Pulmonary Arterial Capacitance Research Articles

Pulmonary artery wave intensity analysis in pulmonary hypertension associated with heart failure and reduced left ventricular ejection fraction.

Wave intensity analysis (WIA) uses simultaneous changes in pressure and flow velocity to determine wave energy, type, and timing of traveling waves in the circulation. In this study, we characterized wave propagation in the pulmonary artery in patients with pulmonary hypertension associated with left-sided heart disease (PHLHD) and the effects of dobutamine. During right heart catheterization, pressure and velocity data were acquired using a dual-tipped pressure and Doppler flow sensor wire (Combowire; Phillips Volcano), and processed offline using customized Matlab software (MathWorks). Patients with low cardiac output underwent dobutamine challenge. Twenty patients with PHLHD (all heart failure with reduced left ventricular ejection fraction) were studied. Right ventricular systole produced a forward compression wave (FCW), followed by a forward decompression wave (FDW) during diastole. Wave reflection manifesting as backward compression wave (BCW) following the FCW was observed in 14 patients. Compared to patients without BCW, patients with BCW had higher mean pulmonary artery pressure (28.7 ± 6.12 vs. 38.6 ± 6.5 mmHg, p = 0.005), and lower pulmonary arterial capacitance (PAC: 2.88 ± 1.75 vs. 1.73 ± 1.16, p = 0.002). Pulmonary vascular resistance was comparable. Mean pulmonary artery pressure of 34.5 mmHg (area under the curve [AUC]: 0.881) and PAC of 2.29 mL/mmHg (AUC: 0.833) predicted BCW. The magnitude of the FCW increased with dobutamine (n = 11) and correlated with pulmonary artery wedge pressure. Wave reflection in PHLHD is more likely at higher pulmonary artery pressures and lower PAC and the magnitude of reflected waves correlated with pulmonary artery wedge pressure. Dobutamine increased FCW but did not affect wave reflection.

Hemodynamic and Management Perspectives in Heart Failure Patients

Introduction Prevalence of heart failure (HF) is increasing, and right ventricular (RV) dysfunction is an independent predictor of mortality. Accurate echocardiographic evaluation of RV function is challenging and novel parameters which can aid in prediction RV function are required. Pulmonary artery Pulsatility index (PAPi) is one such parameter. Patients and Methods We conducted a prospective study in 33 patients admitted with symptoms of HF and severe LV dysfunction (EF < 35) who underwent right heart catheterization and followed them for 6 months. Primary objective was to determine the association of PAPi with hospitalizations and mortality in short-term follow-up in HF patients. Clinical, demographic, echocardiographic, and catheterization data were recorded. PAPi was calculated as a ratio of pulmonary artery pulse pressure and right atrial pressure. Results The mean age of population was 47 years (±12). Males were 20(61%) and females were 13(39%). Median PAPi in the study population was 2.42 (IQR-1.83). The study population were stratified into 3 groups based on 10th, 50th, and 90th percentile PAPi and on comparisons between groups PAPi was significantly associated with hospitalization at 1 and 6 months in univariate ( P = .03 and P = .03 respectively) and in multivariate analysis ( P = .04). PAPi was not found to be associated with mortality at 1 month or 6 months. However, the absolute mortality was low in the study population (n = 4). Conclusion PAPi has been found to be a strong and an independent predictor of hospitalization at 1 month and 6 months. Comments Advanced HF is seen in 1 out of 5 patients with HF. It is characterized by refractory symptoms, multiple hospitalizations, fluid retention, elevated natriuretic peptides, and decreased cardiac output often requiring inotropes. The survival rate is poor. The presence of right ventricular dysfunction is an independent predictor of mortality in these patients. Hemodynamic assessment is of importance in these patients to guide regarding further management, ie, use of inotropes, left ventricular assist devices, etc. The PAPi is a marker derived from the formula (PASP-PADP/RAP). 1 The outcome worsens as the PAPi decreases. However, the stroke volume, pulmonary artery capacitance (PAC), and right atrial pressure all have an impact on PAPi. Patients with high PAC will have better PAPi compared to those with low PAC with the stroke volume being constant. 2 Different subsets of HF population have varying PAPI thresholds, with isolated RV infarction having the lowest (0.9) and severe HF having the highest (3.2). 2 Future research should examine the impact of exercise, inotropes, and vasodilators.

Exertional Cardiac and Pulmonary Vascular Hemodynamics in Patients With Heart Failure With Reduced Ejection Fraction

BackgroundExertional dyspnea is a cardinal manifestation of heart failure with reduced ejection fraction (HFrEF), but quantitative data regarding exertional hemodynamics are lacking. ObjectivesWe sought to characterize exertional cardiopulmonary hemodynamics in patients with HFrEF. MethodsWe studied 35 patients with HFrEF (59 ± 12 years old, 30 males) who completed invasive cardiopulmonary exercise testing. Data were collected at rest, at submaximal exercise and at peak effort on upright cycle ergometry. Cardiovascular and pulmonary vascular hemodynamics were recorded. Fick cardiac output (Qc) was determined. Hemodynamic predictors of peak oxygen uptake (VO2) were identified. ResultsLeft ventricular ejection fraction and cardiac index were 23% ± 8% and 2.9 ± 1.1 L/min/m2, respectively. Peak VO2 was 11.8 ± 3.3 mL/kg/min, and the ventilatory efficiency slope was 53 ± 13. Right atrial pressure increased from rest to peak exercise (4 ± 5 vs 7 ± 6 mmHg,). Mean pulmonary arterial pressure increased from rest to peak exercise (27 ± 13 vs 38 ± 14 mmHg). Pulmonary artery pulsatility index increased from rest to peak exercise, while pulmonary arterial capacitance and pulmonary vascular resistance declined. ConclusionsPatients with HFrEF suffer from marked increases in filling pressures during exercise. These findings provide new insight into cardiopulmonary abnormalities contributing to impairments in exercise capacity in this population. Clinical Trial Registrationclinicaltrials.gov identifier: NCT03078972

Associations of right ventricular pulsatile load and cardiac power output to clinical outcomes in heart failure: Difference from systemic circulation

BackgroundAlthough left ventricular (LV) cardiac power output (CPO) is a powerful prognostic indicator in heart failure (HF), the significance of right ventricular (RV) CPO is unknown. In contrast, RV pulsatile load is a key prognostic marker in HF. We investigated the impact of RV-CPO and pulsatile load on cardiac outcome and the prognostic performance of the combined systemic and pulmonary circulation parameters in HF. MethodsRight heart catheterization and echocardiography were performed in 231 HF patients (62 ± 16 years, LV ejection fraction 42 ± 18 %). Invasive and noninvasive CPOs were calculated from mean systemic or pulmonary arterial pressure and cardiac output. LV-CPO was then normalized to LV mass (LV-P/M). Pulmonary arterial capacitance and the ratio of acceleration time to ejection time (AcT/ET) of RV outflow were used as parameters of RV pulsatile load. The primary endpoints, defined as a composite of cardiac death, HF hospitalization, ventricular arrythmia, and LVAD implantation after the examination, were recorded. ResultsNoninvasive CPOs were moderately correlated with invasive ones (LV: ρ = 0.787, RV: ρ = 0.568, and p < 0.001 for both). During a median follow-up period of 441 days, 57 cardiovascular events occurred. Lower LV-P/M and higher RV pulsatile load were associated with cardiovascular events; however, RV-CPO was not associated with the outcome. Echocardiographic LV-P/M and AcT/ET showed significant incremental prognostic value over the clinical parameters. ConclusionsRV pulsatile load assessed by AcT/ET may be a predictor of clinical events in HF patients. The combination of echocardiographic LV-P/M and AcT/ET could be a novel noninvasive prognostic indicator in HF patients.

Ventricular-arterial decoupling is associated with in-hospital adverse events in normotensive pulmonary embolism.

During acute pulmonary embolism (PE) a compensatory increase in right ventricular (RV) contractility is required to match increased afterload to maintain right ventricular-pulmonary arterial (RV-PA) coupling. The aim of this study was to assess the prognostic utility of RV-PA decoupling in acute PE. We assessed the association between measures of transthoracic echocardiography (TTE)-derived RV-PA coupling including tricuspid annular plane systolic excursion (TAPSE)/right ventricular systolic pressure (RVSP) and right ventricular fractional area change (FAC)/RVSP as well as stroke volume index (SVI)/RVSP (a measure of pulmonary artery capacitance) with adverse PE-related events (in-hospital PE-related mortality or cardiopulmonary decompensation) using logistic regression analysis. In 820 normotensive patients TTE-derived markers of RV-PA coupling were associated with PE-related adverse events. For each 0.1mm/mmHg decrease in TAPSE/RVSP the odds of an adverse event increased by 2.5-fold [adjusted OR (aOR) 2.49, 95% confidence interval (CI) 1.46-4.24, p = 0.001], for every 0.1%/mmHg decrease in FAC/RVSP the odds of an adverse event increased by 1.4-fold (aOR 1.42, CI 1.09-1.86, p = 0.010), and for every 0.1mL/mmHgm2 decrease in SVI/RVSP the odds of an event increased by 2.75-fold (aOR 2.78, CI 1.72-4.50, p < 0.001). In multivariable analysis, TAPSE/RVSP and SVI/RVSP were independent of other risk stratification methods including computed tomography-derived right ventricular dysfunction (RVD), the Bova score, and subjective assessment of TTE-derived RVD. In patients with normotensive acute PE, TTE-derived measures of RV-PA coupling are associated with adverse in-hospital PE-related events and provide incremental value in the risk assessment beyond computed tomography-derived RVD, the Bova score, or subjective TTE-derived RVD.

Reservoir Pressure Analysis in Group 2 Pulmonary Hypertension

<h3>Purpose</h3> The reservoir-wave model, based on the 3-element Windkessel, proposes that the pressure waveform consists of a reservoir pressure (Pres) related to arterial expansion and recoil and a superimposed pressure wave (excess pressure, Pex) generated by forward (ventricular stroke volume and input impedance) and backward travelling waves (related to local arterial properties). In this study we aim to describe Pres in Group 2 isolated post-capillary (IPC) and combined pre and post-capillary (CPC) pulmonary hypertension (PH). <h3>Methods</h3> Pressure and velocity data were acquired simultaneously using a dual-tipped pressure and doppler flow sensor wire during right heart catheterisation. The data were processed offline using customised Matlab software. CPC PH was defined as pulmonary capillary wedge pressure (PCWP) >15mmHg, mean pulmonary arterial pressure (mPAP)>20mmHg and PVR≥3 WU. <h3>Results</h3> Pres but not Pex was higher in CPC compared to IPC PH (Table). A representative pressures and flow tracing is shown in the figure. Higher PA pressures in CPC PH is due to higher Pres secondary to higher PVR, PAC and PCWP. Pres correlated to pulmonary vascular resistance (PVR)(p=0.002;r=0.58),pulmonary capillary wedge pressure(PCWP)(p<0.001;r=0.84) and heart rate(HR)(p=0.01;r=0.487); and negatively correlated to pulmonary artery capacitance(PAC)(p<0.001; r=0.68), but not stroke volume(SV). <h3>Conclusion</h3> This is the first study to compare Pres in group 2 PH. Higher PA pressures in CPC PH is due to higher Pres and not Pex. This suggests input impedance and wave reflection may not be the dominant mechanism in CPC PH.

Prognostication Of Pulmonary Artery Pulsatility Index And Pulmonary Capillary Wedge Pressure In Patients Requiring Impella Support

<h3>Introduction</h3> Pulmonary Artery Pulsatility Index (PaPi) was initially described to identify patients at risk for right ventricular dysfunction after inferior wall myocardial infarctions. The formula has since been applied to patients with advanced heart failure and pulmonary arterial hypertension to predict adverse outcomes. However, there is a lack of data regarding the utility of PaPi in assessing outcomes in patients requiring Impella 2.5 and CP - temporary left ventricular support devices. <h3>Hypothesis</h3> Lower PaPi and higher PCWP will be associated with increased mortality after Impella placement. <h3>Methods</h3> All patients admitted to York Hospital requiring Impella support due to cardiogenic shock between January 1, 2018 and May 1, 2020 were included in this retrospective study. Baseline characteristics and in-hospital mortality months were compared for hemodynamic variables including pulmonary capillary wedge pressure (PCWP) and PaPi. These numbers were collected and analyzed after Impella placement, 24 hours later, and the day of removal using ANOVA, logistic regression, and Fisher's exact test. <h3>Results</h3> There were 32 patients who met inclusion criteria. At time of Impella implantation, the cohort had an average age of 67.6 + 9.9, ejection fraction of 24.62 + 13.09%, brain natriuretic peptide of 772.03 + 1103.8 pg/dL, and lactate of 4.634 + 4.194 mmol/L. The average duration of Impella support was 2.6875 + 1.89 days. Pulmonary artery pulsatility index was strongly associated with in-hospital mortality at values less than 1.2 after Impella placement (p = 0.0325) and on the day of removal (p = 0.0003). Increasing PCWP strongly correlated with in-hospital mortality after Impella placement (p = 0.0179) and on the day of removal (p = 0.0032). Neither PCWP nor PaPi correlated with mortality at 24 hours. <h3>Conclusions</h3> In patients requiring Impella support for cardiogenic shock, PaPi and PCWP are significant predictors of in-hospital mortality. These variables are strongly associated with mortality after Impella placement and on the day of removal. PaPi is a better predictor of poor outcomes at lower values, as values less than 1.2 strongly correlated with mortality. Increasing PCWP will invariably increase the value of PaPi due to the effects of PCWP on pulmonary artery capacitance. Patients with worsening left ventricular dysfunction will thus have higher values of PaPi. A lower PaPi may be an ominous sign in patients requiring mechanical support, but further studies should be done to further assess its prognostic role.

Pulmonary artery capacitance and pulmonary vascular resistance as prognostic indicators in acute pulmonary embolism.

AimsThe non-invasive calculation of right ventricular (RV) haemodynamics as pulmonary artery (PA) capacitance (PAC) and pulmonary vascular resistance (PVR) have proved to be feasible, easy to perform, and of high prognostic value. We, therefore, evaluated whether baseline PAC and PVR could predict clinical outcomes for patients with acute pulmonary embolism (PE).Methods and resultsWe prospectively followed 373 patients [mean (standard deviation) age, 64.1 (14.9) years; 58.4% were men, and 27.9% had cancer] who had acute PE and transthoracic echocardiography within 1 day of diagnosis from 1 March 2013 through 30 June 2020. Pulmonary artery capacitance was calculated as left ventricular stroke volume/(PA systolic pressure − PA diastolic pressure). Pulmonary vascular resistance was calculated as (tricuspid regurgitant velocity/RV outflow tract velocity time integral) × 10 + 0.16. These two variables were calculated retrospectively from the values obtained with transthoracic echocardiography. Pulmonary artery capacitance was acquired in 99 (27%) patients and PVR in 65 (17%) patients. Univariable and bivariable logistic regression analyses, and receiver operating characteristic curves were used to evaluate the ability of these haemodynamic measurements to predict mortality up to 6 months. After using bivariable models to adjust individually for age, cancer, and pulmonary hypertension. Pulmonary vascular resistance was associated with all-cause mortality at 3 months [area under the curve (AUC) 0.75, 95% confidence interval (CI) 0.61–0.86; P = 0.01], and 6 months (AUC 0.81; 95% CI 0.69–0.91; P≤ 0.03). Pulmonary artery capacitance was associated with all-cause mortality at 30 days (AUC 0.95; 95% CI 0.82–0.99; P < 0.001) and 3 months (AUC 0.84; 95% CI 0.65–0.99; P = 0.003).ConclusionNon-invasive measurement of RV haemodynamics could provide prognostic information of patients with acute PE. Pulmonary artery capacitance and PVR are potentially important predictors of all-cause mortality in these patients and should be explored in future studies.

Ischaemic versus non-ischaemic: how does heart failure aetiology affect pulmonary arterial capacitance and pulmonary artery pulsatility index in end-stage heart failure?

Background The aetiology of heart failure may have different effects on right ventricular (RV) function, pulmonary pressures and RV afterload. Pulmonary arterial capacitance (PAC) and pulmonary artery pulsatility index (PAPi) are novel haemodynamic indices used in determining RV afterload and RV function, respectively. We aimed to investigate whether there was a difference in PAC and PAPi between ischaemic cardiomyopathy (ICMP) and non-ischaemic cardiomyopathy (NICMP) in patients with end-stage heart failure. Methods and results A total of 215 subjects undergoing evaluation for heart transplantation or left ventricular (LV) assist device were classified into two groups: ICMP (n = 101) and NICMP (n = 114). The patients with LV ejection fraction ≤ 25% were included in the study. ICMP group had lower PAC and higher PAPi values compared to NICMP group [1.25 (0.82–1.86) vs. 1.58 (1.02–2.21), p = 0.002 and 3.4 (2.2–5.0) vs. 2.5 (1.7–4.0); p = 0.007]. Pulmonary vascular resistance, pulmonary artery systolic and mean pressure were higher in ICMP group compared to NICMP group [3.5 ± 1.8 vs. 2.9 ± 2.3, p = 0.004; 59.0 (42.0–73.0) vs. 46.0 (37.0–59.0), p < 0.001, 35.0 (27.0–46.0) vs. 31.0 (23.0–39.0), p = 0.002]. The patients with ICMP had higher tricuspid annular plane systolic excursion and less RV dilatation. ICMP was an independent risk factor for pulmonary hypertension (OR: 4.02, 95% CI: 1.13-14.24, p = 0.031). Conclusion ICMP was associated with lower PAC and higher PAPi. These results indicated that an ischaemic aetiology is associated with higher RV afterload and better RV function in the end-stage heart failure.

Pulmonary artery capacitance a simple and novel prognostic variable in acute pulmonary embolism

Abstract Background The non-invasive calculation of right ventricular hemodynamics such as the pulmonary artery capacitance (PAC) has proven to be feasible and easy to perform. The simplified pulmonary embolism severity index (sPESI) and pulmonary vascular resistance (PVR) are other prognostic tools that have been used in the past. Purpose To evaluate if baseline PAC can outperform PVR and sPESI to predict all-cause short-term mortality in patients with acute pulmonary embolism (PE). Methods 373 patients with acute PE and a transthoracic echocardiogram performed within one day of diagnosis from March 2013 through June 2020 were followed prospectively. PAC was calculated as: Left ventricular stroke volume/ (Pulmonary artery systolic pressure – Pulmonary artery diastolic pressure). PVR was calculated as: Tricuspid regurgitant velocity / Right ventricular outflow tract velocity time integral x 10 + 0.16. The sPESI was used to evaluate prognosis by categorizing patients into low and high-risk categories. Multiple logistic regression analyses and receiver-operating characteristic curves were used to evaluate the ability of PAC, PVR, and sPESI to predict all-cause mortality up to six months. The Youden index was used to determine the cut-off value with the highest sensitivity and specificity. Kaplan–Meier curves were performed to determine event-free survival rate, differences between groups were assessed using the Wilcoxon Test. Results Mean age was 64±15 years (58% male, 28% cancer). PAC was associated with mortality at thirty days (p 0.0003), three months (p 0.003), and six months (p 0.011) (Table). PVR was associated with mortality at thirty days, three months, and six months (p 0.045, 0.012, and 0.031 respectively). The sPESI score ≥1 (high risk) was associated with all-cause mortality at three months and six months (p 0.0136 and &amp;lt;0.0001 respectively). PAC was the strongest predictor of all-cause mortality with an AUC of 0.95 (CI 0.82- 0.99) at thirty days, 0.84 (CI 0.65–0.99) at three months, and 0.77 (CI 0.57–0.96) for six months. Corresponding Kaplan-Meier survival curve of PAC and thirty days all-cause mortality is presented in the Figure. PVR had an AUC of 0.75 (CI 0.48–0.95) at thirty days, 0.79 (CI 0.58–0.94) at three months, and 0.72 (CI 0.50–0.90) at six months. The sPESI had an AUC of 0.62 (CI 0.54–0.66) at three months and 0.64 (CI 0.59–0.67) at six months. Conclusion In patients with acute PE, PAC outperforms sPESI and PVR as a predictor of short-term all-cause mortality at thirty days, three months, and six months. These three variables should be explored head to head prospectively for their utility to predict short term all-cause mortality. Funding Acknowledgement Type of funding sources: None.

Prognostic Importance of Pulmonary Arterial Capacitance in Acute Decompensated Heart Failure With Preserved Ejection Fraction.

BackgroundAlthough the prognostic importance of pulmonary arterial capacitance (PAC; stroke volume/pulmonary arterial pulse pressure) has been elucidated in heart failure with reduced ejection fraction, whether its significance in patients suffering from heart failure with preserved ejection fraction is not known. We aimed to examine the association of PAC with outcomes in inpatients with heart failure with preserved ejection fraction.Methods and ResultsWe prospectively studied 705 patients (median age, 83 years; 55% women) registered in PURSUIT‐HFpEF (Prospective Multicenter Observational Study of Patients With Heart Failure With Preserved Ejection Fraction). We investigated the association of echocardiographic PAC at discharge with the primary end point of all‐cause death or heart failure rehospitalization with a mean follow‐up of 384 days. We further tested the acceptability of the prognostic significance of PAC in a subgroup of patients (167/705 patients; median age, 81 years; 53% women) in whom PAC was assessed by right heart catheterization. The median echocardiographic PAC was 2.52 mL/mm Hg, with a quartile range of 1.78 to 3.32 mL/mm Hg. Univariable and multivariable Cox regression testing revealed that echocardiographic PAC was associated with the primary end point (unadjusted hazard ratio, 0.82; 95% CI, 0.72–0.92; P=0.001; adjusted hazard ratio, 0.86; 95% CI, 0.74–0.99; P=0.035, respectively). Univariable Cox regression testing revealed that PAC assessed by right heart catheterization (median calculated PAC, 2.82 mL/mm Hg) was also associated with the primary end point (unadjusted HR, 0.70; 95% CI, 0.52–0.91; P=0.005).ConclusionsA prospective cohort study revealed that impaired PAC diagnosed with both echocardiography and right heart catheterization was associated with adverse outcomes in inpatients with heart failure with preserved ejection fraction.RegistrationURL: https://upload.umin.ac.jp/cgi‐open‐bin/ctr_e/ctr_view.cgi?recptno=R000024414. Unique identifier: UMIN000021831.

Hemodynamics Prior to Valve Replacement for Severe Aortic Stenosis and Pulmonary Hypertension during Long-Term Follow-Up.

(1) Background: Pulmonary hypertension after aortic valve replacement (AVR; post-AVR PH) carries a poor prognosis. We assessed the pre-AVR hemodynamic characteristics of patients with versus without post-AVR PH. (2) Methods: We studied 205 patients (mean age 75 ± 10 years) with severe AS (indexed aortic valve area 0.42 ± 0.12 cm2/m2, left ventricular ejection fraction 58 ± 11%) undergoing right heart catheterization (RHC) prior to surgical (70%) or transcatheter (30%) AVR. Echocardiography to assess post-AVR PH, defined as estimated systolic pulmonary artery pressure > 45 mmHg, was performed after a median follow-up of 15 months. (3) Results: There were 83/205 (40%) patients with pre-AVR PH (defined as mean pulmonary artery pressure (mPAP) ≥ 25 mmHg by RHC), and 24/205 patients (12%) had post-AVR PH (by echocardiography). Among the patients with post-AVR PH, 21/24 (88%) had already had pre-AVR PH. Despite similar indexed aortic valve area, patients with post-AVR PH had higher mPAP, mean pulmonary artery wedge pressure (mPAWP) and pulmonary vascular resistance (PVR), and lower pulmonary artery capacitance (PAC) than patients without. (4) Conclusions: Patients presenting with PH roughly one year post-AVR already had worse hemodynamic profiles in the pre-AVR RHC compared to those without, being characterized by higher mPAP, mPAWP, and PVR, and lower PAC despite similar AS severity.

Right ventricular pressure-volume loop shape and systolic pressure change in pulmonary hypertension.

Right ventricular (RV) function determines outcome in pulmonary arterial hypertension (PAH). RV pressure-volume loops, the gold standard for measuring RV function, are difficult to analyze. Our aim was to investigate whether simple assessments of RV pressure-volume loop morphology and RV systolic pressure differential reflect PAH severity and RV function. We analyzed multibeat RV pressure-volume loops (obtained by conductance catheterization with preload reduction) in 77 patients with PAH and 15 patients without pulmonary hypertension in two centers. Patients were categorized according to their pressure-volume loop shape (triangular, quadratic, trapezoid, or notched). RV systolic pressure differential was defined as end-systolic minus beginning-systolic pressure (ESP - BSP), augmentation index as ESP - BSP/pulse pressure, pulmonary arterial capacitance (PAC) as stroke volume/pulse pressure, and RV-arterial coupling as end-systolic/arterial elastance (Ees/Ea). Trapezoid and notched pressure-volume loops were associated with the highest afterload (Ea), augmentation index, pulmonary vascular resistance (PVR), mean pulmonary arterial pressure, stroke work, B-type natriuretic peptide, and the lowest Ees/Ea and PAC. Multivariate linear regression identified Ea, PVR, and stroke work as the main determinants of ESP - BSP. ESP - BSP also significantly correlated with multibeat Ees/Ea (Spearman's ρ: -0.518, P < 0.001). A separate retrospective analysis of 113 patients with PAH showed that ESP - BSP obtained by routine right heart catheterization significantly correlated with a noninvasive surrogate of RV-arterial coupling (tricuspid annular plane systolic excursion/pulmonary arterial systolic pressure ratio; ρ: -0.376, P < 0.001). In conclusion, pressure-volume loop shape and RV systolic pressure differential predominately depend on afterload and PAH severity and reflect RV-arterial coupling in PAH.

Role of pulmonary arterial capacitance in predicting mortality in patients with pulmonary hypertension: A systematic review and meta-analysis

BackgroundPulmonary arterial capacitance or compliance (PAC) has been reported as an independent predictor of mortality in patients with pulmonary arterial hypertension (PAH) and pulmonary hypertension secondary to left heart disease (PH-LHD). MethodsWe conducted a literature search of PubMed/Medline, Google Scholar, and Cochrane library databases from July 30th to September 4th, 2020, and identified all the relevant studies reporting mortality outcomes in patients with PAH and PH-LHD. Pooled data from these studies were used to perform a meta-analysis to identify the role of PAC in predicting all-cause mortality in this subset of patients. ResultsPooled data on 4997 patients from 15 individual studies showed that the mortality risk in patients with PAH and PH-LHD varies significantly per unit change in PAC either from baseline or during follow-up. A reduction in PAC per 1 ml/mmHg was associated with a 4.25 times higher risk of all-cause mortality (95% CI 1.42–12.71; p = 0.021) in PAH patients. Among patients with PH-LHD, mortality risk increased by ~30% following a unit decrease in PAC (HR, 1.29; p = 0.019), whereas an increase in PAC by 1 ml/mmHg lowered the mortality risk by 30% (HR, 0.70). ConclusionPAC is a strong and independent predictor of all-cause mortality in both patients with PAH and PH-LHD. A decrease in PAC by 1 ml/mmHg from baseline or during follow-up significantly increases the risk of all-cause mortality among both patients with PAH and PH-LHD. Treatment modalities targeted at PAC improvement can affect the overall survival and quality of life in such patients.

Presence and significance of mid-systolic notch on right ventricular outflow tract velocity envelopes in pulmonary hypertension due to heart failure

Abstract Funding Acknowledgements Type of funding sources: None. Background A mid-systolic notch (MSN) of the right ventricular outflow tract (RVOT) pulsed-wave Doppler envelope, which is recognized as a characteristic finding in pre-capillary pulmonary hypertension (PH), is often observed in heart failure (HF) patients. However, clinical significance of MSN formation in HF has not been elucidated. Methods Consecutive 233 HF patients who underwent right heart catheterization and echocardiography within 24 hours were enrolled. Isolated post-capillary PH (IpcPH) was defined as mean pulmonary arterial pressure (mPAP) &amp;gt;20 mmHg, mean pulmonary artery wedge pressure (mPAWP) &amp;gt;15 mmHg, and pulmonary vascular resistance (PVR) &amp;lt;3 Wood units and combined pre- and post-capillary PH (CpcPH) was as mPAP &amp;gt;20 mmHg, mPAWP &amp;gt;15 mmHg, and PVR ≥3 Wood units. Pulmonary arterial capacitance (PAC) was calculated as stroke volume / pulmonary arterial pulse pressure [mL/mmHg]. MSN was defined as formation of notch within first half of the RVOT pulsed-wave Doppler envelope. Results Prevalence of IpcPH, CpcPH, and without PH were 87 (37%), 45 (19%), and 101 (43%), respectively and MSN was observed in 8 (9%) of IpcPH, 17 (38%) of CpcPH, and 1 (1%) of patients without PH. Among the hemodynamic and echocardiographic parameters, mPAP and PAC independently determined occurrence of MSN in all the multivariable models (Table). Interestingly, when the PH patients were dimidiated according to median PAC (3.2 mL/mmHg), 25 out of 102 PH patients (25%) with low PAC showed MSN whereas any of PH patients with high PAC did not (Figure). Conclusion MSN was frequently observed in HF patients showing CpcPH. Combination of elevated pressure and reduced compliance of the pulmonary circulation could determine occurrence of MSN in HF. Determinants of MSN occurrence Univariable analysis Multivariable analysis Model 1 Model 2 Model 3 Model 4 variables OR (95% CI) p OR (95% CI) p OR (95% CI) p OR (95% CI) p OR (95% CI) p LV ejection fraction 0.97 (0.94-0.99) 0.007 1.00 (0.96-1.03) 0.795 LV mass index 1.00 (1.00-1.02) 0.143 PAW pressure 1.13 (1.08-1.18) &amp;lt;0.001 0.92 (0.82-1.03) 0.135 Mean PA pressure 1.14 (1.09-1.19) &amp;lt;0.001 1.08 (1.02-1.14) 0.006 1.15 (1.04-1.27) 0.004 1.08 (1.00-1.17) 0.030 1.07 (1.01-1.14) 0.025 Mean RA pressure 1.14 (1.06-1.22) &amp;lt;0.001 1.00 (0.90-1.11) 0.978 Pulmonary vascular resistance 1.97 (1.45-2.67) &amp;lt;0.001 1.20 (0.88-1.63) 0.225 Pulmonary arterial capacitance 0.27 (0.15-0.48) &amp;lt;0.001 0.49 (0.26-0.92) 0.010 0.44 (0.23-0.85) 0.004 0.47 (0.24-0.93) 0.011 0.49 (0.26-0.93) 0.011 Abstract Figure.

Echocardiographic assessment of pulmonary arterial capacitance predicts mortality in pulmonary hypertension

BackgroundPulmonary arterial capacitance (PAC) is one of the strongest predictors of clinical outcomes in patients with pulmonary hypertension (PH). We examined the value of an echocardiographic surrogate for PAC (ePAC) as a predictor of mortality in patients with PH. MethodsWe performed a retrospective study of 302 patients with PH managed at a PH comprehensive care center over a cumulative follow-up time of 858 patient-years. Charts from 2004 to 2018 were reviewed to identify patients in whom a right heart catheterization (RHC) was performed within two months of an echocardiogram. Standard invasive, non-invasive, functional, and biochemical prognostic markers were extracted from the time of RHC. The primary outcome was all-cause mortality. Cox proportional hazards models were used to model the time from RHC to the primary outcome or last medical contact. ResultsVariables associated with all-cause mortality included ePAC [standardized hazard ratio (HR) 0.68, 95% CI 0.48−0.98, p = 0.036], RHC-PAC (HR 0.68, 95% CI 0.48−0.96, p = 0.027), echocardiographic pulmonary vascular resistance (HR 1.29, 95% CI 1.05–1.60, p = 0.017), six-minute walk distance (HR 0.43, 95% CI 0.23−0.82, p = 0.01), and B-type natriuretic peptide (HR 1.29, 95% CI 1.03–1.62, p = 0.027). In multivariable-adjusted Cox analysis, ePAC predicted all-cause mortality independently of age, gender, and multiple comorbidities. There was a graded and stepwise association between low (<0.15 cm/mmHg), medium (0.15−0.25 cm/mmHg), and high (>0.25 cm/mmHg) tertiles of ePAC and all-cause mortality. ConclusionsWe have demonstrated that ePAC is a readily available echocardiographic marker that independently predicts mortality in PH, and have provided clinically relevant ranges by which to risk-stratify patients and predict mortality.

Modeling survival using decision tree analysis in pulmonary hypertension due to left heart disease. the prognostic significance of PVR &amp;lt;3WU when TAPSE &amp;lt;16mm

Abstract Aims In 2019, PVR&amp;lt;3 WU was adopted to stratify patients at low risk of pulmonary hypertension due to left heart disease (PH-LHD) as well those with isolated PH-LHD. We sought to evaluate whether the supervised machine learning with Decision Tree analysis that provides more information than Cox Proportional analysis by forming a hierarchy of multiple covariates, confirms this risk stratification. Methods 202 consecutive patients (mean age: 69±11 y, females 42%) with mean pulmonary artery pressure (mPAP)≥20mmHg and wedge pressure&amp;gt;15mmHg were recruited. Transpulmonary pressure gradient ≥12mmHg, pulmonary vascular resistance (PVR) ≥3WU, diastolic pressure gradient ≥7mmHg, pulmonary arterial capacitance&amp;lt;1.1 ml/mmHg, TAPSE&amp;lt;16 mm, peak systolic tissue Doppler velocity&amp;lt;10cm/s and right ventricular end-diastolic area ≥25 cm2 were the seven categorical values to enter the model. To predict the mortality from the Decision Tree, we used the CHAID method. Each node and branch were compared using survival analysis at 6-year follow-up. Results Mean PAP, wedge pressure, cardiac index, and PVR were 40.3±10.0mmHg, 22.3±7.1mm Hg, 2.9±0.8L/min/m2, and 3.6±2.1WU, respectively. Among the seven dichotomous values linked to the prognosis in PH-LHD, only 2 variables entered the model. To predict the mortality, TAPSE was first selected following by PVR. Compared to patients with PVR&amp;lt;3WU and TAPSE ≥16mm, patients with PVR ≥3WU and TAPSE ≥16mm or patients with PVR ≥3WU and TAPSE &amp;lt;16 mm has significant increased mortality (HR=3,0, 95% CI: [1,4–6,4], p=0.006 and HR=3,3, 95% CI: [1,6–6,9], p=0.002, respectively), while patients with PVR &amp;lt;3WU and TAPSE &amp;lt;16 mm exhibiting the worst prognosis (HR=7,2, 95% CI: [3,3–15,9], p=0.0001). Conclusion Used for solving regression and classification problems, decision tree analysis indicates that among 7 prognostic factors, TAPSE and PVR have to be interpreted altogether and simultaneously in PH-LHD for mortality assessment. Therefore, in future research, PVR &amp;lt;3 WU should be understood primarily based on right ventricular systolic function assessed by echocardiography whether TAPSE is or not ≥16 mm. Funding Acknowledgement Type of funding source: None

METASTATIC PULMONARY CALCIFICATION: A RARE CAUSE OF PULMONARY HYPERTENSION

SESSION TITLE: Fellows Pulmonary Vascular Disease Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Metastatic calcification is seen at autopsy in 60-75% of CKD patients on hemodialysis (HD) due to increased calcium phosphate product (normal 40 mg2/dl2; MPC >70 mg2/dl2) (1,2). Metastatic pulmonary calcification associated with pulmonary hypertension (PH) is rare. We present a case of MPC associated combined postcapillary and precapillary PH (CpcPH). CASE PRESENTATION: A 58-year-old woman with SLE, CTD-ILD (FVC 64%, TLC 56 %), ESRD on HD since 2008 and diastolic heart failure was admitted to the hospital with worsening dyspnea, leg edema and orthopnea. Her calcium phosphate product was 61. CT chest showed diffuse ground glass opacity with mosaic perfusion, enlarged pulmonary artery (PA 4.3 cm) and chest wall calcifications. Echocardiogram showed grade 3 diastolic dysfunction, severely dilated left atrium and elevated right ventricular systolic pressure. Heart catheterization showed mean PA pressure 62 mm Hg, PA wedge pressure 29 mm Hg, transpulmonary gradient (TPG) 33, diastolic pulmonary gradient (DPG) 11, pulmonary vascular resistance 9 WU, LV end diastolic pressure 27 mm Hg, cardiac output 3.6, cardiac index 2.1. Given her severe PH, low CI and NYHA functional class IV, she was started on inhaled treprostinil with improvement in leg edema and orthopnea at 6-month follow up. DISCUSSION: Hyperphosphatemia in ESRD causes increased calcium phosphate product leading to calcium crystallization. Metastatic calcifications are usually seen in lamina propria of stomach, lung alveoli, renal tubules and interstitium(2). Acidosis between HD sessions causes leaching of calcium from bone, leading to deposition during post dialysis alkalosis. Uremia alters the configuration of tissue protein, rendering them more calcifiable. Three main CT patterns of MPC include centrilobular ground glass nodules, dense consolidation and small dense nodules(1). It is usually peripheral in distribution with upper lung zone dominance due to increased alkalinity (higher V/Q ratio causing low PaCO2) causing calcium salt deposition. Vascular calcification in chest and abdominal wall is a common finding as noted in our case. 30-50% of CKD and ESRD patients have PH. Vascular calcification can affect pulmonary arterial capacitance (low PAC in our case 0.81) and increase RV afterload. In this case, contributing factors to her PH are elevated LVEDP, ILD and ESRD (WHO group II, III and V). TPG >12 and DPG >7 suggested pulmonary vascular remodeling from shear stress and downstream pressure. This is an interesting case of MPC with associated PH. Initiation of the pulmonary vasodilator treprostinil reduced her PVR allowing for a better coupling of the RV-PA system. CONCLUSIONS: Treatment of MPC includes intensification of HD sessions and use of calcium and phosphate binders. In this case, inhaled pulmonary vasodilators for treatment of CpcPH after medical treatment optimization of other co-morbidities led to symptomatic improvement. Reference #1: Metastatic pulmonary calcification: HRCT findings in 23 cases, Radiol Bras.2017 Jul-Aug; 50(4): 231–236 Reference #2: Metastatic pulmonary calcification: State-of-the-art review focused on imaging findings, Respiratory Medicine Feb 2014 (108): 668-676 Reference #3: Pulmonary hypertension with extensive calcification in small pulmonary vessels and alveolar capillary wall in a chronic hemodialysis patient, Journal of Cardiology Cases 8 (Feb 2013) e13–e16 DISCLOSURES: No relevant relationships by Moises Cossio, source=Web Response No relevant relationships by Domingo Franco-Palacios, source=Web Response No relevant relationships by Kushagra Gupta, source=Web Response No relevant relationships by Shahzad Hussain, source=Web Response No relevant relationships by Venkateswara Kollipara, source=Web Response No relevant relationships by Toribiong Uchel, source=Web Response

The dangerous and contradictory prognostic significance of PVR

AimsIn 2019, pulmonary vascular resistance (PVR) < 3WU was adopted to stratify patients at low risk in pulmonary hypertension due to left heart disease (PH‐LHD) as well those with isolated PH‐LHD. We sought to evaluate whether supervised machine learning with decision tree analysis, which provides more information than Cox Proportional analysis by forming a hierarchy of multiple covariates, confirms this risk stratification.Methods and resultsTwo hundred two consecutive patients (mean age: 69 ± 11 years, female: 42%) with mean pulmonary artery pressure ≥ 20 mmHg and wedge pressure > 15 mmHg were recruited. Transpulmonary pressure gradient ⩾̸ 12 mmHg, PVR ⩾̸ 3WU, diastolic pressure gradient ⩾̸ 7 mmHg, pulmonary arterial capacitance < 1.1 mL/mmHg, tricuspid annular plane systolic excursion (TAPSE) < 16 mm, peak systolic tissue Doppler velocity < 10 cm/s, right ventricular end‐diastolic area ⩾̸ 25 cm2 were the seven categorical values entered into the model due to their prognostic significance in PH. We used the chi‐squared automatic interaction detection method to predict mortality. Each node and branch were compared using survival analysis at 6‐year follow‐up. Mean pulmonary artery pressure, wedge pressure, cardiac index, and PVR were 40.3 ± 10.0 mmHg, 22.3 ± 7.1 mmHg, 2.9 ± 0.8 L/min/m2, and 3.6 ± 2.1WU, respectively. Among the seven dichotomous, TAPSE was first selected following by PVR. Compared with patients with PVR < 3WU and TAPSE ⩾̸ 16 mm, patients with PVR ⩾̸ 3WU and TAPSE ⩾̸ 16 mm, or patients with PVR ⩾̸ 3WU and TAPSE<16 mm had significantly increased mortality, HR = 3.0, 95% CI = [1.4–6.4], P = 0.006 and HR = 3.3, 95% CI = [1.6–6.9], P = 0.002, respectively, while patients with PVR < 3WU and TAPSE < 16 mm exhibited the worst prognosis, HR = 7.2, 95% CI = [3.3–15.9], P = 0.0001.ConclusionsUsed for solving regression and classification problems, decision tree analysis confirms that PVR and TAPSE have to be analysed together in PH‐LHD and revealed the dangerous and contradictory prognostic significance of PVR < 3WU when TAPSE<16 mm.

Pulmonary arterial capacitance predicts outcomes in patients with pulmonary hypertension independent of race/ethnicity, sex, and etiology.

Pulmonary arterial capacitance (PAC) is a strong hemodynamic predictor of outcomes in patients with pulmonary hypertension (PH). Its value across subgroups of race/ethnicity, sex, and PH etiologies is unclear. We hypothesized that the association of PAC with outcomes would not vary across World Health Organization (WHO) PH group, race/ethnicity, or sex. We performed a retrospective study in patients with PH diagnosed and managed at the Pulmonary Hypertension Comprehensive Care Center of a tertiary care hospital (n=270). Demographic, diagnostic, treatment, and outcome data were extracted from the electronic medical record. Cox proportional hazards models were used to model time from right heart catheterization to event in univariate and multivariable models. Our primary outcome was all-cause mortality and our secondary outcome was PH hospitalization. The median age of the cohort was 56 years (±14.6), and 67% were female. In multivariable Cox models adjusted for significant covariates, decreased PAC remained independently and significantly associated with both all-cause mortality (p=0.029) and hospitalization for PH (p=0.010). No significant interactions were observed between PAC and race, sex, or WHO group. Hispanic patients exhibited a significant independent association with increased hospitalizations (p=0.030), and there was a trend toward increased all-cause mortality in African Americans. WHO group 2PH was associated with more frequent hospitalization (p=0.004). Decreased PAC is significantly associated with mortality and hospitalization in PH patients independent of race, sex, and PH subgroups. Further investigation is required to characterize the effects and determinants of racial disparities in PH.