The utility of considering right ventricular (RV) contractility and afterload as independent entities and summarising their balance or "coupling" using single beat methods has become widely appreciated [1][2][3]. Typically expressed as the ratio of end-systolic ventricular elastance (Ees, a load-independent measure of contractility), to arterial elastance (Ea, a lumped parameter measure of afterload) data suggest that when Ees/Ea reaches a critical threshold, the risk of cardiovascular decompensation begins to rise [4].Pressure-based single beat methods have two central features: prediction of Pmax, the theoretical pressure generated within the RV if contraction remained isovolumic, and definition of end-systolic pressure (ESP). These variables are then used to calculate Ees as (Pmax−ESP)/SV, and Ea as ESP/SV, where SV is the stroke volume. However, it remains unclear what a "normal" RV Ees/Ea value is, due in part to variation in how ESP is defined [5,6], a consideration highlighted in a recent clinical study comparing single and multi-beat determination of Ees/Ea [7]. Additionally, directly relating Ees/Ea to right ventricular ejection fraction (RVEF), a variable clinicians are more familiar with, is challenging. RVEF has been repeatedly shown to predict outcomes in patients with severe pulmonary hypertension (PH) [8], and while cardiac magnetic resonance imaging (cMRI) or three-dimensional echocardiography allow for direct measurement of RVEF, they are not routinely used for repeated measurement of RVEF during a clinically indicated right heart study. The present proof of concept study was designed to test the hypothesis that a method using readily available software and based entirely on analysis of the right ventricular pressure (RVP) waveform can effectively track acute changes in RVEF.Archived measurements of RVP and RV volume provided by conductance/micromanometer catheter were retrospectively analysed. Data had been acquired from 15 anaesthetised swine (∼55 kg) under Institutional Animal Care and Use Committee-approved protocols and in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. Prospective clinical data were acquired under a protocol approved by the Yale Human Investigation Committee. Input signals were sampled at 200 Hz and measured reference values for RVEF calculated from beat-to-beat RV volume as SV/end-diastolic volume. Experimental data had been recorded before and during interventions to alter RV afterload alone or in combination with inotropic depression or augmentation.The Dynamic Fit Wizard within SigmaPlot (version 13, Systat Software, Inc., San Jose, CA) was used to predict Pmax with a distribution function (the 4 parameter Weibull peak fit). In a pilot study involving 15 RVP waveforms with peak pressures ranging from ∼20 to 50 mmHg, the distribution function was found to yield Pmax values that were within 3±7 mmHg of those derived using a more conventional sinusoidal function (figure 1a). For ejection fraction estimation, an alternativ...
Background: Pulmonary hypertension (PH) is commonly associated with heart failure with preserved ejection fraction (HFpEF). In HFpEF, the elevated left sided filling pressures results in isolated post-capillary PH (Ipc-PH) or combined pre- and post-capillary PH (Cpc-PH). Although right heart catheterization (RHC) is the gold standard for diagnosis, it is an invasive test with associated risks. Echocardiogram on the other hand does not help distinguish between Ipc-PH and Cpc-PH. The ability of sub-maximum cardiopulmonary exercise test (CPET) as an adjunct diagnostic tool in PH associated HFpEF is not known. Methods: 46 patients with HFpEF and PH (27 patients with Cpc-PH and 19 patients with Ipc-PH) underwent sub-maximum CPET followed by RHC. The study also included 18 age and gender matched control subjects. Several sub-maximum gas exchange parameters were examined to determine the ability of sub-maximum CPET to distinguish between Ipc-PH and Cpc-PH. Results: Echocardiogram did not distinguish between Ipc-PH and Cpc-PH. Compared to Ipc-PH, Cpc-PH had greater ventilatory equivalent for carbon dioxide (VE/VCO2) slope, reduced delta end-tidal CO2 change during exercise, reduced oxygen uptake efficiency slope (OUES), and reduced gas exchange determined pulmonary vascular capacitance (GXCAP). The latter was significantly associated with RHC determined pulmonary artery compliance (r=0.5; p=0.0004). Conclusion: Sub-maximum gas exchange parameters obtained during CPET in an ambulatory setting allows for discrimination between Ipc-PH and Cpc-PH. Sub-maximum CPET may be a useful end-point measure in HFpEF population.
Right ventricular (RV) functional adaptation to afterload determines outcome in pulmonary hypertension (PH). RV afterload is determined by the dynamic interaction between pulmonary vascular resistance (PVR), characteristic impedance (Zc) and wave reflection. Zc and wave reflection can be estimated from RV pressure waveform analysis and cardiac output. Estimations of Zc and wave reflection coefficient (l) were validated relative to conventional spectral analysis in an animal model. Zc, l, and single beat ratio of end-systolic to arterial elastance (Ees/Ea) to estimate RV-pulmonary arterial (PA) coupling were determined from right heart catheterization (RHC) data. The study included 30 pulmonary artery hypertension (PAH) and 40 heart failure with preserved ejection fraction (HFpEF) patients (20 combined pre- and post-capillary PH; Cpc-PH and 20 isolated post-capillary PH; Ipc-PH). Also included were 10 age and sex-matched controls. There was good agreement with minimal bias between estimated and spectral analysis-derived Zc and l. Zc in PAH and Cpc-PH exceeded that in Ipc-PH and controls. l was increased in Ipc-PH (0.84±0.02), Cpc-PH (0.87±0.05), and PAH (0.85±0.04) compared to controls (0.79±0.03), all p-value<0.05. l was the only afterload parameter associated with RV-PA coupling in PAH. In PH-HFpEF, RV-PA uncoupling was independent of RV afterload. Our findings indicate that Zc and l derived from RV pressure curve, can be used to improve estimation of RV afterload. l is the only afterload measure associated with RV-PA uncoupling in PAH while RV-PA uncoupling in PH-HFpEF appears to be independent of afterload consistent with an inherent abnormality of the RV myocardium.
Functional adaptation of the right ventricle (RV) to its afterload plays an important prognostic role in pulmonary hypertension (PH) [1]. The preferred “multibeat” (MB) method for assessing RV–pulmonary vascular interaction involves the measurement of end-systolic elastance ( E es ), the slope of the end-systolic pressure (ESP) to end-systolic volume over sequential heart beats with varying preload. The E es value is then matched to simultaneous pulmonary arterial (PA) elastance at end systole ( E a ), calculated as ESP pressure divided by stroke volume (SV). The ratio of E es to E a ( E es / E a ) is termed RV–PA coupling, preservation of which indicates maintenance RV functioning in the face of increasing afterload [1]. However, while the MB method is generally regarded as the reference standard, it requires continuous, accurate measurement of RV volume and is therefore not readily applicable in most clinical settings.
Aims A method for estimating right ventricular ejection fraction (RVEF) from RV pressure waveforms was recently validated in an experimental model. Currently, cardiac magnetic resonance imaging (MRI) is the clinical reference standard for measurement of RVEF in pulmonary arterial hypertension (PAH). The present study was designed to test the hypothesis that the pressure-based method can detect clinically significant reductions in RVEF as determined by cardiac MRI in patients with PAH. Methods and results RVEF estimates derived from analysis of RV pressure waveforms recorded during right heart catheterization (RHC) in 25 patients were compared with cardiac MRI measurements of RVEF obtained within 24 h. Three investigators blinded to cardiac MRI results independently performed pressure-based RVEF estimation with the mean of their results used for comparison. Linear regression was used to assess correlation, and a receiver operator characteristic (ROC) curve was derived to define ability of the pressure-based method to detect a maladaptive RV response, defined as RVEF <35% on cardiac MRI. In 23 patients, an automated adaptation of the pressure-based RVEF method was also applied as proof of concept for beat-to-beat RVEF monitoring. The study cohort was comprised of 16 female and 9 male PAH patients with an average age of 53 ± 13 years. RVEF measured by cardiac MRI ranged from 16% to 57% (mean 37.7 ± 11.6%), and estimated RVEF from 15% to 54% (mean 36.2 ± 11.2%; P = 0.6). Measured and estimated RVEF were significantly correlated (r 2 = 0.78; P < 0.0001). ROC curve analysis demonstrated an area under the curve of 0.94 ± 0.04 with a sensitivity of 81% and specificity of 85% for predicting a maladaptive RV response. As a secondary outcome, with the recognized limitation of non-coincident measures, Bland-Altman analysis was performed and indicated minimal bias for estimated RVEF (À1.5%) with limits of agreement of ± 10.9%. Adaptation of the pressure-based estimation method to provide beat-to-beat RVEF also demonstrated significant correlation between the median beat-to-beat value over 10 s with cardiac MRI (r 2 = 0.66; P < 0.001), and an area under the ROC curve of 0.94 ± 0.04 (CI = 0.86 to 1.00) with sensitivity and specificity of 78% and 86%, respectively, for predicting a maladaptive RV response. Conclusions Pressure-based estimation of RVEF correlates with cardiac MRI and detects clinically significant reductions in RVEF. Study results support potential utility of pressure-based RVEF estimation for assessing the response to diagnostic or therapeutic interventions during RHC.
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