Non-invasive assessment of ventriculo-arterial coupling using aortic wave intensity analysis combining central blood pressure and phase-contrast cardiovascular magnetic resonance.
Ontology highlight
ABSTRACT: Background
Wave intensity analysis (WIA) in the aorta offers important clinical and mechanistic insight into ventriculo-arterial coupling, but is difficult to measure non-invasively. We performed WIA by combining standard cardiovascular magnetic resonance (CMR) flow-velocity and non-invasive central blood pressure (cBP) waveforms.Methods and results
Two hundred and six healthy volunteers (age range 21-73 years, 47% male) underwent sequential phase contrast CMR (Siemens Aera 1.5 T, 1.97 × 1.77 mm2, 9.2 ms temporal resolution) and supra-systolic oscillometric cBP measurement (200 Hz). Velocity (U) and central pressure (P) waveforms were aligned using the waveform foot, and local wave speed was calculated both from the PU-loop (c) and the sum of squares method (cSS). These were compared with CMR transit time derived aortic arch pulse wave velocity (PWVtt). Associations were examined using multivariable regression. The peak intensity of the initial compression wave, backward compression wave, and forward decompression wave were 69.5 ± 28, -6.6 ± 4.2, and 6.2 ± 2.5 × 104 W/m2/cycle2, respectively; reflection index was 0.10 ± 0.06. PWVtt correlated with c or cSS (r = 0.60 and 0.68, respectively, P < 0.01 for both). Increasing age decade and female sex were independently associated with decreased forward compression wave (-8.6 and -20.7 W/m2/cycle2, respectively, P < 0.01) and greater wave reflection index (0.02 and 0.03, respectively, P < 0.001).Conclusion
This novel non-invasive technique permits straightforward measurement of wave intensity at scale. Local wave speed showed good agreement with PWVtt, and correlation was stronger using the cSS than the PU-loop. Ageing and female sex were associated with poorer ventriculo-arterial coupling in healthy individuals.
SUBMITTER: Bhuva AN
PROVIDER: S-EPMC7306860 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundTo date, no experimental or clinical study provides detailed analysis of vascular impedance changes after total aortic arch replacement. This study investigated ventriculoarterial coupling and vascular impedance after replacement of the aortic arch with conventional prostheses vs. decellularized allografts.MethodsAfter preparing decellularized aortic arch allografts, their mechanical, histological and biochemical properties were evaluated and compared to native aortic arches and conventional prostheses in vitro. In open-chest dogs, total aortic arch replacement was performed with conventional prostheses and compared to decellularized allografts (n?=?5/group). Aortic flow and pressure were recorded continuously, left ventricular pressure-volume relations were measured by using a pressure-conductance catheter. From the hemodynamic variables end-systolic elastance (Ees), arterial elastance (Ea) and ventriculoarterial coupling were calculated. Characteristic impedance (Z) was assessed by Fourier analysis.ResultsWhile Ees did not differ between the groups and over time (4.1±1.19 vs. 4.58±1.39 mmHg/mL and 3.21±0.97 vs. 3.96±1.16 mmHg/mL), Ea showed a higher increase in the prosthesis group (4.01±0.67 vs. 6.18±0.20 mmHg/mL, P<0.05) in comparison to decellularized allografts (5.03±0.35 vs. 5.99±1.09 mmHg/mL). This led to impaired ventriculoarterial coupling in the prosthesis group, while it remained unchanged in the allograft group (62.5±50.9 vs. 3.9±23.4%). Z showed a strong increasing tendency in the prosthesis group and it was markedly higher after replacement when compared to decellularized allografts (44.6±8.3 dyn·sec·cm(-5) vs. 32.4±2.0 dyn·sec·cm(-5), P<0.05).ConclusionsTotal aortic arch replacement leads to contractility-afterload mismatch by means of increased impedance and invert ventriculoarterial coupling ratio after implantation of conventional prostheses. Implantation of decellularized allografts preserves vascular impedance thereby improving ventriculoarterial mechanoenergetics after aortic arch replacement.
| S-EPMC4117632 | biostudies-literature
Project description:BackgroundWave intensity analysis, traditionally derived from pressure and velocity data, can be formulated using velocity and area. Flow-velocity and area can both be derived from high-resolution phase-contrast cardiovascular magnetic resonance (PC-CMR). In this study, very high temporal resolution PC-CMR data is processed using an integrated and semi-automatic technique to derive wave intensity.MethodsWave intensity was derived in terms of area and velocity changes. These data were directly derived from PC-CMR using a breath-hold spiral sequence accelerated with sensitivity encoding (SENSE). Image processing was integrated in a plug-in for the DICOM viewer OsiriX, including calculations of wave speed and wave intensity. Ascending and descending aortic data from 15 healthy volunteers (30?±?6?years) data were used to test the method for feasibility, and intra- and inter-observer variability. Ascending aortic data were also compared with results from 15 patients with coronary heart disease (61?±?13?years) to assess the clinical usefulness of the method.ResultsRapid image acquisition (11?s breath-hold) and image processing was feasible in all volunteers. Wave speed was physiological (5.8?±?1.3?m/s ascending aorta, 5.0?±?0.7?m/s descending aorta) and the wave intensity pattern was consistent with traditionally formulated wave intensity. Wave speed, peak forward compression wave in early systole and peak forward expansion wave in late systole at both locations exhibited overall good intra- and inter-observer variability. Patients with coronary heart disease had higher wave speed (p <0.0001), and lower forward compression wave (p <0.0001) and forward expansion wave (p <0.0005) peaks. This difference is likely related to the older age of the patients' cohort, indicating stiffer aortas, as well as compromised ventricular function due to their underlying condition.ConclusionA non-invasive, semi-automated and reproducible method for performing wave intensity analysis is presented. Its application is facilitated by the use of a very high temporal resolution spiral sequence. A formulation of wave intensity based on area change has also been proposed, involving no assumptions about the cross-sectional shape of the vessel.
| S-EPMC3472227 | biostudies-literature
Project description:Chronic thromboembolic disease (CTED) is suboptimally defined by a mean pulmonary artery pressure (mPAP) <25 mmHg at rest in patients that remain symptomatic from chronic pulmonary artery thrombi. To improve identification of right ventricular (RV) pathology in patients with thromboembolic obstruction, we hypothesized that the RV ventriculo-arterial (Ees/Ea) coupling ratio at maximal stroke work (Ees/Eamax sw) derived from an animal model of pulmonary obstruction may be used to identify occult RV dysfunction (low Ees/Ea) or residual RV energetic reserve (high Ees/Ea). Eighteen open chested pigs had conductance catheter RV pressure-volume (PV)-loops recorded during PA snare to determine Ees/Eamax sw This was then applied to 10 patients with chronic thromboembolic pulmonary hypertension (CTEPH) and ten patients with CTED, also assessed by RV conductance catheter and cardiopulmonary exercise testing. All patients were then restratified by Ees/Ea. The animal model determined an Ees/Eamax sw = 0.68 ± 0.23 threshold, either side of which cardiac output and RV stroke work fell. Two patients with CTED were identified with an Ees/Ea well below 0.68 suggesting occult RV dysfunction whilst three patients with CTEPH demonstrated Ees/Ea ≥ 0.68 suggesting residual RV energetic reserve. Ees/Ea > 0.68 and Ees/Ea < 0.68 subgroups demonstrated constant RV stroke work but lower stroke volume (87.7 ± 22.1 vs. 60.1 ± 16.3 mL respectively, P = 0.006) and higher end-systolic pressure (36.7 ± 11.6 vs. 68.1 ± 16.7 mmHg respectively, P < 0.001). Lower Ees/Ea in CTED also correlated with reduced exercise ventilatory efficiency. Low Ees/Ea aligns with features of RV maladaptation in CTED both at rest and on exercise. Characterization of Ees/Ea in CTED may allow for better identification of occult RV dysfunction.
| S-EPMC5392517 | biostudies-literature
Project description:BACKGROUND:Tricuspid annular systolic excursion (TAPSE) or velocities (s') and right ventricular (RV) end-systolic dimensions are predictors of outcome in patients with pulmonary hypertension (PH). We explored the value of combining peak s' and RV end-systolic area index (RVESAi) as a surrogate of RV-pulmonary artery (RV-PA) coupling in a large animal of precapillary PH as well as clinically. METHOD:The first experimental group included four control and four piglets with thromboembolic disease. RV-PA coupling was assessed by ventricular to arterial elastance ratio (Ees/Ea) at baseline, after esmolol and dobutamine administration. Echocardiographic metrics included s', TAPSE, fractional area change (RVFAC), and RVESAi. The findings were validated in six piglets with severe PH. Clinical cohorts were stable outpatients (n = 141) and acutely decompensated pulmonary arterial hypertension (n = 48). RESULTS:In the first experimental group, the best linear correlates of Ees/Ea were s' (R2 = .51, p < .001) and RVESAi (R2 = .50, p < .001), while RVFAC (R2 = .17, p = .01) and TAPSE showed weaker association (R2 = .21, p = .39). The ratio s'/RVESAi showed nominally but not significantly (higher) association with Ees/Ea (R2 = .58, p < .01). The association between changes in s'/RVESAi and Ees/Ea was strong (R2 = .56, p < .001). In more severe PH, Ees/Ea and changes in Ees/Ea correlated significantly with s'/RVESAi and changes in s'/RVESAi (R2 = .69; p < .001 and R2 = .64, p < .001, respectively). In the two clinical cohorts, the s'/RVESAi did not emerge as a stronger predictor of outcome than RVESAi. CONCLUSION:RV s'/RVESAi index represents a reasonable bedside-usable surrogate of RV-PA coupling and of its acute variations in PH. Its incremental prognostic value over end-systolic dimension alone remains to be proven.
| S-EPMC6930934 | biostudies-literature
Project description:IntroductionTwo parallel paradigms of cardiovascular efficiency and haemodynamic optimisation coexist in haemodynamic research. Targeting ventriculo-arterial (VA) coupling [i.e., the ratio between arterial and ventricular elastance (EV)] and electromechanical coupling are two promising approaches in acute circulatory failure. However, validation of the parameters of electromechanical coupling in critically ill patients is ongoing. Furthermore, a unifying link between VA and electromechanical coupling may exist, as EV is correlated with different times of the cardiac cycle.Materials and methodsThis study was a retrospective analysis of a prospectively collected observational database from one tertiary center ICU. We analyzed the relationship between electromechanical dyssynchrony and acute circulatory failure hemodynamics before and after treatment (i.e., fluid expansion, dobutamine, or norepinephrine infusion). The relationship between electromechanical coupling and VA coupling was also investigated. Adult patients with haemodynamic instability were included. Haemodynamic parameters, including arterial pressure, cardiac index, VA coupling, stroke work index/pressure-volume area (SWI/PVA), t-IVT, and Tei's index, were collected before and after treatment. A t-IVT of >12 s/min was classified as intraventricular dyssynchrony.ResultsWe included 54 patients; 39 (72.2%) were classified as having intraventricular dyssynchrony at baseline. These patients with baseline dyssynchrony showed a statistically significant amelioration of t-IVT (from 18 ± 4 s to 14 ± 6 s, p = 0.001), left ventricular EV [from 1.1 (0.72-1.52) to 1.33 (0.84-1.67) mmHg mL-1, p = 0.001], VA coupling [from 2 (1.67-2.59) to 1.80 (1.40-2.21), p = 0.001], and SWI/PVA [from 0.58 (0.49-0.65) to 0.64 (0.51-0.68), p = 0.007]. Patients without baseline dyssynchrony showed no statistically significant results. The improvement in VA coupling was mediated by an amelioration of EV. All patients improved their arterial pressure and cardiac index with treatment. The haemodynamic treatment group exhibited no effect on changing t-IVT.ConclusionAcute circulatory failure is associated with electromechanical dyssynchrony. Cardiac electromechanical coupling was improved by haemodynamic treatment only if altered at baseline. The improvement of cardiac electromechanical coupling was associated with the improvement of markers of cardiocirculatory efficacy and efficiency (i.e., SWI/PVA and VA coupling). This study was the first to demonstrate a possible link between cardiac electromechanical coupling and VA coupling in patients with acute circulatory failure.
| S-EPMC9253504 | biostudies-literature
Project description:We present a novel analysis of arterial pulse wave propagation that combines traditional wave intensity analysis with identification of Windkessel pressures to account for the effect on the pressure waveform of peripheral wave reflections. Using haemodynamic data measured in vivo in the rabbit or generated numerically in models of human compliant vessels, we show that traditional wave intensity analysis identifies the timing, direction and magnitude of the predominant waves that shape aortic pressure and flow waveforms in systole, but fails to identify the effect of peripheral reflections. These reflections persist for several cardiac cycles and make up most of the pressure waveform, especially in diastole and early systole. Ignoring peripheral reflections leads to an erroneous indication of a reflection-free period in early systole and additional error in the estimates of (i) pulse wave velocity at the ascending aorta given by the PU-loop method (9.5% error) and (ii) transit time to a dominant reflection site calculated from the wave intensity profile (27% error). These errors decreased to 1.3% and 10%, respectively, when accounting for peripheral reflections. Using our new analysis, we investigate the effect of vessel compliance and peripheral resistance on wave intensity, peripheral reflections and reflections originating in previous cardiac cycles.
| S-EPMC4297358 | biostudies-literature
Project description:Definitive closure of a patent ductus arteriosus (PDA) causes significant changes in loading conditions of the left ventricle (LV) which can lead to cardiorespiratory instability including hypotension, low cardiac output, oxygenation, and ventilation impairment. Physiological insights of the adaptation of the LV can be gained by looking at ventriculo-arterial coupling (VAC) and myocardial work-energetics. We conducted a retrospective cohort study of preterm infants with echocardiographic assessment of VAC parameters, including end-systolic and arterial elastance (EES , EA ), and myocardial work indices derived from longitudinal strain analysis before and 1-h after percutaneous PDA closure. A total of 35 patients were included with mean [±SD] age at intervention of 30.8 ± 9.9 days and median [IQR] weight of 1130 [995, 1318] grams. There was a reduction in preload and stroke volume, an increase in EA (38.6 ± 11.4 vs. 60 ± 15.1 mmHg/ml/kg, p < 0.001) and in EES (72 [61.5, 109.8] vs. 91.6 [72.2, 125.2] mmHg/ml/kg, p = 0.003) post-closure. Myocardial work indices reduced after PDA closure, including global work efficiency (93.9 ± 2.3 vs. 91.1 ± 3.6%, p < 0.001). A total of 17 (48.6%) patients developed post-closure instability which was associated with younger age, lower preload, and higher EA and EES . Percutaneous PDA closure is associated with major short-term changes in VAC and myocardium energetics, which may provide novel insights on the physiology of PDA closure and on the differential vulnerability to changes in loading conditions.
| S-EPMC8606853 | biostudies-literature
Project description:Right ventricular function critically affects the prognosis of patients with pulmonary arterial hypertension. We aimed to analyze the prognostic value of right ventricular indices calculated using magnetic resonance imaging and right heart catheterization metrics in pulmonary arterial hypertension. We retrospectively collected data from 57 Japanese patients with pulmonary arterial hypertension and 18 controls and calculated six indices of right ventricular function: two indices of contractility (end-systolic elastance calculated with right ventricular maximum pressure and with magnetic resonance imaging metrics); two indices of right ventricular-pulmonary arterial coupling (end-systolic elastance/arterial elastance calculated with the pressure method (end-systolic elastance/arterial elastance (P)) and with the volume method (end-systolic elastance/arterial elastance (V)); and two indices of right ventricular diastolic function (stiffness (β) and end-diastolic elastance). We compared the indices between controls and patients with pulmonary arterial hypertension and examined their prognostic role. In patients with pulmonary arterial hypertension, end-systolic elastance (right ventricular maximum pressure) was higher (pulmonary arterial hypertension 0.94 (median) vs control 0.42 (mmHg/mL), p < 0.001), end-systolic elastance/arterial elastance (V) was lower (pulmonary arterial hypertension 0.72 vs control 1.69, p < 0.001), and β and end-diastolic elastance were significantly higher than those in the controls. According to the log-rank test, end-systolic elastance/arterial elastance (P) and end-diastolic elastance were significantly associated with the composite event rate. According to the multivariate Cox regression analysis, decreased end-systolic elastance/arterial elastance (P) was associated with a higher composite event rate (hazard ratio 11.510, 95% confidence interval: 1.954-67.808). In conclusion, an increased right ventricular contractility, diastolic dysfunction, and a trend of impaired right ventricular-pulmonary arterial coupling were observed in our pulmonary arterial hypertension cohort. According to the multivariate outcome analysis, a decreased end-systolic elastance/arterial elastance (P), suggestive of impaired right ventricular-pulmonary arterial coupling, best predicted the pulmonary arterial hypertension-related event.
| S-EPMC7543138 | biostudies-literature
Project description:BackgroundWave intensity analysis provides valuable information on ventriculo-arterial function, hemodynamics, and energy transfer in the arterial circulation. Widespread use of wave intensity analysis is limited by the need for concurrent measurement of pressure and flow waveforms. We describe a method that can estimate wave intensity patterns using only non-invasive pressure waveforms (pWIA).MethodsRadial artery pressure and left ventricular outflow tract (LVOT) flow velocity waveforms were recorded in 12 participants in the Southall and Brent Revisited (SABRE) study. Pressure waveforms were analyzed using custom-written software to derive the excess pressure (P xs ) which was scaled to peak LVOT velocity and used to calculate wave intensity. These data were compared with wave intensity calculated using the measured LVOT flow velocity waveform. In a separate study, repeat measures of pWIA were performed on 34 individuals who attended two clinic visits at an interval of ?1 month to assess reproducibility and reliability of the method.ResultsP xs waveforms were similar in shape to aortic flow velocity waveforms and the time of peak P xs and peak aortic velocity agreed closely. Wave intensity estimated using pWIA showed acceptable agreement with estimates using LVOT velocity tracings and estimates of wave intensity were similar to values reported previously in the literature. The method showed fair to good reproducibility for most parameters.ConclusionThe P xs is a surrogate of LVOT flow velocity which, when appropriately scaled, allows estimation of aortic wave intensity with acceptable reproducibility. This may enable wider application of wave intensity analysis to large studies.
| S-EPMC7260344 | biostudies-literature
Project description:BackgroundWave intensity analysis (WIA) of the coronary arteries allows description of the predominant mechanisms influencing coronary flow over the cardiac cycle. The data are traditionally derived from pressure and velocity changes measured invasively in the coronary artery. Cardiovascular magnetic resonance (CMR) allows measurement of coronary velocities using phase velocity mapping and derivation of central aortic pressure from aortic distension. We assessed the feasibility of WIA of the coronary arteries using CMR and compared this to invasive data.MethodsCMR scans were undertaken in a serial cohort of patients who had undergone invasive WIA. Velocity maps were acquired in the proximal left anterior descending and proximal right coronary artery using a retrospectively-gated breath-hold spiral phase velocity mapping sequence with high temporal resolution (19 ms). A breath-hold segmented gradient echo sequence was used to acquire through-plane cross sectional area changes in the proximal ascending aorta which were used as a surrogate of an aortic pressure waveform after calibration with brachial blood pressure measured with a sphygmomanometer. CMR-derived aortic pressures and CMR-measured velocities were used to derive wave intensity. The CMR-derived wave intensities were compared to invasive data in 12 coronary arteries (8 left, 4 right). Waves were presented as absolute values and as a % of total wave intensity. Intra-study reproducibility of invasive and non-invasive WIA was assessed using Bland-Altman analysis and the intraclass correlation coefficient (ICC).ResultsThe combination of the CMR-derived pressure and velocity data produced the expected pattern of forward and backward compression and expansion waves. The intra-study reproducibility of the CMR derived wave intensities as a % of the total wave intensity (mean ± standard deviation of differences) was 0.0 ± 6.8%, ICC = 0.91. Intra-study reproducibility for the corresponding invasive data was 0.0 ± 4.4%, ICC = 0.96. The invasive and CMR studies showed reasonable correlation (r = 0.73) with a mean difference of 0.0 ± 11.5%.ConclusionThis proof of concept study demonstrated that CMR may be used to perform coronary WIA non-invasively with reasonable reproducibility compared to invasive WIA. The technique potentially allows WIA to be performed in a wider range of patients and pathologies than those who can be studied invasively.
| S-EPMC5154155 | biostudies-literature