Benjimen R. Walker
Keyword(s):  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Vascular Tissue ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Inhibitory Influence ◽  
Enos Expression ◽  
17Β Estradiol ◽  
Spermine Nonoate ◽  
Endothelial Nitric Oxide

Female rats develop less severe pulmonary hypertension (PH) in response to chronic hypoxia compared with males, thus implicating a potential role for ovarian hormones in mediating this gender difference. Considering that estrogen upregulates endothelial nitric oxide (NO) synthase (eNOS) in systemic vascular tissue, we hypothesized that estrogen inhibits hypoxic PH by increasing eNOS expression and activity. To test this hypothesis, we examined responses to the endothelium-derived NO-dependent dilator ionomycin and the NO donors S-nitroso- N-acetylpenicillamine and spermine NONOate in U-46619-constricted, isolated, saline-perfused lungs from the following groups: 1) normoxic rats with intact ovaries, 2) chronic hypoxic (CH) rats with intact ovaries, 3) CH ovariectomized rats given 17β-estradiol (E2β), and 4) CH ovariectomized rats given vehicle. Additional experiments assessed pulmonary eNOS levels in each group by Western blotting. Our findings indicate that E2β attenuated chronic hypoxia-induced right ventricular hypertrophy, pulmonary arterial remodeling, and polycythemia. Furthermore, although CH augmented vasodilatory responsiveness to ionomycin and increased pulmonary eNOS expression, these responses were not potentiated by E2β. Finally, responses to S-nitroso- N-acetylpenicillamine and spermine NONOate were similarly attenuated in all CH groups compared with normoxic control groups. We conclude that the inhibitory influence of E2β on chronic hypoxia-induced PH is not associated with increased eNOS expression or activity.

scholarly journals Different effects on right ventricular function in different etiology of secondary tricuspid regurgitation

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
WC Tsai ◽  
WY Lee ◽  
MS Huang ◽  
WH Lee
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Right Ventricular ◽  
Tricuspid Regurgitation ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Right Atrial ◽  
Left Heart ◽  
Left Heart Disease ◽  
Rv Function

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Ministry of Science and Technology, Excutive Yuan, Taiwan Background Tricuspid regurgitation (TR) is traditionally classified as primary or secondary TR. The effects of TR on right ventricular (RV) function were not consistent. We hypothesized that secondary TR is not a unique group, sophisticated sub-grouping can be useful for studying effects of TR on RV function. Methods 207 consecutive patients identified as significant TR (moderate and severe) by echocardiography were recruited. Standard measurements for right heart were done according to guideline. Lateral tricuspid annulus systolic tissue velocity (S’) and RV fractional area change (FAC) were used for RV function. We classified these patients into primary TR and 6 subgroups of secondary TR according to a new systemic approach. Results Mean age of subjects was 71.2 ± 14.7 years, and there were 84 (40.6%) male. There were 29 (14%) primary TR. Secondary TR was further classified into 6 groups included 18 (8.7%) pacemaker related, 81 (39.1 %) left heart diseases, 6 (2.9%) congenital heart diseases, 3 (1.4%) RV myopathy, 27 (13.0%) pulmonary hypertension, and 43 (20.8%) idiopathic TR. Among 4 major groups (congenital heart disease and RV myopathy were not included in analysis due to low numbers) of secondary TR, S’ was significant higher in idiopathic TR and RV FAC were higher in pacemaker related and idiopathic TR. RV dysfunction was defined as FAC &lt; 35%. RV dysfunction presented mostly in pulmonary hypertension related TR and leastly in idiopathic TR (59.3% vs. 14%, p &lt;0.001). Multivariate analysis using idiopathic TR as reference and controlled TR maximal velocity, RV end-diastolic area, right atrial area, and severity of TR, left heart disease related TR had higher risk of RV dysfunction (OR 4.178, 95% CI 1.490-11.703, p = 0.007). Conclusions Effects of TR on RV function were different among different subgroups of secondary TR. Left heart disease related TR had highest risk for RV dysfunction. Secondary TR should not be regarded as a single disease.

CILP1 as a biomarker for right ventricular maladaptation in pulmonary hypertension

2020 ◽  
pp. 1901192
Author(s):  
Stanislav Keranov ◽  
Oliver Dörr ◽  
Leili Jafari ◽  
Christian Troidl ◽  
Christoph Liebetrau ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Protein Expression ◽  
Right Ventricular ◽  
Predictive Power ◽  
Pressure Overload ◽  
Serum Levels ◽  
Left Ventricular ◽  
Dilative Cardiomyopathy ◽  
Significant Difference ◽  
Rv Function

The aim of our study was to analyse the protein expression of cartilage intermediate layer protein 1 (CILP1) in a mouse model of right ventricular (RV) pressure overload and to evaluate CILP1 as a biomarker of cardiac remodelling and maladaptive RV function in patients with pulmonary hypertension (PH).Pulmonary artery banding was performed in 14 mice; another 9 mice underwent sham surgery. CILP1 protein expression was analysed in all hearts by western blotting and immunostaining. CILP1 serum concentrations were measured in 161 patients (97 with adaptive and maladaptive RV pressure overload caused by PH; 25 with left ventricular (LV) hypertrophy; 20 with dilative cardiomyopathy (DCM); 19 controls without LV or RV abnormalities)In mice, the amount of RV CILP1 was markedly higher after banding than after sham. Control patients had lower CILP1 serum levels than all other groups (p<0.001). CILP1 concentrations were higher in PH patients with maladaptive RV function than those with adaptive RV function (p<0.001), LV pressure overload (p<0.001), and DCM (p=0.003). CILP1 showed good predictive power for maladaptive RV in ROC analysis (AUC 0.79). There was no significant difference between the AUCs of CILP1 and NT-pro-BNP (AUC 0.82). High CILP1 (≥cut-off value for maladaptive RV of 4373 pg·mL−1) was associated with lower TAPSE/PASP ratios (p<0.001) and higher NT-pro-BNP levels (p<0.001).CILP1 is a novel biomarker of RV and LV pathological remodelling that is associated with RV maladaptation and ventriculoarterial uncoupling in patients with PH.

scholarly journals Regional Right Ventricular Abnormalities Implicate Distinct Pathophysiological Conditions in Patients With Chronic Thromboembolic Pulmonary Hypertension

2020 ◽  
Vol 9 (21) ◽  
Author(s):  
Hidenori Moriyama ◽  
Takashi Kawakami ◽  
Masaharu Kataoka ◽  
Takahiro Hiraide ◽  
Mai Kimura ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Area Change ◽  
Thromboembolic Pulmonary Hypertension ◽  
Rv Function

Background Right ventricular (RV) dysfunction is a prognostic factor for cardiovascular disease. However, its mechanism and pathophysiology remain unknown. We investigated RV function using RV‐specific 3‐dimensional (3D)‐speckle‐tracking echocardiography (STE) in patients with chronic thromboembolic pulmonary hypertension. We also assessed regional wall motion abnormalities in the RV and chronological changes during balloon pulmonary angioplasty (BPA). Methods and Results Twenty‐nine patients with chronic thromboembolic pulmonary hypertension who underwent BPA were enrolled and underwent right heart catheterization and echocardiography before, immediately after, and 6 months after BPA. Echocardiographic assessment of RV function included both 2‐dimensional‐STE and RV‐specific 3D‐STE. Before BPA, global area change ratio measured by 3D‐STE was significantly associated with invasively measured mean pulmonary artery pressure and pulmonary vascular resistance ( r =0.671 and r =0.700, respectively). Dividing the RV into the inlet, apex, and outlet, inlet area change ratio showed strong correlation with mean pulmonary artery pressure and pulmonary vascular resistance before BPA ( r =0.573 and r =0.666, respectively). Only outlet area change ratio was significantly correlated with troponin T values at 6 months after BPA ( r =0.470), and its improvement after BPA was delayed compared with the inlet and apex regions. Patients with poor outlet area change ratio were associated with a delay in RV reverse remodeling after treatment. Conclusions RV‐specific 3D‐STE analysis revealed that 3D RV parameters were novel useful indicators for assessing RV function and hemodynamics in pulmonary hypertension and that each regional RV portion presents a unique response to hemodynamic changes during treatment, implicating that evaluation of RV regional functions might lead to a new guide for treatment strategies.

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