Increase In Right Atrial Pressure Research Articles

Intrarenal Venous Doppler as a novel marker for optimal decongestion, management and prognosis in acute heart failure patients.

An increase in right atrial pressure is a common feature of acute decompensated heart failure (ADHF). Such increased pressure leads to persistent kidney congestion. A marker to guide optimal diuretic therapy is missing. We aim to correlate intrarenal Doppler ultrasound (IRD) in ADHF patients with clinical outcomes to assess whether renal hemodynamic parameter changes are useful for monitoring kidney congestion. Between December 2018 and January 2020, ADHF patients requiring intravenous diuretic therapy for at least 48 hours were considered for study selection. IRD blinded examination was performed day on 1, 3, 5 and clinical and laboratory parameters were recorded. Venous Doppler profile (VDP) were classified as continuous (C), pulsatile (P), biphasic (B), or monophasic (M) according to congestion degree; B and M profiles were considered deranged. VDP improvement (VDPimp) was defined as a change of ≥ 1 pattern degree or maintenance of C or P patterns. Arterial resistive index (RI) > 0.8 was considered elevated. Outcomes of death and rehospitalization were gathered at 60 days. Data were assessed by regression and Kaplain Meier analyses. All 177 ADHF patients admitted were screened and 72 were enrolled (27 females - median age 81 [76-87] years - median EF 40% [30-52]). VDP derangement decreased from 79.2% on day 1 to 51.4% on day 5 (p < 0.05). RI elevation decreased from 60.6% on day 1 to 43.1% on day 5 (p < 0.05). At day 5, VDPimp was registered in over half of the patients (59.7%). At day 5, signs of congestion (dyspnea/edema/rales), fluid accumulation (pleural/peritoneal fluid), hematocrit, and BNP improved (p > 0.05).After 60 days, 12 (16.7%) patients were readmitted and 9 (12.5%) died. VDPimp was identified as the unique independent factor associated with readmission (OR 0.22 CI 95% 0.05-0.94, p = 0.04) and death (OR 0.07, CI 95% 0.01-0.68, p = 0.02), with significantly better outcomes identified in VDPimp patients (Log Rank test p < 0.05). Decongestion may be associated with improvements in many clinical and instrumental parameters, but only VDPimp was associated with better clinical outcome. VDPimp should be incorporated in ad hoc AHF clinical trials to better define its role in everyday practice.

Platypnea-Orthodeoxia Syndrome in the Setting of Patent Foramen Ovale Without Pulmonary Hypertension or Major Lung Disease.

BackgroundPatent foramen ovale (PFO)‐associated platypnea‐orthodeoxia syndrome is characterized by dyspnea and hypoxemia when upright. The pathogenesis is thought to involve an increase in right atrial pressure or change in degree of right to left shunting with upright posture.Methods and ResultsWe sought to characterize patients with platypnea‐orthodeoxia syndrome related to PFO without pulmonary hypertension. We retrospectively reviewed databases at 3 tertiary referral hospitals in New South Wales, Australia from 2000 to 2019. Fourteen patients with a mean age of 69±14 years had a PFO with wide tunnel separation. Mean New York Heart Association Classification was II (±0.9) and 7 inpatients had been confined to bed (from postural symptoms). Baseline oxygen saturations supine were 93%±5% and 84%±6% upright. Two patients had a minor congenital heart defect and 4 had mild parenchymal lung disease with preserved lung function. The mean aortic root diameter was 37±6 mm and distance between aortic root and posterior atrial wall was 16±2 mm. Platypnea‐orthodeoxia syndrome was preceded by surgery in 5 patients and 1 patient had mild pneumonia. Successful closure of the PFO using an Amplatzer device was performed in 11 of 14 patients. Post‐closure, all patients had New York Heart Association Classification I (improvement 1.6±0.9, P<0.003) and semi‐recumbent oxygen saturations increased by 13%±8% (P<0.001, n=10).ConclusionsPlatypnea‐orthodeoxia syndrome is a debilitating condition, curable by PFO closure. Anatomical distortion of the atrial septum related to a dilated aortic root or shortening of the distance between the aortic root and posterior atrial wall may contribute to the syndrome.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Reduction in Right Atrial Pressures Is Associated With Hemodynamic Improvements After Transcatheter Edge-to-Edge Repair of the Tricuspid Valve.

Investigational transcatheter edge-to-edge repair (TEER) for severe tricuspid regurgitation (TR) has shown promise as an alternative to surgery, but factors influencing outcomes, optimal patient selection, and procedural timing remain incompletely defined. Given the limitations of determining TR severity by conventional echocardiography, our objectives were to determine whether invasive right atrial (RA) pressures performed during the procedure are related to patient outcomes. This study was a retrospective review of patients who underwent off-label tricuspid TEER using MitraClip (Abbott Vascular, Menlo Park, CA) for significant TR at a single institution. Intraprocedural mean RA pressure, RA peak V-wave, RA pressure nadir, and systolic increase in RA pressure (XV height) were recorded. Thirty-eight patients underwent tricuspid TEER; 33 underwent concomitant mitral TEER for mitral regurgitation. The study cohort was 39% female with a mean age of 78.6±14.3 years. Median follow-up was 339 days (interquartile range, 100-601). Any reduction in mean RA pressure, RA peak V-wave, RA nadir, and XV height occurred in 74%, 82%, 45%, and 87% of patients, respectively. At 1 year, event-free survival was 47%. Postprocedure XV height correlated with TR severity as determined by echocardiography (P<0.0001). The highest quartile of postprocedure XV height (>8 mm Hg) had worse event-free survival compared with those who had concluding XV height ≤8 mm Hg (P=0.02). Attainment of a concluding XV height less than or equal to median value was associated with a lower creatinine the next day (1.27±0.47 versus 1.64±0.47 mg/dL, P=0.04). Intraprocedural XV height correlates with TR severity after tricuspid TEER, and lower concluding pressures are associated with improved outcomes. Analysis of RA pressures may serve as a complementary tool for the evaluation of disease severity and procedural guidance.

Echocardiographic Findings in Patients (pts) Receiving Tyrosine Kinase Inhibitors (TKIs) for the Treatment of Chronic Myeloid Leukemia (CML)

INTRODUCTIONTKIs are standard therapy for pts with CML, with therapy continued over several years and in many instances indefinitely. Cardiac effects of TKIs have been described, including prolongation of QTc and arterio-thrombotic events. Echocardiographic manifestations have been reported including a reduction in left ventricular ejection fraction (EF) and an increase in right atrial pressure (RAP) and right ventricular systolic pressure (RVSP). However, no systematic description of these changes over the course of therapy has been presented. We retrospectively examined features and course of treatment of CML pts who had undergone echocardiogram during or following treatment with TKI therapy.METHODSWe interrogated medical records for pts with CML who had undergone echocardiogram (ECHO). Pts were grouped by TKI and analyzed their age, race, sex, line of therapy, duration of therapy, and change of TKIs. Variables were analyzed using general linear model (for continuous variables), or chi-square test or Fisher's exact test (for categorical variables). T-test was used to compare EF, RVSP, and RAP measure before vs. during and during vs. after index TKI for patients with sequential ECHOs. To compare echocardiograph findings by TKI we used separate repeated measures ANOVAs for EF, RVSP, and RAP for patients with sequential ECHOs. All statistical analyses were conducted using SAS v9.4.RESULTSA total of 146 ECHOs were performed on 111 pts. 11 pts had ECHO before, during, and after TKI treatment, 17 pts had ECHO before and during TKI treatment, and 20 had ECHO during and after TKI. Their median age was 53 yrs (range, 15-83), and 53.1% were male. 95 (86%) were in CP at the time of TKI start; 71 (64%) were receiving their 1st TKI. TKIs used included imatinib in 53 (400 mg n=19, 800 mg n=34), dasatinib in 39, and nilotinib in 19. Among patients with 3 sequential ECHOs, 9 were on dasatinib, 1 on imatinib (400 mg), and 1 on nilotinib. Among patients with ECHOs before and during treatment, 13 were on dasatinib, 2 on imatinib (800 mg), and 2 on nilotinib, while among patients with ECHOs during and after treatment, 16 were on dasatinib, 1 on nilotinib, 1 on imatinib (800 mg), and 1 on imatinib (400 mg). Pt characteristics are presented in Table 1.Considering all ECHOs in all pts, median EF was 62.5% before TKI, 60% during, and 60% after index TKI. Median RVSP was 30 mmHg before index TKI, 33 mmHg during, and 28 mmHg after TKI. Median RAP was stable at 5 mmHg throughout index TKI use. For patients with two sequential ECHOs, EF decreased significantly during TKI therapy (compared to baseline, difference=-3.1%, N=16, p=0.0186), and marginally after TKI (vs during, difference=-2.8%, N=20, p=0.091). There was a mild, non-statistically significant increase in RVSP from baseline to during TKI (difference=3.6 mmHg, N=16, p=0.30) and from during TKI to after TKI use (difference=1.9 mmHg, N=18, p=0.51). RAP did not differ from baseline to during TKI use (difference=1.1 mmHg, N=13, p=0.19), or during TKI to after TKI (difference=-0.71 mmHg, N=14, p=0.16). The results of these pairwise comparisons are presented in Figure 1. In repeated measures ANOVA of those patients with three sequential ECHOs, EF did not differ significantly among TKIs used (F=0.22, N=10, p=0.68), nor did RVSP (F=0.04, N=11, p=0.86). RAP was marginally different among TKIs used (F=9.53, N=11, p=0.054) (Figure 2). Full model results for these repeated measures ANOVAs are presented in Table 2.CONCLUSIONChronic administration of TKIs results in modest ECHO changes, particularly a slight decline in EF. There was also a modest increase in RAP with dasatinib and, to some extent, nilotinib but small sample size make these results preliminary. Still, monitoring of patients on TKIs with ECHOs at baseline and during therapy might be advisable. [Display omitted] DisclosuresKantarjian:ARIAD: Research Funding; Delta-Fly Pharma: Research Funding; Amgen: Research Funding; Pfizer: Research Funding; Bristol-Meyers Squibb: Research Funding; Novartis: Research Funding. Wierda:The University of Texas MD Anderson Cancer Center: Employment; GSK/Novartis: Consultancy, Honoraria, Research Funding; Genzyme: Consultancy, Honoraria; Acerta: Research Funding; Celgene: Consultancy, Honoraria; Gilead: Consultancy, Honoraria, Research Funding; Genentech/Roche: Consultancy, Honoraria, Research Funding; Pharmacyclics: Consultancy, Honoraria, Research Funding; Janssen: Research Funding; Juno: Research Funding; AbbVie: Consultancy, Honoraria, Research Funding; Merck: Consultancy, Honoraria; Emergent: Consultancy, Honoraria, Research Funding; Karyopharm: Research Funding; Kite: Research Funding; Sanofi: Consultancy, Honoraria. Jabbour:Bristol-Myers Squibb: Consultancy. Cortes:Pfizer: Consultancy, Research Funding; ImmunoGen: Consultancy, Research Funding; Novartis Pharmaceuticals Corporation: Consultancy, Research Funding; ARIAD: Consultancy, Research Funding; BMS: Consultancy, Research Funding; Sun Pharma: Research Funding; Teva: Research Funding.

RA pressure waveforms as a means for describing right ventricular diastolic stiffness

Introduction Exercise-induced changes in right atrial (RA) pressure associates with morality in patients with pulmonary hypertension (PH). Increased right ventricular (RV) diastolic stiffness impairs right ventricular filling during atrial contraction. Right atrial waveforms consist of the a-wave (atrial contraction) and v-wave (RA passive filling), as well as x and y descents representing atrial relaxation and ventricular filling, respectively. Ventricular distensibility has been associated with the difference between the x- and y-descents (x-y difference) in RA pressure. A positive x-y difference correlates with increased ventricular stiffness. The study aim was to investigate the relationship between RA pressure waveforms and RV diastolic function in patients with pulmonary arterial hypertension (PAH). We hypothesized that exercise-induced increases in RA pressure associate with increased RV diastolic stiffness and a positive x-y difference. Methods Participants (n = 52) with a right heart catheterization (RHC) and invasive cardiopulmonary exercise test were selected from the University of Arizona Pulmonary Hypertension Registry. Resting (REST) and peak exercise (EX) measurements of RA pressure (RAP), pulmonary artery pressure (PAP), cardiac output (CO), and heart rate (HR) were analyzed. Raw RA waveforms were analyzed to identify the a-wave, v-wave, and x- and y-descents using a custom MATLAB program. Single-beat methods were used to calculate end-diastolic elastance (Eed) a measure of RV stiffness. Wilcoxon signed-rank test was used test differences between rest and exercise conditions (R version 4.0.3). Data is presented as mean ± standard deviation or median [IQR]. A p< 0.05 is considered significant. Results Forty-three participants with pulmonary arterial hypertension diagnosis (age: 53 ± 13, sex: 73% female) and 9 participants without PH (age: 61 ± 13 years, sex: 100% female) were included. At rest, patients with pulmonary hypertension have increased PAP (37 ± 11 vs 16 ± 5 mmHg, p < 0.001) but no significant differences in RAP (2.7 [0.5-4.7] vs 0.1 [-0.1 – 3.0] mmHg, p = 0.4). There is a non-significant increase in Eed (0.61 [0.34-0.93] vs. 0.31 [0.26-0.53] mmHg/ml, p = 0.07) compared to controls. At peak exercise (PAH: 20 [10-50] W and controls: 30 [10-60] W), RA pressure significantly increased (Figure 1A). Participants with PAH had an exercise-induced increase in RA x-descent (Figure 1B) and y-descent (Figure 1C). There was an exercise-induced decrease in the x-y descent in participants with PAH but not Controls (Figure 1D). The x-y difference did not correlate with resting Eed at rest (p = 0.58) or peak exercise (p = 0.22). Discussion/Conclusion Exercise significantly increased average RA, x-descent, and y-descent pressure. The RA x-y difference did not correlate with end-diastolic elastance, another measure of ventricular stiffness. Overall, exercise decreased the x-y difference in participants with PAH that suggests an exercise-induced increase in ventricular distensibility. Further investigations are needed to determine if exercise-induced changes in RA pressure can unmask structural or pressure induced changes in RV diastolic function.

More Than Just Suckdown: Hemodynamics of Intermittent Inflow Cannula Obstruction

<h3>Introduction</h3> Waveforms can provide important insights on patient hemodynamics after durable left ventricular assist device (LVAD) implantation. Herein we describe a case of LVAD implanted as BTC complicated by intermittent inflow cannula obstruction. <h3>Case Report</h3> A 55-year old male was admitted decompensated heart failure. He had a Heartware device implanted as a bridge to candidacy (BTC) due to pulmonary hypertension and ischemic cardiomyopathy. In the 8 months since LVAD implant, the patient had gained 25 kg weight and had struggled to maintain a euvolemic state. Examination revealed an elevated jugular venous pressure, normal VAD sounds, peripheral edema and mean arterial pressure of 88mmHg. Monitoring of the LVAD demonstrated abnormal waveforms suggestive of intermittent suction events (Panel 1A). The patient was transferred to the ICU for invasive monitoring and transesophageal echocardiography to allow a ramp study. The imaging and hemodynamic data confirmed occlusion of the LVAD inflow cannula on each cardiac cycle (B,C) at his existing VAD settings (2740 rpm). A ramp study revealed a paradoxical increase in right atrial pressure and no improvement in blood pressure at higher speeds (D). Thoracic CT imaging confirmed cannula malposition and review of LVAD log files determined that there had been an abrupt change in pulsatility two months after implant and there had been increasingly frequent suction events since. Surgical reintervention was considered, however, given the chronicity of the changes, the consensus was to list the patient for urgent transplantation. <h3>Summary</h3> We describe a case of covert suction events where increasing body mass by 25kg (41%) may have contributed. In LVAD patients who are challenging to decongest, waveforms, hemodynamic and imaging guided optimization can improve function and identify complications.

Abstract 276: The Effects of Peep and Blood Pressure on Cerebral Tissue Oxygen Saturation During Hemorrhage in Swine

Introduction: Positive end-expiratory pressure (PEEP) is used to increase oxygen delivery by preventing end-expiratory alveolar collapse. However, the associated increased intrathoracic pressure can lead to an increase in right atrial pressure, and a decrease in venous return and cardiac output. Near infrared spectroscopy (NIRS) can be used as a non-invasive tool to continuously monitor cerebral tissue oxygen saturation. In this pilot study, we examined the effects of PEEP on cerebral oxygen saturation during a controlled hemorrhage. Methods: Four female, domestic swine (~30 kg), were bled to 3 target levels of mean arterial pressure (MAP; 55, 45, and 35 mm Hg). At each MAP target, 3 levels of PEEP were applied using a mechanical ventilator (5, 10, and 15 cm H 2 O) for ~10 minutes each. Following the reinfusion of shed blood and a recovery period, these interventions were repeated. Measurements included invasive aortic pressure and cerebral oxygen saturation using a commercially available tissue oximeter. A total of 61 epochs were entered into the following regression model: cerebral oxygen saturation = MAP + PEEP + animal number. Each epoch contained data from the last ~2 minutes of each MAP target and PEEP level. Results: The regression model yielded a coefficient of 0.30 for MAP ( P &lt; 0.001) and -0.08 for PEEP ( P = 0.09) and overall, explained 94% of the variance in cerebral oxygenation (adjusted R 2 = 0.94, P &lt; 0.001). While MAP was a stronger predictor in the model, higher PEEP levels appear to result in lower levels of cerebral oxygenation (see figure). Conclusions: Cerebral tissue oxygen saturation declines with lower mean arterial pressures and increased levels of PEEP. NIRS to measure cerebral oxygen saturation may be a useful clinical tool to ensure adequate cerebral oxygenation in patients with hypotension related to hemorrhage, particularly in those patients that require greater than physiologic PEEP to maintain central oxygenation.

Efficacy of Almitrine in the Treatment of Hypoxemia in Sars-Cov-2 Acute Respiratory Distress Syndrome

Efficacy of Almitrine in the Treatment of Hypoxemia in Sars-Cov-2 Acute Respiratory Distress Syndrome

PLATYPNEA-ORTHODEOXIA SYNDROME: KEY PATHOGENETIC ROLE OF PATENT FORAMEN OVALE (PFO) AND DRAMATIC RESPONSE TO PFO CLOSURE

PFO-associated platypnea-orthodeoxia syndrome (POS) is characterised by dyspnoea and hypoxaemia when upright. The pathogenesis is thought to involve an increase in right atrial pressure or change in degree of right to left shunting with upright posture due to structural change. We sought to

676 Platypnea-Orthodeoxia Syndrome: Key Pathogenetic Role of Patent Foramen Ovale (PFO) and Dramatic Response to PFO Closure

PFO-associated platypnea-orthodeoxia syndrome (POS) is characterised by dyspnoea and hypoxaemia when upright. The pathogenesis is thought to involve an increase in right atrial pressure or change in degree of right to left shunting with upright posture. We sought to characterise patients with POS related to PFO without pulmonary hypertension. We retrospectively reviewed databases at three tertiary referral hospitals in New South Wales, Australia from 2000 to 2019. Fourteen patients with a mean age of 69±14 years of age had a PFO with wide tunnel separation. Median NYHA Class was II and 7 inpatients had been confined to bed (from postural symptoms). It was 30±33 days from onset of POS to diagnosis. Baseline oxygen saturations supine were 93±5% and 84±6% upright. 2 patients had a minor congenital heart Platypnea-orthodeoxia Syndromedefect and 4 had mild parenchymal lung disease with preserved lung function. The mean aortic root diameter was 37±6mm and distance between aortic root and posterior atrial wall was 16±2mm. POS was preceded by surgery in 5 patients and 1 patient had mild pneumonia. Successful closure of the PFO using an Amplatzer device was performed in 11 of 14 patients. Post-closure, NYHA Class improved by 2±0.9 (p<0.001, n=11) and supine oxygen saturations increased by 13±8% (p<0.001, n=10). POS is a debilitating condition, curable by PFO closure. Anatomical distortion of the atrial septum related to a dilated aortic root or shortening of the distance between the aortic root and posterior atrial wall may contribute to the syndrome.

Preoperative Bleeding and Blood Product Transfusion Association with the Preoperative Use of Aspirin and Heparin in Left Ventricular Assist Device Implantation

Introduction Perioperative bleeding in the setting of LVAD implantation adversely impact outcomes. Hypothesis This project aims to determine pre-operative and intraoperative risk factors for this complication. Methods A retrospective cohort study was conducted including 90 consecutive advanced heart failure patients who underwent LVAD implantation as a bridge to transplantation or destination therapy from 2008 to 2017. By protocol, all anti-platelet therapies other than aspirin were discontinued 7 days pre-implantation. Aspirin was continued if clinically indicated. Additionally, any patients on anti-coagulant therapy were transitioned to intravenous heparin. Heparin infusion was discontinued 6 hours pre-operatively. Perioperative hemodynamics, laboratory values, cardiopulmonary bypass parameters, and blood product utilization were collected. Results Observable bleeding within 7 days of implant occurred in 15 patients (16%). This was significantly associated with the pre-operative use of heparin (OR 6.4; 95% CI 1.8-23.2; p=0.005) and its incidence increased for each 1 mmHg increase in right atrial pressure during pre-operative right heart catheterization (OR 1.1; 95% CI 1.0-1.2; p=0.03). Aspirin use within 3 days of implant increased the need of packed RBC transfusion both intra-operatively (OR 3.2; 95% CI 1.3-8.2; p=0.01) and post-operatively (OR 3.0; 95% CI 1.1-8.4; p=0.04) as well as increased the risk of hemoglobin drop ≥3 gm/dl on post-operative day 1 or the need of more than 2 packed RBC units peri-operatively (OR 4.2; 95% CI 1.6-11.4; p=0.004). Cardiopulmonary bypass time > 60 minutes increased the need for packed RBC transfusion post-operatively (OR 3.07; 95% CI 1.05-9.01; p=0.04). Conclusions Pre-operative aspirin and heparin are reversible factors that may affect the need for peri-operative blood products transfusion. This may indicate that these agents may need to be withheld longer or alternative antithrombotic preoperative agents should be considered.

Hemodynamic changes after acute fluid loading in patients with systemic sclerosis without pulmonary hypertension.

A fluid challenge with a rapid infusion of saline helps to discriminate between pre- and post-capillary pulmonary hypertension (PH) and allows unmasking hidden post-capillary PH. Systemic sclerosis (SSc) patients may present with biventricular systolic and diastolic dysfunction. The aim of this study was to evaluate the hemodynamic changes of the pulmonary circulation in SSc patients without PH after a fluid challenge. Twenty-five SSc patients and 25 controls underwent right heart catheterization in basal conditions and after volume loading with saline infusion of 7 mL/kg over 5–10 min. At baseline, there was no difference in hemodynamics between SSc patients and controls. Rapid volume loading resulted in a significant increase in pressures and flows in both groups. Increases in right atrial pressure (3 ± 1 vs. 2 ± 1 mmHg, P = 0.03), mean pulmonary artery pressure (5 ± 1 vs. 3 ± 1 mmHg, P < 0.001), and pulmonary artery wedge pressure (PAWP; 5 ± 2 vs. 3 ± 1 mmHg, P < 0.001) were larger in SSc patients than in controls. Conversely, cardiac index (0.4 ± 0.2 vs. 0.6 ± 0.3 L/min/m2, P = 0.005) increased less in SSc patients than in controls. Pulmonary vascular resistance did not differ between groups before and after volume loading. Four SSc patients and only one of the controls reached a PAWP > 18 mmHg suggesting latent left heart failure. Even if differences are small and not diagnostic for heart failure, SSc patients without PH have a larger increase in pulmonary vascular pressures and a smaller increase in cardiac output than controls after an acute volume loading, probably due to subclinical left ventricular diastolic dysfunction.

Heart-lung interactions during mechanical ventilation: the basics.

The hemodynamic effects of mechanical ventilation can be grouped into three clinically relevant concepts. First, since spontaneous ventilation is exercise. In patients increased work of breathing, initiation of mechanical ventilatory support may improve O2 delivery because the work of breathing is reduced. Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As lung volume increases so does the pressure difference between airway and pleural pressure. When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular resistance. Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection. Anything that over distends lung units will increase their vascular resistance, and if occurring globally throughout the lung, increase pulmonary vascular resistance. Decreases in end-expiratory lung volume cause alveolar collapse increases pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers that restore alveolar oxygenation without over distention will reduce pulmonary artery pressure. Third, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, it can induce profound decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload and will augment left ventricular ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved left ventricular ejection, increased cardiac output and reduced myocardial O2 demand. This brief review will focus primarily on mechanical ventilation and intrathoracic pressure as they affect right and left ventricular function and cardiac output.

Abstract 21298: Surveillance Invasive Hemodynamics in Pediatric Heart Transplant Patients: Utility or Futility?

Introduction: Although first year survival after pediatric heart transplant is improving, late-onset rejection, cardiac allograft vasculopathy (CAV), and graft failure remain significant challenges. Patients routinely undergo endomyocardial biopsy with invasive hemodynamics as the gold standard for rejection surveillance and assessment of long-term graft performance. However, it remains unclear how hemodynamic measures contribute to the monitoring of rejection, CAV, and graft dysfunction. This study aims to assess changes in hemodynamics as the graft ages in patients with or without a history of rejection or CAV. Hypothesis: We hypothesize that abnormal hemodynamics, particularly elevated filling pressures, are associated with CAV, rejection and graft aging. Methods: A total of 2,764 patients from the Pediatric Heart Transplant Study database from 1995-2014 met study criteria of survival to 1 year after transplant with available surveillance biopsy and hemodynamics. Retrospective analyses of 16,489 hemodynamic sets were performed. Results: The median age at transplant was 4.89 years [0.73, 12.95]. Average follow up time was 4.05 years [2.04, 7.17]. Fifty-six percent of patients were male, and 46% had history of congenital heart disease. When comparing hemodynamics collected at the first annual catheterization to 10 years after transplant, those who never had rejection or CAV showed statistically significant increases in right atrial pressure (RAP) (p=&lt;0.001), and pulmonary capillary wedge pressure (PCWP) (p = &lt;0.001) with concomitant decrease in cardiac index (p=0.01). When comparing hemodynamics from patients with a history of CAV or rejection to those without such events, patients with history of CAV or rejection had higher RAP (p=&lt;0.001) and PCWP (p = &lt;0.001), and lower cardiac index (p=0.003) and systemic vascular resistance (p=0.0001). Conclusions: Despite freedom from CAV or rejection, RAP and PCWP increase and cardiac index decreases as the graft ages. Additionally, the diagnosis of CAV or rejection during the life of the graft leads to further derangement in graft performance, which can be detected in hemodynamics. Serial hemodynamic assessment may contribute to the ongoing monitoring of graft function in pediatric recipients.

The right ventricle: interaction with the pulmonary circulation.

The primary role of the right ventricle (RV) is to deliver all the blood it receives per beat into the pulmonary circulation without causing right atrial pressure to rise. To the extent that it also does not impede left ventricular (LV) filling, cardiac output responsiveness to increased metabolic demand is optimized. Since cardiac output is a function of metabolic demand of the body, during stress and exercise states the flow to the RV can vary widely. Also, instantaneous venous return varies widely for a constant cardiac output as ventilatory efforts alter the dynamic pressure gradient for venous return. Normally, blood flow varies with minimal changes in pulmonary arterial pressure. Similarly, RV filling normally occurs with minimal increases in right atrial pressure. When pulmonary vascular reserve is compromised RV ejection may also be compromised, increasing right atrial pressure and limiting maximal cardiac output. Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, rapidly spiraling to acute cardiogenic shock and death. Treatments include reversing the causes of pulmonary hypertension and sustaining mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Chronic pulmonary hypertension induces progressive RV hypertrophy to match RV contractility to the increased pulmonary arterial elastance. Once fully developed, RV hypertrophy is associated with a sustained increase in right atrial pressure, impaired LV filling, and decreased exercise tolerance. Treatment focuses on pharmacologic therapies to selectively reduce pulmonary vasomotor tone and diuretics to minimize excessive RV dilation. Owning to the irreversible nature of most forms of pulmonary hypertension, when the pulmonary arterial elastance greatly exceeds the adaptive increase in RV systolic elastance, due to RV dilation, progressive pulmonary vascular obliteration, or both, end stage cor pulmonale ensues. If associated with cardiogenic shock, it can effectively be treated only by artificial ventricular support or lung transplantation. Knowing how the RV adapts to these stresses, its sign posts, and treatment options will greatly improve the bedside clinician’s ability to diagnose and treat RV dysfunction.

Simultaneous presentation of giant aneurysms of the coronary sinus and superior vena cava

Aneurysms of the coronary sinus and superior vena cava are rare and their aetiologies remain controversial. Some studies have shown that these acquired venous aneurysms are caused by an increase in right atrial pressure, which may be related to right heart failure. However, few reports have provided direct evidence to support this hypothesis. We present a rare case of combined giant aneurysms of the coronary sinus and vena cava, diagnosed using multiple imaging modalities. This case strongly supports the hypothesis that right heart diastolic failure may be an important mechanism underlying the pathogenesis of combined giant aneurysms.

Predictors of mortality after transjugular portosystemic shunt.

To investigate if echocardiographic and hemodynamic determinations obtained at the time of transjugular intrahepatic portosystemic shunt (TIPS) can provide prognostic information that will enhance risk stratification of patients. We reviewed medical records of 467 patients who underwent TIPS between July 2003 and December 2011 at our institution. We recorded information regarding patient demographics, underlying liver disease, indication for TIPS, baseline laboratory values, hemodynamic determinations at the time of TIPS, and echocardiographic measurements both before and after TIPS. We recorded patient comorbidities that may affect hemodynamic and echocardiographic determinations. We also calculated Model for End-stage Liver Disease (MELD) score and Child Turcotte Pugh (CTP) class. The following pre- and post-TIPS echocardiographic determinations were recorded: Left ventricular ejection fraction, right ventricular (RV) systolic pressure, subjective RV dilation, and subjective RV function. We recorded the following hemodynamic measurements: Right atrial (RA) pressure before and after TIPS, inferior vena cava pressure before and after TIPS, free hepatic vein pressure, portal vein pressure before and after TIPS, and hepatic venous pressure gradient (HVPG). We reviewed 418 patients with portal hypertension undergoing TIPS. RA pressure increased by a mean ± SD of 4.8 ± 3.9 mmHg (P < 0.001), HVPG decreased by 6.8 ± 3.5 mmHg (P < 0.001). In multivariate linear regression analysis, a higher MELD score, lower platelet count, splenectomy and a higher portal vein pressure were independent predictors of higher RA pressure (R = 0.55). Three variables predicted 3-mo mortality after TIPS in a multivariate analysis: Age, MELD score, and CTP grade C. Change in the RA pressure after TIPS predicted long-term mortality (per 1 mmHg change, HR = 1.03, 95%CI: 1.01-1.06, P < 0.012). RA pressure increased immediately after TIPS particularly in patients with worse liver function, portal hypertension, emergent TIPS placement and history of splenectomy. The increase in RA pressure after TIPS was associated with increased mortality. Age, splenectomy, MELD score and CTP grade were independent predictors of long-term mortality after TIPS.

Late-onset right ventricular dysfunction after mechanical support by a continuous-flow left ventricular assist device

Right heart failure (RHF) is a serious post-operative complication of left ventricular assist device (LVAD) implantation, with significant morbidity and mortality. Many clinical, hemodynamic and laboratory variables have been shown to have prognostic value for appearance of RHF. We sought to investigate the incidence of new-onset right ventricular dysfunction (RVD) complicating the long-term use of LVADs. We retrospectively examined all patients supported with a continuous-flow LVAD for >1 year at our center. Twenty patients (mean age 54 ± 10 years, 95% men, 60% with ischemic cardiomyopathy, left ventricular ejection fraction 22 ± 6%, pulmonary capillary wedge pressure 23.5 ± 7.5 mm Hg, brain natriuretic peptide [BNP] 1,566 ± 1,536 pg/ml, serum creatinine 1.6 ± 0.64 mg/dl, furosemide dose 643 ± 410 mg/day) underwent long-term mechanical support as destination therapy support with a continuous-flow LVAD (HeartMate II) at our center. During follow-up (1,219 ± 692 days), 9 patients (45%) manifested symptoms and signs of RVD (increase in right atrial pressure [RAP], BNP and daily furosemide dose compared with the early post-operative period). In these patients, RAP was increased by 6.6 ± 2.6 mm Hg and BNP by 526 ± 477 pg/ml, whereas furosemide dose increased by 145 ± 119 mg. The mean and median times of RVD onset were 2.3 ± 1.5 and 2.1 years, respectively, after LVAD implantation (range 0.4 to 4.8 years). Four of these patients (44.4%) demonstrated further deterioration of RV function and died 73 ± 106 days (median 25 days, range 9 to 231 days) after first manifestation of RVD. Comparisons of baseline variables regarding medical history and clinical status did not demonstrate significant differences between the patients with or without RVD, including parameters related to RV function at the time of implantation. Late-onset RVD is a complication of LVAD support, which can manifest several months to years from device implantation. This complication has significant adverse implications with regard to patient outcome. Prognostic factors need to be identified to follow and treat high-risk patients more efficiently.

Differential hemodynamic effects of exercise and volume expansion in people with and without heart failure.

Invasive hemodynamic exercise testing is commonly used in the evaluation of patients with suspected heart failure with preserved ejection fraction (HFpEF) or pulmonary hypertension. Saline loading has been suggested as an alternative provocative maneuver, but the hemodynamic changes induced by the 2 stresses have not been compared. Twenty-six subjects (aged, 67±10 years; n=14 HFpEF; n=12 control) underwent right heart catheterization at rest, during supine exercise, and with acute saline loading in a prospective study. Exercise and saline each increased cardiac output and pressures in the right atrium, pulmonary artery, and pulmonary capillary wedge positions. Changes in heart rate, blood pressure, rate-pressure product, and cardiac output were greater with exercise compared with saline. In controls subjects, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure increased similarly with saline and exercise, whereas in HFpEF subjects, exercise led to ≈2-fold greater increases in right atrial pressure (10±4 versus 6±3 mm Hg; P=0.02), pulmonary arterial pressure (22±8 versus 11±4 mm Hg; P=0.0001), and pulmonary capillary wedge pressure (18±5 versus 10±4 mm Hg; P<0.0001) compared with saline. Systolic reserve assessed by stroke work and cardiac power output was lower in HFpEF subjects with both exercise and saline. Systemic and pulmonary arterial compliances were enhanced with saline but reduced with exercise. Exercise elicits greater pulmonary capillary wedge pressure elevation compared with saline in HFpEF but not controls, suggesting that hemodynamic stresses beyond passive stiffness and increased venous return explain the development of pulmonary venous hypertension in HFpEF. Exercise testing is more sensitive than saline loading to detect hemodynamic derangements indicative of HFpEF. http://www.clinicaltrials.gov. Unique identifier: NCT01418248.