Wave Intensity Analysis of Left Ventricular Filling

2005 ◽  
Vol 127 (5) ◽  
pp. 862-867 ◽  
Author(s):  
L. L. Lanoye ◽  
J. A. Vierendeels ◽  
P. Segers ◽  
P. R. Verdonck

Wave intensity analysis (WIA) is a powerful technique to study pressure and flow velocity waves in the time domain in vascular networks. The method is based on the analysis of energy transported by the wave through computation of the wave intensity dI=dPdU, where dP and dU denote pressure and flow velocity changes per time interval, respectively. In this study we propose an analytical modification to the WIA so that it can be used to study waves in conditions of time varying elastic properties, such as the left ventricle (LV) during diastole. The approach is first analytically elaborated for a one-dimensional elastic tube-model of the left ventricle with a time-dependent pressure-area relationship. Data obtained with a validated quasi-three dimensional axisymmetrical model of the left ventricle are employed to demonstrate this new approach. Along the base-apex axis close to the base wave intensity curves are obtained, both using the standard method and the newly proposed modified method. The main difference between the standard and modified wave intensity pattern occurs immediately after the opening of the mitral valve. Where the standard WIA shows a backward expansion wave, the modified analysis shows a forward compression wave. The proposed modification needs to be taken into account when studying left ventricular relaxation, as it affects the wave type.

2020 ◽  
Author(s):  
A.D. Hughes ◽  
C. Park ◽  
A. Ramakrishnan ◽  
J. Mayet ◽  
N. Chaturvedi ◽  
...  

AbstractBackgroundWave 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, and its reproducibility.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 analysed using custom-written software to derive the excess pressure (Pxs) which was compared with the LVOT flow velocity waveform, and used to calculate wave intensity. In a separate study, repeat measures of wave intensity and other wave and reservoir parameters were performed on 34 individuals who attended 2 clinic visits at an interval of approximately 1 month to assess reproducibility and reliability of the method.ResultsPxs waveforms were similar in shape to aortic flow velocity waveforms and the time of peak Pxs and maximum aortic velocity agreed closely (mean difference = 0.00 (limits of agreement −0.02, 0.02)s). Wave intensity patterns when scaled to peak LVOT velocity gave credible estimates of wave intensity similar to values reported previously in the literature. The method showed fair to good reproducibility for most parameters.ConclusionsThe Pxs is a surrogate of LVOT flow velocity allowing estimation of aortic wave intensity with acceptable reproducibility. This enables widespread application of wave intensity analysis to large studies.


2016 ◽  
Vol 310 (5) ◽  
pp. H619-H627 ◽  
Author(s):  
Christopher J. Broyd ◽  
Sukhjinder Nijjer ◽  
Sayan Sen ◽  
Ricardo Petraco ◽  
Siana Jones ◽  
...  

Wave intensity analysis (WIA) has found particular applicability in the coronary circulation where it can quantify traveling waves that accelerate and decelerate blood flow. The most important wave for the regulation of flow is the backward-traveling decompression wave (BDW). Coronary WIA has hitherto always been calculated from invasive measures of pressure and flow. However, recently it has become feasible to obtain estimates of these waveforms noninvasively. In this study we set out to assess the agreement between invasive and noninvasive coronary WIA at rest and measure the effect of exercise. Twenty-two patients (mean age 60) with unobstructed coronaries underwent invasive WIA in the left anterior descending artery (LAD). Immediately afterwards, noninvasive LAD flow and pressure were recorded and WIA calculated from pulsed-wave Doppler coronary flow velocity and central blood pressure waveforms measured using a cuff-based technique. Nine of these patients underwent noninvasive coronary WIA assessment during exercise. A pattern of six waves were observed in both modalities. The BDW was similar between invasive and noninvasive measures [peak: 14.9 ± 7.8 vs. −13.8 ± 7.1 × 104 W·m−2·s−2, concordance correlation coefficient (CCC): 0.73, P < 0.01; cumulative: −64.4 ± 32.8 vs. −59.4 ± 34.2 × 102 W·m−2·s−1, CCC: 0.66, P < 0.01], but smaller waves were underestimated noninvasively. Increased left ventricular mass correlated with a decreased noninvasive BDW fraction ( r = −0.48, P = 0.02). Exercise increased the BDW: at maximum exercise peak BDW was −47.0 ± 29.5 × 104 W·m−2·s−2 ( P < 0.01 vs. rest) and cumulative BDW −19.2 ± 12.6 × 103 W·m−2·s−1 ( P < 0.01 vs. rest). The BDW can be measured noninvasively with acceptable reliably potentially simplifying assessments and increasing the applicability of coronary WIA.


2007 ◽  
Vol 292 (3) ◽  
pp. H1533-H1540 ◽  
Author(s):  
Tracy N. Hobson ◽  
Jacqueline A. Flewitt ◽  
Israel Belenkie ◽  
John V. Tyberg

The left atrium (LA) acts as a booster pump during late diastole, generating the Doppler transmitral A wave and contributing incrementally to left ventricular (LV) filling. However, after volume loading and in certain disease states, LA contraction fills the LV less effectively, and retrograde flow (i.e., the Doppler Ar wave) into the pulmonary veins increases. The purpose of this study was to provide an energetic analysis of LA contraction to clarify the mechanisms responsible for changes in forward and backward flow. Wave intensity analysis was performed at the mitral valve and a pulmonary vein orifice. As operative LV stiffness increased with progressive volume loading, the reflection coefficient (i.e., energy of reflected wave/energy of incident wave) also increased. This reflected wave decelerated the forward movement of blood through the mitral valve and was transmitted through the LA, accelerating retrograde blood flow in the pulmonary veins. Although total LA work increased with volume loading, the forward hydraulic work decreased and backward hydraulic work increased. Thus wave reflection due to increased LV stiffness accounts for the decrease in the A wave and the increase in the Ar wave measured by Doppler.


2005 ◽  
Vol 289 (1) ◽  
pp. H270-H276 ◽  
Author(s):  
A. Zambanini ◽  
S. L. Cunningham ◽  
K. H. Parker ◽  
A. W. Khir ◽  
S. A. McG. Thom ◽  
...  

The study of wave propagation at different points in the arterial circulation may provide useful information regarding ventriculoarterial interactions. We describe a number of hemodynamic parameters in the carotid, brachial, and radial arteries of normal subjects by using noninvasive techniques and wave-intensity analysis (WIA). Twenty-one normal adult subjects (14 men and 7 women, mean age 44 ± 6 yr) underwent applanation tonometry and pulsed-wave Doppler studies of the right common carotid, brachial, and radial arteries. After ensemble averaging of the pressure and flow-velocity data, local hydraulic work was determined and a pressure-flow velocity loop was used to determine local wave speed. WIA was then applied to determine the magnitude, timings, and energies of individual waves. At all sites, forward-traveling (S) and backward-traveling (R) compression waves were observed in early systole. In mid- and late systole, forward-traveling expansion waves (X and D) were also seen. Wave speed was significantly higher in the brachial (6.97 ± 0.58 m/s) and radial (6.78 ± 0.62 m/s) arteries compared with the carotid artery (5.40 ± 0.34 m/s; P < 0.05). S-wave energy was greatest in the brachial artery (993.5 ± 87.8 mJ/m2), but R-wave energy was greatest in the radial artery (176.9 ± 19.9 mJ/m2). X-wave energy was significantly higher in the brachial and radial arteries (176.4 ± 32.7 and 163.2 ± 30.5 mJ/m2, respectively) compared with the carotid artery (41.0 ± 9.4 mJ/m2; P < 0.001). WIA illustrates important differences in wave patterns between peripheral arteries and may provide a method for understanding ventriculo-arterial interactions in the time domain.


2017 ◽  
Vol 2017 (1) ◽  
Author(s):  
C J Broyd ◽  
J E Davies ◽  
J E Escaned ◽  
A Hughes ◽  
K Parker

Wave intensity analysis (WIA) is a technique developed from the field of gas dynamics that is now being applied to assess cardiovascular physiology. It allows quantification of the forces acting to alter flow and pressure within a fluid system, and as such it is highly insightful in ascribing cause to dynamic blood pressure or velocity changes.When co-incident waves arrive at the same spatial location they exert either counteracting or summative effects on flow and pressure. WIA however allows waves of different origins to be measured uninfluenced by other simultaneously arriving waves. It therefore has found particular applicability within the coronary circulation where both proximal (aortic) and distal (myocardial) ends of the coronary artery can markedly influence blood flow. Using these concepts, a repeating pattern of 6 waves has been consistently identified within the coronary arteries, 3 originating proximally and 3 distally. Each has been associated with a particular part of the cardiac cycle. The most clinically relevant wave to date is the backward decompression wave, which causes the marked increase in coronary flow velocity observed at the start of the diastole. It has been proposed that this wave is generated by the elastic re-expansion of the intra-myocardial blood vessels that are compressed during systolic contraction. Particularly by quantifying this wave, WIA has been used to provide mechanistic and prognostic insight into a number of conditions including aortic stenosis, left ventricular hypertrophy, coronary artery disease and heart failure. It has proven itself to be highly sensitive and as such a number of novel research directions are encouraged where further insights would be beneficial. 


2008 ◽  
Vol 295 (3) ◽  
pp. H1198-H1205 ◽  
Author(s):  
Nearchos Hadjiloizou ◽  
Justin E. Davies ◽  
Iqbal S. Malik ◽  
Jazmin Aguado-Sierra ◽  
Keith Willson ◽  
...  

Despite having almost identical origins and similar perfusion pressures, the flow-velocity waveforms in the left and right coronary arteries are strikingly different. We hypothesized that pressure differences originating from the distal (microcirculatory) bed would account for the differences in the flow-velocity waveform. We used wave intensity analysis to separate and quantify proximal- and distal-originating pressures to study the differences in velocity waveforms. In 20 subjects with unobstructed coronary arteries, sensor-tipped intra-arterial wires were used to measure simultaneous pressure and Doppler velocity in the proximal left main stem (LMS) and proximal right coronary artery (RCA). Proximal- and distal-originating waves were separated using wave intensity analysis, and differences in waves were examined in relation to structural and anatomic differences between the two arteries. Diastolic flow velocity was lower in the RCA than in the LMS (35.1 ± 21.4 vs. 56.4 ± 32.5 cm/s, P < 0.002), and, consequently, the diastolic-to-systolic ratio of peak flow velocity in the RCA was significantly less than in the LMS (1.00 ± 0.32 vs. 1.79 ± 0.48, P < 0.001). This was due to a lower distal-originating suction wave (8.2 ± 6.6 × 103 vs. 16.0 ± 12.2 × 103 W·m−2·s−1, P < 0.01). The suction wave in the LMS correlated positively with left ventricular pressure ( r = 0.6, P < 0.01) and in the RCA with estimated right ventricular systolic pressure ( r = 0.7, P = 0.05) but not with the respective diameter in these arteries. In contrast to the LMS, where coronary flow velocity was predominantly diastolic, in the proximal RCA coronary flow velocity was similar in systole and diastole. This difference was due to a smaller distal-originating suction wave in the RCA, which can be explained by differences in elastance and pressure generated between right and left ventricles.


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