Changes In Pulmonary Pressure Research Articles

GABA-immunoreactivity in Neuroepithelial Bodies of Spontaneously Hypertensive Rats

Neuroepithelial bodies (NEBs) are complex sensory receptors dispersed throughout the intrapulmonary airways. They are composed of pulmonary neuroendocrine cells (PNECs) which have a large amount of dense-core vesicles containing calcitonin gene-related peptide (CGRP), serotonin (5HT), substance P (SP) and δ-aminobutyric acid (GABA). NEBs are densely innervated by vagal sensory terminals, dorsal root afferents and intrinsic motor fibres. Their location, neurochemical composition and dense innervation make NEBs a key component for the regulation of lung homeostasis. Pulmonary arterial hypertension is a rare disease characterized by morphological alterations in the microcirculation of the lungs causing a wide array of complications and high mortality. Spontaneously hypertensive rats (SHRs) are a common model for essential hypertension, that may develop secondary pulmonary hypertension and thus can be used as an animal model to study pulmonary pressure changes. The present study focuses on the immunohistochemical demonstration of GABA in the NEBs and its potential role in the regulation of the pulmonary pressure. Two groups of SHRs were used and age-matched normotensive Wistar Kyoto (WKY) rats served as controls. We found single PNECs and clusters of GABA-immunoreactive cells protruding into the lumen of the intrapulmonary airways in all examined groups of SHRs and in the normotensive WKY rats. However, the expressional levels statistically differed within the two age groups of SHRs and the controls. Specifically, the NEBs and PNECs in 1-month-old SHRs and particularly in 3-month-old SHRs showed more intense GABA-immunostaining compared to the WKY rats. In conclusion, NEBs and PNECs react to the alterations of the pulmonary pressure homeostasis by an increased GABA expression as a preventive or reactive regulation mechanism against developing pulmonary hypertension.

Prevalence of non pulmonary vein triggers and pulmonary pressure change in atrial fibrillation ablation for cardiac amyloidosis patients

Abstract Background Cardiac amyloidosis (CA) has been associated with an increased risk of atrial arrhythmias and high risk to develop pulmonary hypertension due to infiltration of the amyloid protein in the atrial wall. Though non-PV triggers are commonly seen in left atrium, they are also seen in the right side of the heart, so identifying them at the time of ablation is essential. Objective The study evaluates the prevalence of non-PV triggers during catheter ablation in atrial fibrillation (AF) patients affected by cardiac amyloidosis and how restoration of sinus rhythm affects pulmonary pressures. Methods This is a study including 74 consecutive patients with an established diagnosis of amyloidosis ATTR diagnosed with cardiac MRI or myocardial biopsy that underwent their first AF catheter ablation. All have a transthoracic echocardiogram before ablation. They underwent pulmonary vein (PV) isolation + isolation of left atrial posterior wall and superior vena cava. Additionally, extrapulmonary triggers, which are defined as ectopic triggers originating from sites other than PVs including left atrial appendage (LAA), coronary sinus (CS), interatrial septum, crista terminalis, mitral valve anulus were identified. Post procedure, patients were followed up routinely with ECG during office visits, echocardiogram, 7-day Holter monitor and event recorders during the first year followed by biannual checkups during the remaining part of the follow-up period. Student’s t-test was used to compare pulmonary pressure between the groups. Results Isoproterenol-challenge revealed non-PV triggers in 51 (68.9%) patients. These triggers were mostly mapped to LAA (39, 52.7%), CS (30, 40,5%), and crista terminalis (35, 47.3%). Besides, ectopic beats were seen originating from inter-atrial septum (19, 25.6%), mitral valve annulus (10, 13.5%). More than one trigger was found in (68%) patients. At 1-year after the ablation, 65 (87.8%) were arrhythmia-free off antiarrhythmic drugs. Moreover, in patients who maintained sinus rhythm post-ablation, there was either a non progression or a reduction in pulmonary pressures (PAPm before ablation: 44.8 ± 8.9 mmHg vs PAPm after ablation 45.1 ± 11.1 mmHg, P value =0.87). Conversely, those experiencing arrhythmic recurrences demonstrated an increase in pulmonary pressures (PAPm before ablation: 41.9 ± 7.7 mmHg vs PAPm after ablation 47.8 ± 10.2 mmHg, P value =0.019). Fig.1 Conclusion Our findings suggest that non-PV triggers are highly prevalent in cardiac amyloidosis AF patients including a high rate crista terminalis firing. Notably, restoration of sinus rhythm post-ablation was linked to stable or reduced pulmonary arterial pressures, whereas patients with arrhythmic recurrences experienced a significant increase.

Immediate cardiopulmonary responses to consecutive pulmonary embolism: a randomized, controlled, experimental study

BackgroundAcute pulmonary embolism (PE) induces ventilation-perfusion mismatch and hypoxia and increases pulmonary pressure and right ventricular (RV) afterload, entailing potentially fatal RV failure within a short timeframe. Cardiopulmonary factors may respond differently to increased clot burden. We aimed to elucidate immediate cardiopulmonary responses during successive PE episodes in a porcine model.MethodsThis was a randomized, controlled, blinded study of repeated measurements. Twelve pigs were randomly assigned to receive sham procedures or consecutive PEs every 15 min until doubling of mean pulmonary pressure. Cardiopulmonary assessments were conducted at 1, 2, 5, and 13 min after each PE using pressure-volume loops, invasive pressures, and arterial and mixed venous blood gas analyses. ANOVA and mixed-model statistical analyses were applied.ResultsPulmonary pressures increased after the initial PE administration (p < 0.0001), with a higher pulmonary pressure change compared to pressure change observed after the following PEs. Conversely, RV arterial elastance and pulmonary vascular resistance was not increased after the first PE, but after three PEs an increase was observed (p = 0.0103 and p = 0.0015, respectively). RV dilatation occurred following initial PEs, while RV ejection fraction declined after the third PE (p = 0.004). RV coupling exhibited a decreasing trend from the first PE (p = 0.095), despite increased mechanical work (p = 0.003). Ventilatory variables displayed more incremental changes with successive PEs.ConclusionIn an experimental model of consecutive PE, RV afterload elevation and dysfunction manifested after the third PE, in contrast to pulmonary pressure that increased after the first PE. Ventilatory variables exhibited a more direct association with clot burden.

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.

Hemodynamic and Respiratory Changes following Prone Position in Acute Respiratory Distress Syndrome Patients: A Clinical Study.

Limited data are available for the oxygenation changes following prone position in relation to hemodynamic and pulmonary vascular variations in acute respiratory distress syndrome (ARDS), using reliable invasive methods. We aimed to assess oxygenation and hemodynamic changes between the supine and prone posture in patients with ARDS and identify parameters associated with oxygenation improvement. Eighteen patients with ARDS under protective ventilation were assessed using advanced pulmonary artery catheter monitoring. Physiologic parameters were recorded at baseline supine position, 1 h and 18 h following prone position. The change in the Oxygenation Index (ΔOI) between supine and 18 h prone significantly correlated to the concurrent change in shunt fraction (r = 0.75, p = 0.0001), to the ΔOI between supine and 1 h prone (r = 0.73, p = 0.001), to the supine acute lung injury score and the OI (r = -0.73, p = 0.009 and r = 0.69, p = 0.002, respectively). Cardiac output did not change between supine and prone posture. Moreover, there was no change in pulmonary pressure, pulmonary vascular resistances, right ventricular (RV) volumes and the RV ejection fraction. The present investigation provides physiologic clinical data supporting that oxygenation improvement following prone position in ARDS is driven by the shunt fraction reduction and not by changes in hemodynamics. Moreover, oxygenation improvement was not correlated with RV or pulmonary circulation changes.

Extent and determinants of dynamic mitral regurgitation unmasked by handgrip exercise in patients with primary mitral regurgitation

Abstract Background Bicycle exercise is the exercise modality of choice to unmask the dynamic nature of mitral regurgitation (MR). Handgrip exercise may serve as alternative exercise intervention, as it can be performed physically accomplished by the majority of patients. Until now, there are only scarce data on the prevalence and magnitude of dynamic MR during handgrip exercise. Purpose To assess extent and predictors of exercise-induced dynamic MR during handgrip exercise in patients with primary MR. Methods We prospectively included patients with primary MR and at least mild severity that underwent echocardiography at rest and during three minutes of handgrip exercise according to a standardized protocol. Results The final patient cohort included 166 patients. Mean age was 72±12 years, 57% were female and 53% had atrial fibrillation. At rest, MR severity was graded as mild in 57% of patients, moderate MR in 27% and severe in 16%. Handgrip exercise led to an increase in at least one grade in MR severity in 31 patients (19%), while 15 patients (9%) experienced a decrease of MR severity (Fig. 1B). Twenty patients (14%) of those with non-severe MR at rest, developed severe MR during handgrip exercise (Fig. 1B). According to a pre-defined cutoff of increase in effective orifice regurgitant area (EROA) &amp;gt;10 mm2 during exercise, 19% of patients revealed a marked exercise-induced increase in MR, irrespective of the severity of MR at rest. Patients with marked exercise-induced increases in MR severity (EROA &amp;gt;10 mm2) had elevated left- (53±22ml/m2 vs. 44±19ml/m2; p=0.036), and right atrial volumes (43±19ml/m2 vs. 34±18ml/m2; p=0.014), more often pathology of the anterior mitral leaflet (e.g. prolapse; flail leaflet) (65% vs. 33%; p&amp;lt;0.001), and increased mitral annulus diameter (38±5mm vs. 36±4mm; p=0.003). The exercise-induced changes in EROA correlated with changes in estimated systolic pulmonary pressure from rest to exercise (r=0.438 (0.287 to 0.568); p&amp;lt;0.001) (Fig. 1C). Conclusion(s) In patients with primary MR, handgrip echocardiography unmasks marked exercise-induced increases of MR severity in every fifth patient independent of the severity at rest. A relevant number of patients with non-severe MR at rest developed severe MR during exercise. Dynamic MR is associated with bi-atrial dilatation, increased mitral annulus diameter, and pathology of the anterior mitral valve leaflet. Moreover, 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 Maximilian Spieker for a Clinician Scientist Track.

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.

Role of Circulating Inflammation in Regulating Pulmonary Pressure at Altitude

A patent foramen ovale (PFO) is a right-to-left shunt present in ~30% of the population that has been shown to worsen the degree of hypoxemia at sea level, and hypoxia is a known inflammatory stimulus. At altitude, the alveolar hypoxia results in increased pulmonary pressures, but it is unknown if this effect is more pronounced in those with a PFO, or if inflammation plays a role in regulating pulmonary pressures. Therefore, the purpose of this study is to determine whether changes in circulating inflammation correlate with changes in pulmonary pressures during 10 hours of normobaric hypoxia and determine whether those changes are different in those with a PFO. 36 participants matched for biological sex (18 female) and presence/absence of a PFO (18 PFO+) were exposed to 10 hours of normobaric hypoxia (11.5% O2). Venous blood samples were taken at 0 and 10 hours, and plasma was later analyzed via flow cytometry for the presence of 1 anti- and 12 pro-inflammatory cytokines. Pulmonary artery systolic pressure (PASP) and cardiac output (Q) were measured via echocardiography at 0, 4, 7, and 10 hours. Total pulmonary resistance (TPR) was calculated as PASP/Q. PASP (p < 0.0001), Q (p < 0.0001), and TPR (p = 0.0002) all significantly increased from baseline to 10 hours but plateaued at 7 hours. There were no differences in PASP, Q, or TPR between PFO- and PFO+ participants. The absolute change in each cytokine individually did not correlate with the absolute change in PASP. However, in a multiple linear regression model using the cytokines IL-18, IL-23, and IL-33, the change in IL-18 (p = 0.0021), IL-23 (p = 0.0031), and IL-33 (p = 0.0492) significantly predicted the change in PASP (significance of overall model, p = 0.0071). Our findings indicate that there are no effects of PFO on pulmonary pressures in response to 10 hrs of normobaric hypoxia. However, there is a positive association between the change in inflammation and the change in PASP during hypoxia exposure. These data suggest that individuals with highest levels of circulating inflammation may have an increased risk of developing higher pulmonary pressures under hypoxic conditions.

Effects and Outcomes of Pulmonary Function Testing after Left Ventricular Assist Device Implantation

Purpose The use of left ventricular assist device (LVAD) has increased significantly over the past several years. The physiologic effects of LVAD implantation on pulmonary function are not well elucidated. Studies evaluating the effects of LVAD implantation on pulmonary function testing (PFT) are inconsistent and data regarding the prognostic implications of PFT data on survival are scarce. Our study aims to evaluate the changes of PFT data after LVAD implantation in our own patient population and to assess the impact of pre-operative PFT data in regards to patient survival. Methods This was a single-center, retrospective analysis. Electronic medical records of all patients who underwent LVAD implantation at our institution between October 2011 to December 2019 were reviewed. PFTs prior to implantation were reviewed and were compared to records at 3 months and 12 months, when available. A change in a PFT value of greater than 10% was considered significant. Kaplan-Meier analysis and multivariable Cox regressions were performed to evaluate mortality. Results A total of 318 patients who underwent LVAD implantation at our center were reviewed. 44 patients who underwent pump exchanges were excluded. 81% of the patients were male and the mean age was 60 years old ± 12 years with a range of 24-83 years. Overall, there were no significant changes in FEV1 or FVC after LVAD implantation, with a mean increase of 2% and 4% in FEV1 at 3 months and 12 months respectively and a mean increase of 6% at both 3 months and 12 months in FVC. On the other hand, DLCO worsened at 3 months and 12 months and decreased by 21% and 10% respectively. A pre-operative DLCO of Conclusion Pulmonary physiology following LVAD implantation is complex. While patients with heart failure historically report improvement in dyspnea and exercise tolerance following their implant, our study indicates that a majority of their PFT values either remain unchanged or even worsen. Our analysis demonstrates a decrease in DLCO after LVAD implantation, which may be related to changes in pulmonary pressures following implantation. A pre-operative DLCO of

Acute pulmonary pressure change after transition to sacubitril/valsartan in patients with heart failure reduced ejection fraction.

AimsSacubitril/valsartan combines renin–angiotensin–aldosterone system inhibition with amplification of natriuretic peptides. In addition to well‐described effects, natriuretic peptides exert direct effects on pulmonary vasculature. The effect of sacubitril/valsartan on pulmonary artery pressure (PAP) has not been fully defined.Methods and resultsThis was a retrospective case‐series of PAP changes following transition from angiotensin‐converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) to sacubitril/valsartan in patients with heart failure reduced ejection fraction and a previously implanted CardioMEMS™ sensor. Pre‐sacubitril/valsartan and post‐sacubitril/valsartan PAPs were compared for each patient by examining averaged consecutive daily pressure readings from 1 to 5 days before and after sacubitril/valsartan exposure. PAP changes were also compared between patients based on elevated trans‐pulmonary gradients (trans‐pulmonary gradient ≥ 12 mmHg) at time of CardioMEMS™ sensor implantation. The cohort included 18 patients, 72% male, mean age 60.1 ± 13.6 years. There was a significant decrease in PAPs associated with transition from ACEI/ARB to sacubitril/valsartan. The median (interquartile range) pre‐treatment and post‐treatment change in mean, systolic and diastolic PAPs were −3.6 (−9.8, −0.7) mmHg (P < 0.001), −6.5 (−15.0, −2.0) mmHg (P = 0.001), and −2.5 (−5.7, −0.7) (P = 0.001), respectively. The decrease in PAPs was independent of trans‐pulmonary gradient (F(1,16) = 0.49, P = 0.49).ConclusionsIn this retrospective case series, transition from ACEI/ARB to sacubitril/valsartan was associated with an early and significant decrease in PAPs.

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.

Echocardiographic and clinical outcomes of MitraClip therapy in patients with severe mitral regurgitation

Abstract Background MitraClip implantation improves mitral regurgitation (MR), however its impact on pulmonary hypertension (PHT) is not fully elucidated. Our hypothesis was that changes in pulmonary pressure after MitraClip implantation might predict outcomes. Methods We studied a cohort of 149 consecutive patients who underwent MitraClip implantation between August 2015 and September 2019. We compared echocardiographic and clinical variables between a group with not-severe PHT and a group with severe PHT according to Pulmonary artery systolic pressure (PASP) &amp;gt;55 mmHg. Results Mean age of the cohort was 73±10 years, 75% were men, and 80% had functional MR. There are no differences in baseline characteristics between the two groups. There was a significant reduction of 13.6 mmHg in PASP at the severe PHT group from 68.2±10.9 mmHg before the procedure to 54.6±14.9 after (P=0.001) compared to the absence of a significant change in the second group. This reduction was maintained in the 6 months follow-up. Although PHT is considered a poor prognostic measure, and the severe PHT group had a baseline PASP higher than the not-severe group (P&amp;lt;0.001), however the Kaplan Meier curve did not show any significant difference in overall survival (p=0.468), and there is also no difference in one-year survival. Conclusions MitraClip therapy improves PASP in patients with severe MR and severe PHT. These patients showed the same survival as patients with not-severe PHT. MitraClip is a safety and effective procedure even for patients with severe PHT, that should not be excluded. Funding Acknowledgement Type of funding source: None

Remote Dielectric Sensing (reds) Use In The Prevention of Heart Failure Rehospitalizations- A Meta-analysis

Introduction Acute decompensated heart failure (ADHF) is a major cause of hospital readmissions despite technological advances and multiple guidelines. Remote dielectric sensing (ReDS) is a non-invasive electromagnetic-based tool that measures absolute lung fluid content. This technology identifies changes in pulmonary pressures before the development of symptoms, hence assists physicians to adjust the medical therapy before clinical worsening. The objective of this meta-analysis is to see the use of Remote Dielectric Sensing (ReDS) in the prevention of heart failure rehospitalizations. Methods Using PubMed, Ovid (MEDLINE), and Cochrane database we searched using the MeSH terms including,” Radar Sensing,” “Remote Dielectric Sensing (ReDS)” Heart failure exacerbations,” Heart failure rehospitalizations,”. The primary outcome was to assess the rate of heart failure rehospitalization with the use of the device. Unadjusted odds ratios were calculated using a random-effect model using RevMan V 5.3. Results Our analysis included a total of 568 patients in the ReDS group and 1167 patients without ReDS. The mean age of the sample was 65.2±12.8 with 66% males and 34% females. We found that patients with ReDS monitoring had lower odds of heart failure rehospitalizations (Odds ratio=0.41; 95% CI=0.31-0.54; p-value Conclusion ReDS monitoring can be beneficial in lowering heart failure rehospitalization by remote monitoring. However, large clinical studies are warranted to further assess its efficacy in reducing hospital readmissions and mortality.

Value of Chest Radiography and Electrocardiography in Diagnosis of Congenital Heart Diseases in Pediatrics in Comparison with Echocardiography

Background: Advances in echocardiographic technology have made a revolution in the quality of image and acquisition of data; however, it has also increased the cost of this diagnostic test. Objective: To determine if chest x ray (CXR) and electrocardiography (ECG) are still valuable in evaluation of new patients with heart murmurs in presence of echocardiography (ECHO). Patients and Methods: This was a six month, prospective clinical study undertaken in the Outpatient Pediatric Cardiology Unit, Zagazig University Children Hospital, between April 2018 and October 2018. The study included 44 patients (boys and girls) between the ages of 1 month and 14 years. All cases were subjected to detailed history, full clinical examination and imaging modalities as CXR, ECG and ECHO. Results: The highest accuracy of CXR was detection of right atrium (96.9%) followed by left ventricle (95.1%). The highest accuracy of ECG was detection of right atrium (98.5%) and left ventricle (95.5%). The agreement between CXR and ECHO in detection of pulmonary hypertension was 0.4 while that for ECG was 0.6. The agreement between CXR and ECHO in diagnosis of congenital heart diseases was 0.6 and that for ECG was 0.9. The accuracy of ECG in diagnosis of congenital heart disease was 95.4% while that for CXR was 70.4%. Conclusion: ECG is more accurate than CXR in detection of cardiac chamber enlargement and heart diseases in general but echocardiography still the most accurate method in this regard. The chest radiograph and electrocardiogram had limited values in the diagnosis of pulmonary pressure changes and echocardiography is the method to be used in this regard.

Value of Chest Radiography and Electrocardiography in Diagnosis of Congenital Heart Diseases in Pediatrics in Comparison with Echocardiography

Background: Advances in echocardiographic technology have made a revolution in the quality of image and acquisition of data; however, it has also increased the cost of this diagnostic test. Objective: To determine if chest x ray (CXR) and electrocardiography (ECG) are still valuable in evaluation of new patients with heart murmurs in presence of echocardiography (ECHO). Patients and Methods: This was a six month, prospective clinical study undertaken in the Outpatient Pediatric Cardiology Unit, Zagazig University Children Hospital, between April 2018 and October 2018. The study included 44 patients (boys and girls) between the ages of 1 month and 14 years. All cases were subjected to detailed history, full clinical examination and imaging modalities as CXR, ECG and ECHO. Results: The highest accuracy of CXR was detection of right atrium (96.9%) followed by left ventricle (95.1%). The highest accuracy of ECG was detection of right atrium (98.5%) and left ventricle (95.5%). The agreement between CXR and ECHO in detection of pulmonary hypertension was 0.4 while that for ECG was 0.6. The agreement between CXR and ECHO in diagnosis of congenital heart diseases was 0.6 and that for ECG was 0.9. The accuracy of ECG in diagnosis of congenital heart disease was 95.4% while that for CXR was 70.4%. Conclusion: ECG is more accurate than CXR in detection of cardiac chamber enlargement and heart diseases in general but echocardiography still the most accurate method in this regard. The chest radiograph and electrocardiogram had limited values in the diagnosis of pulmonary pressure changes and echocardiography is the method to be used in this regard.

P6467Pressure-mediated changes in the ventricular septum shape during exercise in patients with pulmonary hypertension: a 3-d echocardiography study

Abstract Background The role of interventricular (IV) septum in mediating the mechanical interaction between the two ventricles is well recognized. This interaction is promoted by several structural and hemodynamic determinants. We aimed at assessing the geometrical RV changes in patients with pulmonary hypertension (PH) compared to normal, evaluating RV curvature at rest and during stress testing addressing the specific role of pressure-induced changes in IV septum curvature. Methods Thirty-four subjects (15 controls; 19 PH patients) underwent RV real-time 3D full volume acquisition at rest and during exercise-echo. The 3D data were analysed off-line using the 4D RV TomTec software. The 3D mesh of the RV model was post-processed using a custom developed software. The value of mean regional curvature was assessed for the interventricular septum (IVS) at end-diastole (ED) and at end systole (ES). Results In controls the IVS curvature, assessed at end-diastole (ED) and end-systole (ES), was significantly (p&lt;0.001) more concave (at rest −0.31±0.06 at ED, and −0.29±0.06 at ES; during exercise −0.28±0.09 at ED, and −0.28±0.08 at ES) than in PH patients (at rest −0.09±0.14 at ED, and −0.09±0.11 at ES ; during exercise −0.05±0.18 at ED, and −0.02±0.18 at ES). There was no significant variation in any of RV IVS curvatures between rest and exercise or between ES and ED. In PH subjects, IVS curvature at ES weakly increased from −0.09±0.11 (SD) at rest to −0.02±0.18 during exercise (p=0.179).Nonetheless, the degree of IVS curvature was strongly related to systolic pulmonary artery pressure (PASP), both at rest (r=0.743 at ES, p&lt;0.01; r=0.794, p&lt;0.001 at ED) and during exercise (r=0.823 at ES, p&lt;0.0001; r=0.812 at ED, p&lt;0.0001). Conclusions These data provide new perspectives on how the interventricular septum morphology adapts during exercise in PH patients vs controls. Changes in IVS curvature are linearly related to pulmonary pressure changes and occur with different slope (rest-exercise) in PH vs controls.

Dobutamine stress echocardiography in pulmonary arterial hypertension

BackgroundThere is a growing interest in exploring the concept of right ventricular functional reserve in patients with pulmonary arterial hypertension. However, it is still unclear how it should be assessed. Aim of the study was to investigate the determinants of the changes in cardiac output and in pulmonary pressure during dobutamine stress echocardiography in pulmonary arterial hypertension. MethodsLow-dose dobutamine stress echocardiography was performed in 55 patients and 28 controls. Tricuspid annular plane systolic excursion, its ratio to systolic pulmonary artery pressure, right ventricular area change, degree of tricuspid regurgitation, right ventricular end-systolic pressure-area ratio, cardiac output were assessed at rest and at peak stress. ResultsAccording to the stress induced increase in cardiac output, patients were classified into 2 groups: above/equal to the median of 2.8 L/min (high cardiac output) or below the median (low cardiac output). High cardiac output patients were characterized by a greater increase in heart rate (+45.1 ± 17.5 vs +21.3 ± 17.7 bpm), a greater improvement in tricuspid annular plane systolic excursion (+4.2 ± 3.3 vs +1.9 ± 2.6 mm, P = 0.005) and a decrease in tricuspid regurgitation (P = 0.010) as compared to low cardiac output patients. Changes in pulmonary pressure were not associated with changes in indicators of right ventricular function but only with changes in heart rate. ConclusionsThe increase in cardiac output during dobutamine is associated with an improvement in longitudinal right ventricular function, a decrease in tricuspid regurgitation and an increase in heart rate. Changes in pulmonary pressure only reflect the changes in heart rate.

Hypoxia, not pulmonary vascular pressure, induces blood flow through intrapulmonary arteriovenous anastomoses.

Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms. Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal pulmonary pressure change. Hypoxic pulmonary vasoconstriction was attenuated in humans following acetazolamide administration and partially restored with bicarbonate infusion, indicating that the effects of acetazolamide on hypoxic pulmonary vasoconstriction may involve an interaction between arterial pH and PCO2. We observed that IPAVA blood flow during hypoxia was similar before and after acetazolamide administration, even after acid-base status correction, indicating that pulmonary pressure, pH and PCO2 are unlikely regulators of IPAVA blood flow. Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased with exposure to acute hypoxia and has been associated with pulmonary artery systolic pressure (PASP). We aimed to determine the direct relationship between blood flow through IPAVA and PASP in 10 participants with no detectable intracardiac shunt by comparing: (1) isocapnic hypoxia (control); (2) isocapnic hypoxia with oral administration of acetazolamide (AZ; 250 mg, three times a day for 48 h) to prevent increases in PASP; and (3) isocapnic hypoxia with AZ and 8.4% NaHCO3 infusion (AZ + HCO3 (-) ) to control for AZ-induced acidosis. Isocapnic hypoxia (20 min) was maintained by end-tidal forcing, blood flow through IPAVA was determined by agitated saline contrast echocardiography and PASP was estimated by Doppler ultrasound. Arterial blood samples were collected at rest before each isocapnic-hypoxia condition to determine pH, [HCO3(-)] and Pa,CO2. AZ decreased pH (-0.08 ± 0.01), [HCO3(-)] (-7.1 ± 0.7 mmol l(-1)) and Pa,CO2 (-4.5 ± 1.4 mmHg; P < 0.01), while intravenous NaHCO3 restored arterial blood gas parameters to control levels. Although PASP increased from baseline in all three hypoxic conditions (P < 0.05), a main effect of condition expressed an 11 ± 2% reduction in PASP from control (P < 0.001) following AZ administration while intravenous NaHCO3 partially restored the PASP response to isocapnic hypoxia. Blood flow through IPAVA increased during exposure to isocapnic hypoxia (P < 0.01) and was unrelated to PASP, cardiac output and pulmonary vascular resistance for all conditions. In conclusion, isocapnic hypoxia induces blood flow through IPAVA independent of changes in PASP and the influence of AZ on the PASP response to isocapnic hypoxia is dependent upon the H(+) concentration or Pa,CO2.

Abstract 16602: Pulmonary Vascular Response to Metaboreflex Stimulation During Submaximal Exercise in Heart Failure

Introduction: Neural feedback from skeletal muscle during exercise contributes to changes in pulmonary pressures in healthy individuals. Heart failure patients (HF) often develop pulmonary hypertension; however, the relationship between muscle afferent feedback and the pulmonary vasculature in HF remains unclear. Hypothesis: We examined the influence of metaboreceptor stimulation on pulmonary vascular capacitance using a validated non-invasive gas exchange equivalent (GX CAP ) in HF. Methods: Eleven HF patients (age 51±5 yrs; EF, 32±3%; NYHA class, 1.6±0.2) and 11 controls (CTL; age 43±3 yrs) completed 3 cycling session (4-min at 60% of peak oxygen consumption, VO 2 ). Session one: baseline control trial. Sessions 2 and 3: bilateral upper-thigh tourniquets inflated suprasystolic for 2 min at end-exercise (regional circulatory occlusion, RCO) with or without addition of inspired CO 2 to maintain end-exercise end-tidal CO 2 (P ET CO 2 ) (RCO+CO 2 ) (randomized). Rest, exercise, and recovery heart rate (HR), P ET CO 2 , and VO 2 were measured. O 2 pulse (VO 2 /HR) and GX CAP (O 2 pulseхP ET CO 2 ) were calculated. Results: During all conditions at end-exercise, HF demonstrated significantly lower GX CAP compared to CTL (p&lt;0.01). Percent change in GX CAP from end-exercise to 2 min post-exercise was attenuated in HF compared to CTL (41±5% vs 64±1%, respectively, p&lt;0.01) during the baseline trial. During RCO, HF had a 55±6% reduction in GX CAP from end-exercise compared to 77±2% in CTL (p&lt;0.01). During RCO+CO 2 , HF had a 49±4% reduction in GX CAP from end-exercise compared to 69±2% in CTL (p&lt;0.01). GX CAP was similar between sessions within HF. The CTL group demonstrated an attenuated return of GX CAP during RCO compared to both baseline and RCO+CO 2 (p&lt;0.01) with no difference between baseline and RCO+CO 2 . Conclusion: These data suggest the exercise mediated rise and post-exercise recovery of pulmonary vascular capacitance are attenuated in HF during constant-load submaximal exercise compared to CTL. Additionally, our data confirm previous reports that locomotor muscle afferent feedback influences pulmonary vascular capacitance in CTL; however, this model of locomotor muscle metaboreflex stimulation appears to a differential response in HF compared to CTL.

Intravenous Sildenafil in Right Ventricular Dysfunction with Pulmonary Hypertension following a Heart Transplant

The objective of the present work is to describe the experience with intravenous (IV) sildenafil in heart transplant (HT) patients with reactive pulmonary hypertension (PH) who developed right ventricular dysfunction (RVD) in the immediate postoperative period. The first 5 patients who received IV sildenafil followinga HT are presented. The HTs took place between March 2011 and September 2012 in patients aged 37 to 64 years; all patients were male. Prior to the HT, mean pulmonary artery pressure (mPAP) was 32-56 mmHg. In all cases, the hemodynamic study demonstrated PH reactivity (positive vasodilator test with nitric oxide). All 5 patients developed RVD with hemodynamic instability immediately after the HT, despite the administration of nitric oxide from the time of intubation prior to the implant, optimal medical treatment in all cases, and a ventricular assist in 2 cases. In all patients, IV sildenafil was initiated at 10 mg/8 h for 48 h and was subsequently increased to 20 mg/8 h. in its oral formulation until discharge from the hospital. The change in pulmonary pressure was assessed using a Swan-Ganz catheter. Ventricular function was assessed using echocardiography. Length of stay in the Resuscitation Unit and mid-term survival were also assessed. Average time of extracorporeal circulation was 200 ± 110 min and organ ischemic time was 210 ± 95 min. All of the patients demonstrated pulmonary and systemic hemodynamic improvement, as well as recovery of right ventricular function after completing the treatment with IV sildenafil. The stay in the Resuscitation Unit lasted 3-25 days. All the patients were discharged from hospital with no mortality to date. Intravenous sildenafil improves right ventricle hemodynamics associated with pulmonary hypertension post-HT. Prophylactic prevention with this drug could be indicated for patients with reactive PH who are about to receive a transplant.