Pulmonary Artery Stiffness Research Articles

Relationship between Pulmonary Artery Stiffness and Functional Capacity in Patients with Heart Failure with Reduced Ejection Fraction.

Background and ObjectivesFunctional capacity varies significantly among patients with heart failure with reduced ejection fraction (HFrEF), and it remains unclear why functional capacity is severely compromised in some patients with HFrEF while it is preserved in others. In this study, we aimed to evaluate the role of pulmonary artery stiffness (PAS) in the functional status of patients with HFrEF.MethodsA total of 46 heart failure (HF) patients without overt pulmonary hypertension or right HF and 52 controls were enrolled in the study. PAS was assessed on parasternal short-axis view using pulsed-wave Doppler recording of pulmonary flow one centimeter distal to the pulmonic valve annulus at a speed of 100 mm/sec. PAS was calculated according to the following formula: the ratio of maximum flow velocity shift of pulmonary flow to pulmonary acceleration time.ResultsPAS was significantly increased in the HFrEF group compared to the control group (10.53±2.40 vs. 7.41±1.32, p<0.001). In sub-group analysis of patients with HFrEF, PAS was significantly associated with the functional class of the patients. HFrEF patients with poor New York Heart Association (NYHA) functional capacity had higher PAS compared those with good functional capacity. In multivariate regression analysis, NYHA class was independently correlated with PAS.ConclusionPAS is associated with functional status and should be taken into consideration as an underlying pathophysiological mechanism of dyspnea in patients with HFrEF.

The predictive capabilities of a novel cardiovascular magnetic resonance derived marker of cardiopulmonary reserve on established prognostic surrogate markers in patients with pulmonary vascular disease: results of a longitudinal pilot study

BackgroundNo unified method exists to effectively predict and monitor progression of pulmonary arterial hypertension (PAH). We assessed the longitudinal relationship between a novel marker of cardiopulmonary reserve and established prognostic surrogate markers in patients with pulmonary vascular disease.Methods and ResultsTwenty participants with confirmed (n = 14) or at high risk (n = 6) for PAH underwent cardiovascular magnetic resonance (CMR) at baseline and after ~6 months of guideline-appropriate management. Ten PAH participants underwent RHC within 48 h of each CMR. RHC (mean pulmonary arterial pressure, mPAP; pulmonary vascular resistance index, PVRI; cardiac index, CI) and phase-contrast CMR (mean pulmonary arterial blood flow velocity, meanPAvel) measurements were taken at rest and during continuous adenosine infusion (70/140/210 mcg/kg/min). Initial meanPAvel’s (rest and hyperemic) were correlated with validated surrogate prognostic parameters (CMR: RV ejection fraction, RVEF; RV end systolic volume indexed, RVESVI; RHC: PVRI, CI; biomarker: NT-pro brain natriuretic peptide, NTpBNP; clinical: 6-min walk distance, 6MWD), a measure of pulmonary arterial stiffness (elastic modulus) and volumetric estimation of RV ventriculoarterial (VA) coupling. Changes in meanPAvel’s were correlated with changes in comparator parameters over time.At initial assessment, meanPAvel at rest correlated significantly with PVRI (inversely), CI (positively) and elastic modulus (inversely) (R2 > 0.37,P < 0.05 for all), whereas meanPAvel at peak hyperemia correlated significantly with PVRI, RVEF, RVESVI, 6MWD, elastic modulus and VA coupling (R2 > 0.30,P < 0.05 for all). Neither resting or hyperemia-derived meanPAvel correlated with NTpBNP levels. Initial meanPAvel at rest correlated significantly with RVEF, RVESVI, CI and VA coupling at follow up assessment (R2 > 0.2,P < 0.05 for all) and initial meanPAvel at peak hyperemia correlated with RVEF, RVESVI, PVRI and VA coupling (R2 > 0.37,P < 0.05 for all). Change in meanPAvel at rest over time did not show statistically significant correlation with change in prognostic parameters, while change in meanPAvel at peak hyperemia did show a significant relationship with ΔRVEF, ΔRVESVI, ΔNTpBNP and ΔCI (R2 > 0.24,P < 0.05 for all).ConclusionMeanPAvel during peak hyperemia correlated with invasive, non-invasive and clinical prognostic parameters at different time points. Further studies with predefined clinical endpoints are required to evaluated if this novel tool is a marker of disease progression in patients with pulmonary vascular disease.

Pulmonary vascular collagen content, not cross-linking, contributes to right ventricular pulsatile afterload and overload in early pulmonary hypertension.

The present study found an important role for collagen content, but not collagen cross-linking, in the pulsatile right ventricular (RV) afterload, which is correlated with RV hypertrophy. These results uncover a new collagen-mediated mechanical mechanism of RV dysfunction in early pulmonary hypertension progression. Furthermore, our results suggest that measures and metrics of pulsatile hemodynamics such as pulse pressure and pulse wave velocity are potentially important to cardiovascular mortality in patients with pulmonary hypertension.

Chronic Obstructive Pulmonary Disease and Arterial Stiffness

Comorbidities are common in chronic obstructive pulmonary disease (COPD). Cardiovascular comorbidity is a leading cause of morbidity and mortality in COPD patients. Low lung function is a risk factor for increased arterial stiffness, a condition that is common in COPD patients, independent of conventional cardiovascular risk factors. Arterial stiffness is an independent risk factor both for all-cause and for cardiovascular mortality, and carotid–femoral pulse wave velocity is the gold standard for the assessment of arterial stiffness. Various mechanisms proposed in the development of arterial stiffness include systemic inflammation, ageing, advanced glycation end products, renin–angiotensin–aldosterone system, increased elastolysis, and vitamin D deficiency. Early detection of arterial stiffness in COPD patients is warranted to detect cardiovascular comorbidity at the subclinical stage, which would help to prevent overt vascular events in the future. We need well-designed studies to see the impact of therapy that targets increased arterial stiffness on future cardiovascular events in COPD. This review discusses the epidemiology, diagnosis, and therapy of increased arterial stiffness in COPD patients.

Assessment of proximal pulmonary arterial stiffness using magnetic resonance imaging: effects of technique, age and exercise.

IntroductionTo compare the reproducibility of pulmonary pulse wave velocity (PWV) techniques, and the effects of age and exercise on these.Methods10 young healthy volunteers (YHV) and 20 older healthy volunteers (OHV) with no cardiac or lung condition were recruited. High temporal resolution phase contrast sequences were performed through the main pulmonary arteries (MPAs), right pulmonary arteries (RPAs) and left pulmonary arteries (LPAs), while high spatial resolution sequences were obtained through the MPA. YHV underwent 2 MRIs 6 months apart with the sequences repeated during exercise. OHV underwent an MRI scan with on-table repetition. PWV was calculated using the transit time (TT) and flow area techniques (QA). 3 methods for calculating QA PWV were compared.ResultsPWV did not differ between the two age groups (YHV 2.4±0.3/ms, OHV 2.9±0.2/ms, p=0.1). Using a high temporal resolution sequence through the RPA using the QA accounting for wave reflections yielded consistently better within-scan, interscan, intraobserver and interobserver reproducibility. Exercise did not result in a change in either TT PWV (mean (95% CI) of the differences: −0.42 (−1.2 to 0.4), p=0.24) or QA PWV (mean (95% CI) of the differences: 0.10 (−0.5 to 0.9), p=0.49) despite a significant rise in heart rate (65±2 to 87±3, p<0.0001), blood pressure (113/68 to 130/84, p<0.0001) and cardiac output (5.4±0.4 to 6.7±0.6 L/min, p=0.004).ConclusionsQA PWV performed through the RPA using a high temporal resolution sequence accounting for wave reflections yields the most reproducible measurements of pulmonary PWV.

Fever, abdominal distension, polyserositis

Objective To provide useful information for the diagnosis and differentiation through exploring the tumor with polyserositis as the initial symptom. Methods There was a case present with fever, poor spirit, abdominal distention and edema in Children′s Hospital of Hebei Province.The characteristics and results of physical examination were summarized and discussed according to the condition evolution phases.The possible etiological factors were analyzed.The treatment was adjusted.Further physical examination was improved.The final diagnosis was tracked. Results After getting admitted to hospital, the patient received CT scan and ultrasound examination for many times.The results suggested the pericardial effusion, pleural effusion, peritoneal effusion and cardiac insufficiency.The child had made a slight improvement through treatment.However, he had hemiparesis.Cerebral infarction was demonstrated through magnetic resonance imaging(MRI), magnetic resonance angiography(MRA), magnetic resonance venography(MRV). Ultrasound showed that there was more pericardial effusion, aortic root solid low echo mass, pulmonary arterial wall stiffness, left and right pulmonary artery blood flow speed increased.Neck and chest enhanced CT showed mediastinal lesions.Pathology examination results suggested myeloid sarcoma after referral to superior hospital. Conclusions When children had an unexplained polyserositis, more comprehensive analysis were needed.The illness condition should be explained with Monism as far as possible.Repeated inspections would be necessary when the pathogenesis was not clear.Careful watch for the tumor should be kept. Key words: Polyserositis; Heart failure; Cerebral infarction; Tumour

Reduced haemodynamic coupling and exercise are associated with vascular stiffening in pulmonary arterial hypertension

ObjectiveInadequate right ventricular (RV) and pulmonary arterial (PA) functional responses to exercise are important yet poorly understood features of pulmonary arterial hypertension (PAH). This study combined invasive catheterisation with echocardiography...

Ozone and PM2.5 in the air pollution mixture differentially impact cardiopulmonary pathophysiologic mechanisms

Introduction: The relative contributions of ozone (O3) and PM2.5 in air pollution mixtures to cardiopulmonary outcomes remain poorly understood. This study examines whether and how O3 and PM2.5 may differentially impact mechanisms of cardiopulmonary pathophysiology. Methods: Exposures to each pollutant were manipulated for 89 office workers living together on a work campus in China with various combinations of an O3-generating electrostatic precipitator (ESP) and a high efficiency particulate air (HEPA) filter. Subjects were measured for biomarkers of cardiopulmonary pathophysiology at four time points each separated by 2-3 week intervals. Results: Mean 24-hour exposure concentrations during the study were 37 ± 1.5 µg/m3 for PM2.5 and 6.4 ± 0.2 ppb for O3, and they were significantly negatively correlated. Contrary to previous literature showing these biomarkers all being associated with PM2.5 exposure, this study shows that lung inflammation (fractional exhaled nitric oxide and exhaled breath condensate (EBC) nitrite and nitrate), systolic and diastolic blood pressure, and platelet activation (soluble P-selectin (sP-sel)) were tightly associated with short-term and chronic O3 exposure. In contrast, pulmonary oxidative stress (EBC malondialdehyde), arterial stiffness (augmentation index), and endothelial cell dysfunction (von Willebrand factor (VWF)) were significantly associated with chronic PM2.5 exposure. For example, an interquartile range (IQR) increase in 24-hour O3 exposure concentration (4.1 ppb) and 2-week mean ambient O3 (11.0 ppb) was significantly associated with a 12.5% and 27.4% increase in sP-sel, respectively. An IQR increase in 2-week mean ambient PM2.5 (41.4 µg/m3) was associated with a significant 11.2% increase in VWF. Conclusions: These findings have provided insights into biological mechanisms by which O3 and PM2.5 can differentially enhance cardiopulmonary disease risk.

Distal vessel stiffening is an early and pivotal mechanobiological regulator of vascular remodeling and pulmonary hypertension.

Pulmonary arterial (PA) stiffness is associated with increased mortality in patients with pulmonary hypertension (PH); however, the role of PA stiffening in the pathogenesis of PH remains elusive. Here, we show that distal vascular matrix stiffening is an early mechanobiological regulator of experimental PH. We identify cyclooxygenase-2 (COX-2) suppression and corresponding reduction in prostaglandin production as pivotal regulators of stiffness-dependent vascular cell activation. Atomic force microscopy microindentation demonstrated early PA stiffening in experimental PH and human lung tissue. Pulmonary artery smooth muscle cells (PASMC) grown on substrates with the stiffness of remodeled PAs showed increased proliferation, decreased apoptosis, exaggerated contraction, enhanced matrix deposition, and reduced COX-2-derived prostanoid production compared with cells grown on substrates approximating normal PA stiffness. Treatment with a prostaglandin I2 analog abrogated monocrotaline-induced PA stiffening and attenuated stiffness-dependent increases in proliferation, matrix deposition, and contraction in PASMC. Our results suggest a pivotal role for early PA stiffening in PH and demonstrate the therapeutic potential of interrupting mechanobiological feedback amplification of vascular remodeling in experimental PH.

OP-011 The Relationship Between Pulmonary Artery Stiffness and Functional Capacity in Patients With Heart Failure

OP-011 The Relationship Between Pulmonary Artery Stiffness and Functional Capacity in Patients With Heart Failure

OP-075 The Evaluation of the Relationship between Pulmonary Artery Stiffness and Right Ventricular Functions in Patients with Behcet’s Disease

OP-075 The Evaluation of the Relationship between Pulmonary Artery Stiffness and Right Ventricular Functions in Patients with Behcet’s Disease

Pulmonary Artery Stiffness Is Independently Associated with Right Ventricular Mass and Function: A Cardiac MR Imaging Study.

Purpose To determine the relationship between pulmonary artery (PA) stiffness and both right ventricular (RV) mass and function with cardiac magnetic resonance (MR) imaging. Materials and Methods The study was approved by the local research ethics committee, and all participants gave written informed consent. Cardiac MR imaging was performed at 1.5 T in 156 healthy volunteers (63% women; age range, 19-61 years; mean age, 36.1 years). High-temporal-resolution phase-contrast imaging was performed in the main and right PAs. Pulmonary pulse wave velocity (PWV) was determined by the interval between arterial systolic upslopes. RV function was assessed with feature tracking to derive peak systolic strain and strain rate, as well as peak early-diastolic strain rate. RV volumes, ejection fraction (RVEF), and mass were measured from the cine images. The association of pulmonary PWV with RV function and mass was quantified with univariate linear regression. Interstudy repeatability was assessed with intraclass correlation. Results The repeatability coefficient for pulmonary PWV was 0.96. Increases in pulmonary PWV and RVEF were associated with increases in age (r = 0.32, P < .001 and r = 0.18, P = .025, respectively). After adjusting for age (P = .090), body surface area (P = .073), and sex (P = .005), pulmonary PWV demonstrated an independent positive association with RVEF (r = 0.34, P = .026). Significant associations were also seen with RV mass (r = 0.41, P = .004), RV radial strain (r = 0.38, P = .022), and strain rate (r = 0.35, P = .002), and independent negative associations were seen with radial (r = 0.27, P = .003), longitudinal (r = 0.40, P = .007), and circumferential (r = 0.31, P = .005) peak early-diastolic strain rate with the same covariates. Conclusion Pulmonary PWV is reliably assessed with cardiac MR imaging. In subjects with no known cardiovascular disease, increasing PA stiffness is associated with increasing age and is also moderately associated with both RV mass and function after controlling for age, body surface area, and sex. (©) RSNA, 2016 Online supplemental material is available for this article.

Assessment of pulmonary arterial stiffness in obstructive sleep apnea.

Pulmonary hypertension (PH) is one of the major complications of obstructive sleep apnea syndrome (OSAS). Pulmonary arterial stiffness (PAS) can be used in determination of PH. The aim of the present study was to evaluate the PAS and cardiac function of patients with OSAS and analyses the relationship between OSAS severity and PAS. Sixty newly diagnosed patients with OSAS (mean age 49.6±11.7years) and 30 healthy controls (mean age 46.4±14years) were enrolled. Right ventricle (RV) and left ventricle (LV) echocardiographic parameters and PAS values of study groups were compared. There were no significant differences in terms of LV ejection fraction, LV Tei-index and tricuspid annular plane systolic excursion. PAS, mean pulmonary arterial pressure (PAP) and RV Tei-index were significantly higher but tricuspid annulus early diastolic myocardial velocity was lower in patients with OSAS than control subjects (respectively p<0.001, p<0.001, p=0.001, p=0.001). Moreover, we found a higher PAS in OSAS patients without PH compared to controls (p<0.001). When we investigated the relationship between polysomnographic variables and echocardiographic parameters, we found positive correlations between apnea hypopnea index and total oxygen desaturation with PAS and mean PAP (r=0.384, p<0.001; r=0.404, p<0.001; r=0.36, p<0.001; r=0.349, p=0.001 respectively). PAS and mean PAP were increased in patients with OSAS. Pulmonary vascular bed may be affected due to the fluctuation of PAP during day and night time. Therefore, assessment of PAS can be more useful than PAP in OSAS patients.

Relation of elastic properties of pulmonary artery with left ventricular abnormalities and aortic stiffness in patients with moderate to severe obstructive sleep apnea: A cross-sectional echocardiographic study.

In this study, the associations between pulmonary artery stiffness (PAS) and aortic stiffness, left ventricular diastolic parameters, and left ventricular mass (LVM) index in moderate to severe obstructive sleep apnea syndrome (OSAS) patients without coexisting disorders were investigated. A total of 66 non-diabetic, non-hypertensive, and non-smoking volunteers were enrolled. Participants were categorized by apnea-hypopnea index (AHI; event/hour). The control group was defined as no OSAS: AHI<5 (n=35), and OSAS group had moderate to severe OSAS: AHI>15 (n=31).Echocardiographic and biochemical tests, including measurement of C-reactive protein (CRP), were performed. PAS (kHz/s) was calculated by dividing the maximal frequency shift of the pulmonary flow by the acceleration time. PAS (kHz/s), obtained by echocardiography, was statistically significantly higher in the OSAS group than the control group (28±5 vs 18±4, p<0.001), and was positively correlated with AHI, CRP, aortic stiffness index, E/E', and LVM index (p=0.034, p=0.039, p<0.001, p=0.040, and p<0.001, respectively), and negatively correlated with aortic strain (AS), aortic distensibility (AD), E/A, E'/A', and E' (p<0.001). Regression analyses indicated that CRP and PAS are independent predictors of aortic stiffness (p<0.05). E/A and LVM index were independent predictors of PAS (p=0.002 and p=0.001, respectively). Increased PAS is associated with aortic stiffness, left ventricular diastolic function, and increased LVM index. PAS may be a more effective indicator of aortic stiffness in OSAS patients than CRP.

Pulmonary Function and Arterial Stiffness in Chronic Heart Failure.

Arterial stiffness contributes to heart failure and is decreased by angiotensin receptor blockers (ARBs). This cross-sectional study aimed to assess associations of lung function and ARB with arterial stiffness in patients with chronic heart failure. 354 outpatients (168 males; 186 females; 68.2 ± 7.2 years old) with chronic heart failure were evaluated. Lung function parameters, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and FEV1 to FVC ratio (FEV1/FVC), were assessed. The cardio-ankle vascular index (CAVI) was used to estimate arterial stiffness. Unadjusted correlation analyses revealed a positive association of CAVI with ARB but not ACEI, and a negative correlation with FEV1 (r = −0.2987, p < 0.0001). Multiple stepwise regression analyses showed that ARB and FEV1 (p < 0.0001) were independent predicting factors for CAVI. These findings suggest that reduced pulmonary function is associated with increased CAVI. Pulmonary function protection could be used to improve the prognosis in heart failure, but additional studies are necessary.

Both Systemic and Pulmonary Artery Stiffness Predict Ventricular Functional Recovery after Successful Percutaneous Closure of Atrial Septal Defects in Adults.

Percutaneous closure of atrial septal defect (ASD) has become the preferred method in treatment of the majority of cases. The aim of this study was to evaluate the echocardiographic effects of percutaneous closure of secundum ASD in adults and assess which parameters predict good response to closure. We prospectively included 42 patients with secundum ASD treated successfully with percutaneous device closure. All patients underwent transthoracic echocardiography examination with tissue Doppler imaging before, 24 hours after and within 3 months of intervention. Measurements of arterial stiffness were carried out using a Mobil-O-Graph arteriography system. Remodeling of heart chambers occurred immediately and persisted at 3 months after ASD closure. Significant decreases were observed in right ventricle (RV) end-diastolic diameter, right atrium volume index, and tricuspid annular plane systolic excursion both after the procedure and at 3 months (P < .01 for all). The RV and left ventricle (LV) tissue Doppler-myocardial performance index demonstrated to decline during follow up (P = .0001). Significant correlations were found between pulse-wave velocity, augmentation index, pulmonary artery stiffness, and LV-RV tissue Doppler-myocardial performance index at third month. Linear regression analyses showed that pulse-wave velocity is the most effective parameter of LV and pulmonary artery stiffness is the most effective parameter of RV functional recovery, respectively, assessed by tissue Doppler-myocardial performance index. Percutaneous closure of secundum ASD in adults has various sustained benefits on multiple echocardiographic parameters within 3 months. The changes in RV and LV function after device closure were significantly correlated with the degree of pulmonary artery stiffness and pulse-wave velocity, respectively.

Abstract 12451: Pulmonary Artery Stiffness is an Independent Predictor of Right Ventricular Mass and Function

Background: Right ventricular (RV) mass is independently associated with cardiovascular risk in the general population, but the underlying causes are not known. Objectives: We used cardiac magnetic resonance (CMR) imaging to determine if there was a relationship between pulmonary (PA) stiffness and measures of RV function and mass. Methods: 156 healthy volunteers underwent 1.5T cardiovascular magnetic resonance imaging. Pulmonary pulse wave velocity (PWV), derived from phase-contrast imaging, was used to assess vascular stiffness. RV performance was assessed using feature-tracking to derive peak systolic strain and strain rate, as well as peak early-diastolic strain rate (PEDSR). RV volumes, ejection fraction (RVEF) and mass (RVM) were measured from the cine images. The association of pulmonary PWV with RV function and mass was quantified by univariate linear regression. Results: Pulmonary PWV and RV ejection fraction (RVEF) both increased with age (R = +0.32, p &lt; 0.001; R = +0.17, p = 0.04 respectively). Adjusting for the effects of age, body surface area and gender, pulmonary PWV showed an independent association with increased RVEF (R = +0.17, p = 0.03), RVM (R = +0.26, p=0.001), RV radial strain (R = +0.36, p = 0.005) and strain rate (R = +0.38, p &lt; 0.001) and reductions in radial (R = -0.45, p = 0.002), longitudinal (R = -0.42, p = 0.008) and circumferential (R = -0.45, p = 0.003) PEDSR. Conclusions: In subjects with no known cardiovascular disease, PA stiffness increases with age and is independently associated with both RV mass and diastolic dysfunction. These findings suggest that prognostically adverse changes in RV function and morphology are associated with age-related changes in PA stiffness.

Evaluation of Pulmonary Artery Stiffness in Patients with Obstructive Sleep Apnea Syndrome.

To investigate whether obstructive sleep apnea syndrome (OSAS) has any effect on pulmonary artery stiffness (PAS) derived from echocardiographic calculation. Fifty-two patients with newly diagnosed OSAS and forty-two subjects without OSAS matched by age and sex were enrolled in the study. OSAS was categorized according to apnea hypopnea index (AHI, event/h) as follows: normal (AHI<5), mild OSAS (AHI 5-15), moderate and severe OSAS (AHI>15). All participants were evaluated by echocardiography to determine PAS and right ventricle functions. PAS was calculated throughout pulmonary artery flow by the formula; PAS (kHz/sec) = maximal frequency shift/acceleration time. Demographic and clinical parameters were similar in both groups. PAS significantly increased in OSAS compared with the control group (26.9 ± 6.1 vs. 18.0 ± 3.5, P < 0.001). Additionally, PAS in severe and moderate OSAS was considerably high compared with that in mild OSAS and control group (P < 0.001). Right ventricular myocardial performance index (MPI) and mean pulmonary artery pressures (mPAP) were considerably higher in OSAS group than control group (P < 0.001). Tricuspid E/A, right ventricle tissue Doppler E'/A', and right ventricular ejection time (RVET) decreased in OSAS group compared with control group (P < 0.001). There was a significantly positive correlation between PAS and AHI, mPAP, and MPI (P < 0.001), and a significantly negative correlation between PAS and tricuspid E/A, E'/A', and RVET (P < 0.001). Linear regression analyses showed that PAS was an independent factor for mPAP (ß = 0.595, P = 0.034). Elastic properties of pulmonary artery deteriorate with severity of OSAS and may be responsible for right ventricular dysfunctions in OSAS.

17β-Estradiol Attenuates Conduit Pulmonary Artery Mechanical Property Changes With Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH), a rapidly fatal vascular disease, strikes women more often than men. Paradoxically, female PAH patients have better prognosis and survival rates than males. The female sex hormone 17β-estradiol has been linked to the better outcome of PAH in females; however, the mechanisms by which 17β-estradiol alters PAH progression and outcomes remain unclear. Because proximal pulmonary arterial (PA) stiffness, one hallmark of PAH, is a powerful predictor of mortality and morbidity, we hypothesized that 17β-estradiol attenuates PAH-induced changes in mechanical properties in conduit proximal PAs, which imparts hemodynamic and energetic benefits to right ventricular function. To test this hypothesis, female mice were ovariectomized and treated with 17β-estradiol or placebo. PAH was induced in mice using SU5416 and chronic hypoxia. Extra-lobar left PAs were isolated and mechanically tested ex vivo to study both static and frequency-dependent mechanical behaviors in the presence or absence of smooth muscle cell activation. Our static mechanical test showed significant stiffening of large PAs with PAH (P<0.05). 17β-Estradiol restored PA compliance to control levels. The dynamic mechanical test demonstrated that 17β-estradiol protected the arterial wall from the PAH-induced frequency-dependent decline in dynamic stiffness and loss of viscosity with PAH (P<0.05). As demonstrated by the in vivo measurement of PA hemodynamics via right ventricular catheterization, modulation by 17β-estradiol of mechanical proximal PAs reduced pulsatile loading, which contributed to improved ventricular-vascular coupling. This study provides a mechanical mechanism for delayed disease progression and better outcome in female PAH patients and underscores the therapeutic potential of 17β-estradiol in PAH.

OP-146 The Relationship Between Parathyroid Hormone Level and Pulmonary Artery Stiffness in Patients with Chronic Kidney Disease

OP-146 The Relationship Between Parathyroid Hormone Level and Pulmonary Artery Stiffness in Patients with Chronic Kidney Disease