Increase In Pulmonary Artery Systolic Pressure Research Articles

Cardiopulmonary haemodynamics in Tibetans and Han Chinese during rest and exercise.

During sea-level exercise, blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) in humans without a patent foramen ovale (PFO) is negatively correlated with pulmonary pressure. Yet, it is unknown whether the superior exercise capacity of Tibetans well adapted to living at high altitude is the result of lower pulmonary pressure during exercise in hypoxia, and whether their cardiopulmonary characteristics are significantly different from lowland natives of comparable ancestry (e.g. Han Chinese). We found a 47% PFO prevalence in male Tibetans (n=19) and Han Chinese (n=19) participants. In participants without a PFO (n=10 each group), we measured heart structure and function at rest and peak oxygen uptake ( ), peak power output ( ), pulmonary artery systolic pressure (PASP), blood flow through IPAVA and cardiac output ( ) at rest and during recumbent cycle ergometer exercise at 760Torr (SL) and at 410Torr (ALT) barometric pressure in a pressure chamber. Tibetans achieved a higher than Han, and a higher at ALT without differences in heart rate, stroke volume or . Blood flow through IPAVA was generally similar between groups. Increases in PASP and total pulmonary resistance at ALT were comparable between the groups. There were no differences in the slopes of PASP plotted as a function of during exercise. In those without PFO, our data indicate that the superior aerobic exercise capacity of Tibetans over Han Chinese is independent of cardiopulmonary features and more probably linked to differences in local muscular oxygen extraction. KEY POINTS: Patent foramen ovale (PFO) prevalence was 47% in Tibetans and Han Chinese living at 2275m. Subjects with PFO were excluded from exercise studies. Compared to Han Chinese, Tibetans had a higher peak workload with acute compression to sea level barometric pressure (SL) and acute decompression to 5000m altitude (ALT). Comprehensive cardiac structure and function at rest were not significantly different between Han Chinese and Tibetans. Tibetans and Han had similar blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) during exercise at SL. Peak pulmonary artery systolic pressure (PASP) and total pulmonary resistance were different between SL and ALT, with significantly increased PASP for Han compared to Tibetans at ALT. No differences were observed between groups at acute SL and ALT.

Changes in Pulmonary Artery Pressure Late in Life: The Atherosclerosis Risk in Communities (ARIC) Study.

Although the prognostic implications of higher pulmonary artery systolic pressure (PASP) are well established, few data exist regarding longitudinal change in pulmonary pressure in late life. The aim of this study was to quantify changes in PASP over 6 years and determine the relative contributions of cardiac and pulmonary dysfunction. Among 1,420 participants in the ARIC (Atherosclerosis Risk in Communities) study with echocardiographic measures of PASP at both the fifth (2011-2013) and seventh (2018-2019) visits, longitudinal changes in PASP over about 6.5 years were quantified. Multivariable regression was used to determine the extent to which cardiac and pulmonary dysfunction were associated with changes in PASP and to define the relationship of changes in PASP with dyspnea development. The mean age was 75 ± 5 years at visit 5 and 81 ± 5 years at visit 7, 24% of subjects were Black adults, and 68% were women. Over the 6.5 years, PASP increased by 5 ± 8mmHg, from 28 ± 5 to 33 ± 8mmHg. PASP increased more in older participants. Predictors of greater increases in PASP included worse left ventricular (LV) systolic and diastolic function, pulmonary function, and renal function. Increases in PASP were associated with concomitant increases in measures of LV filling pressure, including E/e' ratio and left atrial volume index. Each 5mmHg increase was associated with 16% higher odds of developing dyspnea (OR: 1.16; 95%CI: 1.07-1.27; P< 0.001). Pulmonary pressure increased over 6.5 years in late life, was associated with concomitant increases in LV filling pressure, and predicted the development of dyspnea. Interventions targeting LV diastolic function may be effective at mitigating age-related increases in PASP.

Pulmonary Hypertension and Operative Risk in Mitral Valve and Coronary Surgery

IntroductionPulmonary hypertension (PHT) is a known risk factor for coronary artery bypass grafting (CABG), though less well understood for valve operations. We hypothesized PHT is associated with lower risk during mitral valve operations compared to CABG. MethodsPatients undergoing isolated mitral valve or CABG operations (2011-2019) in a regional Society of Thoracic Surgeons (STS) database were stratified by pulmonary artery systolic pressure (PASP). The association of PASP by procedure type was assessed by hierarchical regression modeling, adjusting for STS predicted risk scores. ResultsOf the 2542 mitral and 11,059 CABG patients, the mitral population had higher mean STS risk of mortality (3.6% versus 2.4%, P < 0.0001) and median PASP (42 mmHg versus 32 mmHg, P < 0.0001). PASP was independently associated with operative mortality and major morbidity in both mitral and CABG patients. However, for mitral patients a 10-mmHg increase in PASP was associated with lower odds of morbidity (odds ratio: 1.06 versus 1.13), mortality (odds ratio: 1.11 versus 1.18) and intensive care unit time (4.3 versus 7.6 h) compared with CABG patients (interaction terms P < 0.0001). Among mitral patients, median PASP was higher in stenotic versus regurgitant disease (57 mmHg versus 40 mmHg, P < 0.0001). However, there was no differential association of PASP on morbidity or mortality (interaction terms P > 0.05). ConclusionsAlthough mitral surgery patients tend to have higher preoperative pulmonary artery pressures, PHT was associated with a lower risk for mitral outcomes compared with CABG. Further research on the management and optimization of patients with PHT perioperatively is needed to improve care for these patients.

The Effect of COVID-19 on Long-Term Cardiac Function in Patients With Chronic Heart Failure

Aim To evaluate functional changes in the heart in the long-term following COVID-19 in patients with chronic heart failure (CHF).Material and methods Case reports of 54 patients aged 69.1±9.7 years who had COVID-19 from January 2021 through January 2022 and had been previously diagnosed with NYHA functional class II-III CHF were studied. Two comparison groups were isolated: HF with LV EF &gt;50 % (n=39) and &lt;50 % (n=15). Echocardiography was used to evaluate changes in LV EF and pulmonary artery systolic pressure (PASP) 5-6 months following COVID-19.Results In all CHF patients after COVID-19 at 5.8 months on average, LV EF decreased (median difference, 2.5 %; 95 % confidence interval (CI): 6.99×10-5- 4.99) and PASP increased (median difference, 8 mm Hg; 95 % CI: 4.5-12.9). In the HF group with LV EF &lt;50 %, the decrease in EF was greater than in the group with LV EF &gt;50 % (6.9 and 0.7 %, respectively; p=0.037); furthermore, the CHF phenotype did not influence the change in PASP (p=0.4). The one-factor regression analysis showed that the dynamics of LV EF decrease was significantly influenced by the baseline decrease in LV EF, whereas the change in PASP was influenced by the dynamics of LV EF decrease, presence of dyslipidemia, and statin treatment. Furthermore, the multifactorial analysis showed that prognostically significant factors for long-term changes in LV EF following COVID-19 were male gender (odds ratio (OR), 5.92; 95 % CI: 1.31-26.75; p=0.014), LV EF at baseline &lt;50 % (OR, 0.88; 95 % CI: 0.8-0.96; p&lt;0.001); changes in PASP depended on the presence of dyslipidemia (OR, 0.08; 95 % CI: 0.01-0.84; p=0.018).Conclusion This study showed that COVID-19 in the long term can influence the course of CHF; in this process, HF patients with EF &lt;50 % have progression of systolic dysfunction and PASP, whereas patients with EF &gt;50 % have an isolated increase in PASP.

Ecocardiografia na hipertensão pulmonar: avaliação das câmaras cardíacas direitas e artéria pulmonar

Introduction: Pulmonary Hypertension (PH) is defined as an increase in mean pulmonary artery (PA) pressure above 25mmHg at rest and an increase of 30mmHg with exertion. In more advanced pathological stages, structural changes may occur in the cardiac chambers due to hemodynamic changes. Objectives: To verify if PH patients present with right-side hemodynamic and structural changes. Material and Methods: The study was carried out using a database of the cardiology service of a local health unit in the central region of mainland Portugal. Patients studied were those with PH and those without PH. Although patients with PH were included, those presenting with uncontrolled arterial hypertension, diabetes mellitus and/or congenital cardiac alterations were excluded. Results: The sample consisted of 113 individuals, of which 35 had PH (31.0%) and 68 did not have PH (69.0%). It was observed that in the group with PH there was a growing increase in the cardiac chambers and PA. It was also observed that the higher the Pulmonary Artery Systolic Pressure (PASP), the higher the value obtained in the cardiac chambers and PA. There was also a decrease in the tricuspid annular plane systolic excursion (TAPSE) value as a function of the increase in PASP, compared to lower values. The tricuspid regurgitation velocity (TRV) did not increase much in regards to the increase in PASP, with a greater accentuation of the 2.9-3.4m/s parameter in this correlation. Conclusion: Our study verified that structural and hemodynamic changes in the right heart chambers and PA occur in the presence of PH.

Abstract 14248: The Impact of Trastuzumab on the Pulmonary Artery Systolic Pressure in Patients With HER-2 Positive Breast Cancer

Introduction: Despite that trastuzumab (TZB) improves life expectancy and prognosis in patients with HER-2 positive breast cancer (BC), cardiotoxicity is a well-established complication. However, other potential cardiac complications of TZB such as pulmonary hypertension (PHTN) are poorly investigated. Aim: Evaluate the effect of TZB on pulmonary artery systolic pressure (PASP) and measure the predictors of developing elevated PASP. Methods: The medical records for all females who received TZB treatment for confirmed HER-2 positive BC at King Hussein Cancer Centre in Jordan between 2014 - 2019 who had a documented normal PASP of ≤35 mmHg before treatment were evaluated. Results: A total of 436 patients with a mean age of 53±11 years were included. The leading comorbidities were hypertension and diabetes mellitus affecting 26.2% and 15.4% of the patients, respectively. 15.6% of the study’s population were active smokers. Prior to initiating TZB, 22.3% had left ventricular hypertrophy (LVH), 14.3% had mild tricuspid valve regurgitation (TR), 11.5% had pericardial effusion, and 4.8% had mild aortic valve regurgitation (AR).Of alarming significance, 24.8% of the patients had their PASP increased after one year. Patients who developed elevated PASP tend to be older (56.9 vs 51.3, P&lt;0.001), had baseline mild TR (26.3% vs 10.3%, P&lt;0.001), LVH (39.4% vs 17.6%, P&lt;0.001), and mild AR (9.1% vs 3.7%, P=0.031).Multivariate analysis showed that the only predictors of elevated PASP are TR at baseline (OR 3.9; 95% CI 1.58-6.17, P=0.001), and age (OR 1.04; 95% CI 1.01-1.06, P=0.005). However, baseline LVH (OR 1.79; 95% CI 0.98-3.26, P=0.057), number of the TZB cycles (OR 0.93; 95% 0.85-1.02, P=0.152), and the total dose of TZB (OR 1; 95% CI 1-1, P=0.284) were non-significant predictors. At 1 year follow up, the mean total cumulative dose of TZB was 6.8±1.8 grams that were given at a mean of 15±3 cycles. Moreover, major events (heart failure exacerbation, pulmonary embolism, and acute coronary syndrome) were recorded in 3.9% of the patients and death occurred in 4.1%. Conclusions: Trastuzumab demonstrated an increase in the PASP in a considerable portion of the patients at 1-year interval with this elevation being substantially concerning due to being highly indicative of PHTN.

Extent and determinants of pulmonary hypertension unmasked by handgrip exercise in patients with mitral regurgitation

Abstract Background Pulmonary hypertension (PH) is an established prognosticator in patients with mitral regurgitation (MR). However, a substantial proportion of patients with MR presents without PH at rest but may develop PH during exercise. Previous studies already demonstrated the prevalence and prognostic impact of PH during bicycle exercise. Until now, there are no data on exercise PH assessed by handgrip exercise. Purpose To assess prevalence and predictors of exercise-induced PH during handgrip exercise in patients with MR. Methods We prospectively included patients with MR and at least mild severity that underwent echocardiography at rest and during three minutes of handgrip exercise according to a standardized protocol. PH was defined by systolic pulmonary artery pressure (SPAP) &amp;gt;50 mmHg. Results The final patient cohort included 371 patients with primary and secondary MR. Mean age was 74±11 years, 48% were female and 59% had atrial fibrillation. Median NT-proBNP was 2017 (845–4976) ng/l. Thirty-eight percent of patients had primary MR, while 62% presented with secondary MR. At rest, MR severity was graded as mild in 56% of patients, moderate in 32% and severe in 12%. Mean SPAP at rest was 40±12 mmHg, and 63 patients (17%) revealed PH at rest (SPAP &amp;gt;50 mmHg). Handgrip exercise leads to an increase in SPAP by 7±12 mmHg. Thus, during exercise 137 patients (37%) exhibited SPAP &amp;gt;50 mmHg. Together, 110 patients (32%) of those patients without PH at rest, showed PH during handgrip exercise. Left- (OR 1.021 (1.010 to 1.033); p&amp;lt;0.001), and right atrial volume index (OR 1.020 (1.009 to 1.035); p&amp;lt;0.001), RV fractional area change (OR 0.972 (0.949 to 0.994); p=0.013), tricuspid regurgitation (OR 1.863 (1.434 to 2.445); p&amp;lt;0.001) and SPAP at rest (OR 1.131 (1.100 to 1.167); p&amp;lt;0.001) were the predictors of exercise PH. Moreover, there was a linear correlation between the change in MR severity assessed by effective regurgitant orifice area (r=0.359; p&amp;lt;0.001) and regurgitation volume (r=0.370; p&amp;lt;0.001) and the change in SPAP. Patients with exercise PH and patients with PH at rest were more symptomatic according to NYHA functional class than patients without PH (p=0.008) (Fig. 1). Conclusion(s) In patients with primary and secondary MR, handgrip echocardiography unmasks exercise PH in every third patient without PH at rest. Bi-atrial dilatation, right ventricular function, tricuspid regurgitation and SPAP at rest were predictors of exercise PH, while changes in MR severity during handgrip exercise correlate with changes in pulmonary pressures. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): This work was supported by the Forschungskommission of the Medical Faculty of the Heinrich Heine University Düsseldorf to Maximilian Spieker for a Clinician Scientist Track.

PULMONARY HYPERTENSION FOLLOWING TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) PLACEMENT DUE TO NEUROHORMONAL VASOACTIVE CAUSES

PULMONARY HYPERTENSION FOLLOWING TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) PLACEMENT DUE TO NEUROHORMONAL VASOACTIVE CAUSES

Augmentation of Pulmonary Perfusion by Conducted Effects of a Pulmonary Artery Ultrasound Catheter.

Ultrasound (US) generated by catheters used clinically for US-facilitated thrombolysis can release shear-dependent vasodilators from endothelial and red blood cells. We hypothesized that catheter-based US in the pulmonary artery (PA) decreases downstream vascular resistance and increases pulmonary blood flow. In rhesus macaques, a U.S. Food and Drug Administration-approved multi-element US catheter was placed in a pulmonary artery. Comprehensive echocardiography was performed (i) at baseline, (ii) during hypoxemia (12% FIO2) to increase pulmonary vascular resistance (PVR) and (c) 15 min after initiating US during hypoxemia. Reduced FIO2 produced intended reductions in oxygen saturation (69 ± 3%) and PaO2 (34 ± 5 mm Hg), yet on echocardiography, hypoxemia did not create the intended model, with only modest hypoxia-related increases in PA systolic pressure (24 ± 4 to 28 ± 4 mm Hg, p=0.05) and no significant change in PVR or multiparametric right ventricular (RV) function. Although US did not further change total PVR, on 99mTc-macroalbumin aggregate single-photon-emission computed tomography imaging, lung perfusion was significantly higher in the lung ipsilateral to the US catheter versus the contralateral control lung (133 ± 48 cpm vs. 103 ± 43×103 cpm, p=0.01). We conclude that PA catheter-based US increases regional lung perfusion, most likely from vasodilators that are conducted downstream.

Pulmonary artery systolic pressure at 1-month predicts 1-year survival after transcatheter aortic valve implantation.

Pulmonary hypertension related to left ventricle heart disease is a common finding in patients with severe aortic stenosis treated with transcatheter aortic valve implantation (TAVI) and is associated with a higher mortality rate. The study aimed to analyze the influence of pulmonary artery systolic pressure (PASP) changes after TAVI on long-term survival. TAVI was performed in 362 patients between January 2013 and December 2018. The study group comprised 210 patients who underwent a detailed 1-month follow-up. At 1-month, 142 had a stable or decreased PASP value (Group 1), while in 68 patients an increase was observed (Group 2). During 1-year follow-up, 20 patients died (9.5%), 9 in Group 1 and 11 in Group 2 (P = 0.02). The receiver operating characteristic (ROC) curve analysis (area under the curve [AUC], 0.750) revealed a significant value of 1-month measurement for 1-year mortality prediction. The cutoff for the PASP value predictive of mortality was ≤41 mm Hg. A Kaplan-Meier analysis showed significantly higher mortality in patients without a 1-month PASP decrease. In the multivariable analysis, PASP measured at 1-month after TAVI (hazard ratio, 1.040; 95% confidence interval, 1.019-1.062; P < 0.001) was an independent predictor of 1-year mortality. Each 1 mm Hg increase in PASP predicts a 4% increase in the risk of death. Decreased or stable value of PASP at 1-month follow-up may predict better 1-year survival after TAVI, while each 1 mm Hg increase in PASP confers a 4% greater risk of 1-year mortality.

Mechanical property evaluation of the right ventricular myocardium in cancer patients with chemotherapy by echocardiography: a systematic review and meta-analysis.

BackgroundCancer therapy-related cardiotoxicity has recently become an area of intense research. As the prognostic role of the right ventricle (RV) in a variety of cardiovascular diseases has been confirmed, and several studies have paid increased attention to RV function in cancer patients who have underwent chemotherapy, we provide a meta-analysis to objectively evaluate the mechanical properties of the right ventricular myocardium by echocardiography in this population.MethodsWe systematically searched Embase, PubMed, and Cochrane databases were applied to search for studies (published before August 11, 2021) comparing RV contraction measured by echocardiography at baseline to follow-up in cancer patients who underwent chemotherapy or radiotherapy. The mechanical properties of the right ventricular myocardium were pulmonary artery systolic pressure (PASP), tricuspid annular plane systolic excursion (TAPSE), systolic velocity of tricuspid annulus (S'), right ventricular free wall longitudinal strain (RVFWLS), right ventricular global longitudinal strain (RVGLS), and right ventricular fractional area change (RVFAC). We analyzed pooled data using a random-effects model and assessed risk of bias in the included studies using the Newcastle-Ottawa Scale.ResultsTwenty-one trials were enrolled (N=1,355 participants). Cancer patients who underwent chemotherapy but not radiotherapy showed an increase in PASP [standardized mean difference (SMD) =0.161, 95% CI: 0.007 to 0.316) compared with the condition at baseline, as well as reductions in TAPSE (SMD =−0.543, 95% CI: −0.698 to −0.389), S' (SMD =−0.507, 95% CI: −0.748 to −0.266), RVFWLS (SMD =0.833, 95% CI: 0.549 to 1.118) and RVGLS (SMD =1.017, 95% CI: 0.751 to 1.283). There was no significant difference in RVFAC (SMD =−0.097, 95% CI: −0.213 to 0.018). Furthermore, these indicators pointed to a deterioration of right ventricular contraction function in cancer patients who underwent chemotherapy and radiotherapy. The risk of bias of the included studies evaluated by the Newcastle-Ottawa Scale was medium to high.DiscussionRight ventricular contraction function would deteriorate in cancer patients who underwent chemotherapy and radiotherapy, especially with the prolongation of chemotherapy duration and accumulation of chemotherapeutic drugs. Further studies are needed to establish the definition of right ventricular systolic dysfunction in clinical practice.

REFRACTORY HYPOXEMIA IN A NONAGENARIAN WITH PATENT FORAMEN OVALE MANAGED MEDICALLY

TOPIC: Pulmonary Vascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Patent foramen ovale (PFO) is a cardiac defect with a prevalence of 25-30%, which notably decreases with age. A study done in 2018 showed an increased incidence of PFO in patients with pulmonary hypertension (pHTN). It is suggested that the presence of PFO in these individuals is a reflection of dilated and dysfunctional right atrium and ventricles, leading to an increased right to left gradient, stretching open a communication between the two atria. CASE PRESENTATION: We present a 96 year old female with heart failure with preserved ejection fraction, chronic respiratory failure secondary to moderate persistent asthma, on 4L of O2 at baseline, recurrent venous thromboembolic disease on apixaban, severe untreated OSA, initially admitted for septic shock due to acute cholecystitis requiring percutaneous cholecystostomy and broad spectrum antibiotics. On admission she also had significant hypoxia with cyanosis requiring intubation. The level of hypoxia was discordant with the clinical picture, with chest x-ray only showing atelectasis. She was extubated to high flow nasal cannula five days later, however we faced challenges in weaning her oxygen requirements. She received systemic steroids, anticoagulation and diuresis without improvement. Subsequently, the patient underwent an echocardiogram that showed a pulmonary artery systolic pressure (PASP) of 79mmHg (previously 47 mmHg in a study done 8 months ago). Given the degree of hypoxia and associated increase in PASP, intracardiac shunting was suspected. A repeat TTE with bubble study confirmed the presence of a small PFO. We discussed surgical closure, however invasive measures were deferred given her advanced age. Instead, the patient was treated with short acting diltiazem every 6 hours and furosemide daily with the goal of reducing pulmonary pressures and R to L shunting of deoxygenated blood. Although diltiazem is associated with negative outcomes in patients with heart failure, there was no evidence of pulmonary vascular congestion, and the immediate benefit outweighed the risk. Many days after initiating our plan, her oxygen requirements suddenly dropped from 60L/min to 4L/min and we were able to discharge her successfully. DISCUSSION: It is postulated that sepsis can lead to pHTN from elevated pulmonary vascular resistance through various mechanisms. Opening of PFO in severe pHTN is a common occurrence - resulting in resistive hypoxemia. Although we lack definitive evidence without right heart catheterization, we were able to exclude other etiologies of hypoxia through trial and error, strengthening our theory that PFO was the main driver of the clinical presentation. CONCLUSIONS: To summarize, hypoxia due to intracardiac shunting is an important cause of hypoxia, not to be missed on our list of differential diagnoses, with timely identification and appropriate therapy being the key to positive outcomes. REFERENCE #1: Sharan L, Stackhouse K, Awerbach JD, Bashore TM, Krasuski RA. Effect of Patent Foramen Ovale in Patients With Pulmonary Hypertension. Am J Cardiol. 2018 Aug 1;122(3):505-510. doi: 10.1016/j.amjcard.2018.04.014. Epub 2018 May 1. PMID: 30201113. REFERENCE #2: William J. Sibbald, NigelA.M. Paterson, Ronald L. Holliday, Richard A. Anderson, Trevor R. Lobb, John H. Duff, Pulmonary Hypertension in Sepsis: Measurement by the Pulmonary Arterial Diastolic-Pulmonary Wedge Pressure Gradient and the Influence of Passive and Active Factors, Chest, Volume 73, Issue 5, 1978, Pages 583-591, ISSN 0012-3692, https://doi.org/10.1378/chest.73.5.583. REFERENCE #3: Islam S, Masiakos P, Schnitzer JJ, Doody DP, Ryan DP. Diltiazem reduces pulmonary arterial pressures in recurrent pulmonary hypertension associated with pulmonary hypoplasia. J Pediatr Surg. 1999 May;34(5):712-4. doi: 10.1016/s0022-3468(99)90361-5. PMID: 10359169. DISCLOSURES: No relevant relationships by Maryam Ahmed, source=Web Response No relevant relationships by Robert McDonald, source=Web Response

Mountain evidence on the relationship between iron status and pulmonary vasoconstriction.

Mountain evidence on the relationship between iron status and pulmonary vasoconstriction.

Non-invasive pulmonary artery pressure estimation by electrical impedance tomography in a controlled hypoxemia study in healthy subjects

Pulmonary hypertension is a hemodynamic disorder defined by an abnormal elevation of pulmonary artery pressure (PAP). Current options for measuring PAP are limited in clinical practice. The aim of this study was to evaluate if electrical impedance tomography (EIT), a radiation-free and non-invasive monitoring technique, can be used for the continuous, unsupervised and safe monitoring of PAP. In 30 healthy volunteers we induced gradual increases in systolic PAP (SPAP) by exposure to normobaric hypoxemia. At various stages of the protocol, the SPAP of the subjects was estimated by transthoracic echocardiography. In parallel, in the pulmonary vasculature, pulse wave velocity was estimated by EIT and calibrated to pressure units. Within-cohort agreement between both methods on SPAP estimation was assessed through Bland–Altman analysis and at subject level, with Pearson’s correlation coefficient. There was good agreement between the two methods (inter-method difference not significant (P > 0.05), bias ± standard deviation of − 0.1 ± 4.5 mmHg) independently of the degree of PAP, from baseline oxygen saturation levels to profound hypoxemia. At subject level, the median per-subject agreement was 0.7 ± 3.8 mmHg and Pearson’s correlation coefficient 0.87 (P < 0.05). Our results demonstrate the feasibility of accurately assessing changes in SPAP by EIT in healthy volunteers. If confirmed in a patient population, the non-invasive and unsupervised day-to-day monitoring of SPAP could facilitate the clinical management of patients with pulmonary hypertension.

Abstract 15318: Longitudinal Changes in Pulmonary Pressure in Late Life: The Atherosclerosis Risk in Communities Study

Introduction: While the prognostic implications of higher pulmonary artery systolic pressure (PASP) are well established, few data exist regarding longitudinal change in pulmonary pressure in the community. We characterized longitudinal changes in PASP over ~6.5 years in late life, and identified predictors of this change. Methods: We studied 1,426 elderly participants in the prospective, community-based Atherosclerosis Risk in Communities (ARIC) study who underwent protocol echocardiography and had assessable tricuspid regurgitation spectral Doppler at 5 th (2011-2013) and 7 th (2018-2019) study visits. We used multivariable linear regression to identify clinical, echocardiographic and biomarker predictors of change in PASP. Results: Mean age was 74±5 years at Visit 5, 32% were men, 24% black, and mean PASP was 27.5±5.0 mmHg. Over a median of 6.5±3.0 years, PASP increased by 5.2±7.7 mmHg on average, with no significant differences by race (white 5.0±7.6, black 5.8±7.9; p=0.40) or sex (women 5.2±7.7, men 5.1±7.8; p=0.95). In models adjusted for heart rate and blood pressure at both visits, and for PASP, clinical and echocardiographic measures at Visit 5, independent predictors of longitudinal increase in PASP at Visit 5 were higher NT-proBNP (p=0.005), larger left atrial volume index (p=0.045), and lower forced expiratory volume at 1 second (p=0.019). Longitudinal increase in PASP was associated with concomitant increases in LAVi, E/e’ ratio, and LV mass index ( Figure ; all p &lt;0.003), but not with changes in LVEF or strain. Conclusions: PASP increased by 5±8 mmHg over 6.5±3.0 years in late life, with greater increases associated with higher filling pressure and worse pulmonary function. Increases in PASP are accompanied by longitudinal worsening in LV diastolic - but not systolic - measures.

Impaired pulmonary gas exchange efficiency, but normal pulmonary artery pressure increases, with hypoxia in men and women with a patent foramen ovale.

What is the central question of this study? Do individuals with a patent foramen ovale (PFO+ ) have a larger alveolar-to-arterial difference in ( ) than those without (PFO- ) and/or an exaggerated increase in pulmonary artery systolic pressure (PASP) in response to hypoxia? What is the main finding and its importance? PFO+ had a greater while breathing air, 16% and 14% O2 , but not 12% or 10% O2 . PASP increased equally in hypoxia between PFO+ and PFO- . These data suggest that PFO+ may not have an exaggerated acute increase in PASP in response to hypoxia. Patent foramen ovale (PFO) is present in 30-40% of the population and is a potential source of right-to-left shunt. Accordingly, those with a PFO (PFO+ ) may have a larger alveolar-to-arterial difference in ( ) than those without (PFO- ) in normoxia and with mild hypoxia. Likewise, PFO is associated with high-altitude pulmonary oedema, a condition known to have an exaggerated pulmonary pressure response to hypoxia. Thus, PFO+ may also have exaggerated pulmonary pressure increases in response to hypoxia. Therefore, the purposes of the present study were to systematically determine whether or not: (1) the was greater in PFO+ than in PFO- in normoxia and mild to severe hypoxia and (2) the increase in pulmonary artery systolic pressure (PASP) in response to hypoxia was greater in PFO+ than in PFO- . We measured arterial blood gases and PASP via ultrasound in healthy PFO+ (n=15) and PFO- (n=15) humans breathing air and 30min after breathing four levels of hypoxia (16%, 14%, 12%, 10% O2 , randomized and balanced order) at rest. The was significantly greater in PFO+ compared to PFO- while breathing air (2.1±0.7vs. 0.4±0.3Torr), 16% O2 (1.8±1.2vs. 0.7±0.8Torr) and 14% O2 (2.3±1.2vs. 0.7±0.6Torr), but not 12% or 10% O2 . We found no effect of PFO on PASP at any level of hypoxia. We conclude that PFO influences pulmonary gas exchange efficiency with mild hypoxia, but not the acute increase in PASP in response to hypoxia.

Impact of Severe Pulmonary Hypertension on Right Heart Hemodynamics and Outcomes Following Cardiac Transplantation: A Single Center Experience

The prognostic impact of pulmonary hypertension (PH) is debated as well as the trend of pulmonary hemodynamic variables after heart transplantation (HTx). We investigated the impact of preoperative PH on postoperative survival and on the evolution of right heart hemodynamics (RHH) after HTx. We reviewed the records of 431 consecutive HTx recipients, divided in a non-PH group (270 pts) and a PH group (161 pts).PH was defined as pulmonary vascular resistance ≥2.5 Wood units (WU) at right heat catheterization: mild (97 pts; PVR: 2.5-3.4WU), moderate (41 pts; PVR: 3.5-4.9WU) and severe PH (23 pts; PVR ≥5.0WU). RHH [systolic/mean/diastolic pulmonary artery-systolic-pressure (PAP), pulmonary-capillary-wedge-pressure (PCWP), transpulmonary gradient (TPG), cardiac output (CO), pulmonary vascular resistance (PVR), pulmonary-arterial-pulsatility-index (PAPi) and right-ventricle-stroke-work-index (RVSWI)] were measured before HTX and 3, 6, 12 months, 3, 5 years after HTX. Survival analysis was conducted using Kaplan-Meier curves. Preoperatively, patients with severe PH had significantly (P<0.001) higher mean PAP (64.5/42.2/28.8 vs. 48.6/32.6/21.8mmHg), TPG (16.8 vs. 9.9mmHg), PVR (6.1 vs. 3.2WU) and RVSWI (568.4 vs. 428.9) than patients with mild/moderate PH. After HTx, the PH-group had a higher incidence of graft dysfunction (20.5 vs. 14.8%;P=0.01), right ventricular failure (9.3 vs. 4.8%;P=0.03), ECMO (10 vs. 5.1%;P=0.01), ICU stay (8.4 vs. 6.8 day;P=0.02) than non-PH patients. In hospital mortality was 10.6% in PH-patients (15.8% vs. 9.9% in severe vs. mild/moderate PH;P=0.04) vs. 6.3% in non-PH group (P=0.01). Ten-years survival rates were 70% in PH-patients (71% in severe PH) vs. 72% in non-PH patients. RHH improved early after HTx, without significant differences between severe PH and mild/moderate PH [PAP (30.1/19.4/10.9 vs. 26.8/17.3/9.8mmHg), TPG (10.9 vs. 8.5mmHg), PVR (1.8 vs. 1.5WU) and RVSWI (506.1 vs. 470.9) but slightly worsened after 3-5 years. Pre-transplant PH is an independent predictor of early mortality after HTx, not affecting long-term survival even when severe. After an early significant improvement of RHH, mean PAP, TPG and PVR increase while CO, PAPi and RVSWI decrease during follow-up. A rigorous monitoring of RHH must be scheduled during FU.

Diagnostic analysis of abnormal increase of PASP in fetus in middle- and late-stage pregnancy by color Doppler echocardiography.

Our study was conducted with an attempt to investigate the diagnostic analysis of abnormal increase of fetal pulmonary artery systolic pressure (PASP) in middle and late pregnancy by color Doppler echocardiography. From August 2017 to January 2019, 52 fetuses with moderate or greater tricuspid high-speed regurgitation were retrospectively analyzed and selected as Group A. 88 fetuses with full-color blood flow of the two ventricles and symmetrical sizes of the cardiac cavities on both sides harboring tricuspid valve and mild regurgitation or a small amount of regurgitation were selected as Group B. The pulmonary artery blood flow acceleration time (AT) and right ventricular ejection time (ET) was measured, and the PASP was calculated. The tricuspid regurgitation velocity, tricuspid regurgitation pressure difference and PASP in Group A were higher than those in Group B (p < 0.05), and the AT and AT/ET values in Group A were lower than those in Group B (p < 0.05). Gestational age, tricuspid regurgitation velocity and tricuspid regurgitation pressure difference were positively correlated with PASP. However, AT/ET and AT value were negatively correlated with PASP. The abnormal increase of pulmonary artery can be assessed by color Doppler echocardiography of fetal tricuspid regurgitation, which is worth popularizing and applying in clinic. It was suggested that the middle- and late-stage fetuses with moderate or greater tricuspid regurgitation and with >20 mmHg regurgitation pressure difference should be followed up in clinic. If PASP was ≥70 mmHg with symptoms of right heart failure, fetuses should be closely observed until 35-36 weeks old to ensure fetal safety and early delivery would be recommended.

High preoperative pulmonary artery systolic pressure is associated with acute kidney injury and prognosis in patients underwent cardiopulmonary bypass surgery

To observe the relationship between pulmonary artery systolic pressure (PASP) and acute renal injury (AKI) and prognosis after cardiopulmonary bypass (CPB) heart surgery. The clinical data of 9 860 patients who underwent CPB heart surgery in Beijing Anzhen Hospital from January 1st, 2015 to December 31st, 2016 were analyzed retrospectively. The patients were divided into two groups according to whether AKI occurred after operation. The clinical data were obtained from hospital information system (HIS) and DoCare including general information, types of operation, preoperative complication, ejection fraction, serum creatinine (SCr), PASP, intraoperative CPB duration, aortic occlusion duration, fluid balance, blood products and drug usage, postoperative mechanical ventilation duration, length of intensive care unit (ICU) and hospital stay, and perioperative central venous pressure (CVP). Multivariate Logistic regression analysis was used to screen the risk factors of AKI after operation. According to the preoperative PASP level, the patients were divided into ≥ 60 mmHg (1 mmHg = 0.133 kPa) group and < 60 mmHg group, and the incidence of AKI and prognosis after operation were compared between the two groups. All patients were followed up by telephone after discharge, and they were divided into survival group and death group according to the follow-up results, and the clinical data were compared between the two groups. Multivariate Cox regression analysis was used to screen the risk factors of long-term prognosis. Kaplan-Meier survival curve was used to analyze the long-term prognosis of two groups with different preoperative PASP levels. 6 285 patients were enrolled in the final analysis. (1) Among the 6 285 patients, 2 592 patients (41.2%) suffered from AKI after operation, of whom 1 697 (65.5%) were stage 1 according to Kidney Disease: Improving Global Outcomes (KDIGO), which was the main type of AKI. Univariate analysis showed that age, preoperative ejection fraction, SCr, PASP, coronary heart disease, hypertension, diabetes, intraoperative CPB duration, aortic occlusion duration, fluid balance, red blood cell input and norepinephrine, dopamine, epinephrine dosage, postoperative mechanical ventilation duration, the length of ICU and hospital stay, and perioperative CVP might be the risk factors of AKI after operation. Multivariate Logistic regression analysis showed that preoperative PASP was one of independent risk factors for AKI in patients undergoing CPB heart surgery [odds ratio (OR) = 4.753, 95% confidence interval (95%CI) was 1.328-8.417, P = 0.004]. The incidence of AKI after operation in PASP ≥ 60 mmHg group was significantly higher than that in < 60 mmHg group [73.8% (712/965) vs. 35.3% (1 880/5 320), P < 0.01]. (2) After a follow-up of (11±3) months, 237 patients (3.8%) died in 6 285 patients. The mortality of patients in PASP ≥ 60 mmHg group was significantly higher than that in < 60 mmHg group [9.5% (92/965) vs. 2.7% (145/5 320), P < 0.01]. Kaplan-Meier survival curve analysis showed that there was a significant difference between the two groups in cumulative survival rate (Log-Rank test: χ2 = 144.400, P < 0.001). Univariate analysis showed that male, age, preoperative hypertension, ejection fraction, PASP, intraoperative CPB duration, aortic occlusion duration, fluid balance, epinephrine dosage, postoperative mechanical ventilation duration, the length of ICU and hospital stay, and perioperative CVP might be risk factors for long-term death of patients undergoing CPB heart surgery. Multivariate Cox regression analysis showed that for every 1 mmHg increase in preoperative PASP, the long-term mortality increased by 1.126 times [hazard ratio (HR) = 1.126, 95%CI was 1.003-1.604, P = 0.021]. The increase of PASP is related to AKI after CPB heart surgery, which is an independent risk factor for long-term mortality.

P1541The relation between right ventricular-pulmonary circulation coupling and aging in healthy population

Abstract Purpose The aim of the study was to evaluate the right ventricular (RV) structure and functional adaptation to age, in particular the RV pulmonary circulation (PC) coupling and physiologic correlates. Methods 1177 healthy subjects aged 16–100 years were enrolled. They underwent general medical evaluation and a comprehensive TTE included RV systolic such as tricuspid annular plane systolic excursion (TAPSE), pulmonary artery systolic pressure (PASP) derived from the tricuspid regurgitation (TR), the derived RV-pulmonary circulation (PC) coupling or TAPSE/PASP, pulmonary vascular resistances (PVR) derived from TR/RV outflow tract velocity (RVOT VTI) and diastolic function parameters. The cohort was divided in 4 groups of age: group 1: 300 subjects from 18 to 35 years; group 2: 383 subjects from 36 to 50; group 3: 451 from 50 to 79 years and group 4: 43 subjects &gt; than 80 years of age The oldest subjects were completely independent in daily living activities. The groups were compared by ANOVA and the difference was adjusted by gender, BMI and mean arterial pressure. For each group the difference between genders was tested by T-Test. Multivariate analysis was used to evaluate the relationship between RV function and structure indexes and covariates selected according to pathologic relevance. Results There was a progressive increase in blood pressure (BP) according to age. The RV longitudinal diameter, right E/A ratio, right ventricular outflow tract acceleration time and TAPSE/PASP decreased according to age increase (p&lt;0.0001). The right atrial volume indexed by BSA, PASP, PVR increase with age (p&lt;0.0001). Either TAPSE or Sm were unaffected by age. Women had constantly smaller RV longitudinal diameters, right atrium volume index, TAPSE and TAPSE/PASP (p&lt;0.001). In the multiple regression analysis, though the proportion of variance of the dependent variables predicted by the independent ones was very small, age, BSA, gender, E/Em and the longitudinal diameter of the RV were independent predictors of TAPSE/PASP. Heart rate, left ventricular (LV) diastolic function, stroke volume (SV) and TR were independently related to Sm, while age, BSA, LV diastolic function and SV were independently related to TAPSE. Conclusion With ageing there is a progressive involvement not only of the LV in terms of adaptation to increase afterload related to arterial stiffness but also of the RV. With age PVR and PASP increase while RV contractility is still unchanged. While the RV adapts very well to volume overload, even the physiologic increase in PASP with age, causes a RV-PC coupling impairment.