scholarly journals WAVE SPEED IN THE HUMAN CORONARY ARTERY DOES NOT DECREASE WITH VASODILATION: EXTENDING THE LIMITS OF VALIDITY OF THE SINGLE–POINT TECHNIQUE FOR WAVE INTENSITY ANALYSIS

2013 ◽  
Vol 61 (10) ◽  
pp. E1761 ◽  
Author(s):  
Cristina Rolandi ◽  
Kalpa de Silva ◽  
Matt Lumley ◽  
Tim Lockie ◽  
Brian Clapp ◽  
...  
2014 ◽  
Vol 109 (2) ◽  
Author(s):  
M. Cristina Rolandi ◽  
Kalpa Silva ◽  
Matthew Lumley ◽  
Timothy P. E. Lockie ◽  
Brian Clapp ◽  
...  

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.


2006 ◽  
Vol 39 ◽  
pp. S614-S615
Author(s):  
J. Aguado-Sierra ◽  
J. Davies ◽  
J. Mayet ◽  
D. Francis ◽  
A.D. Hughes ◽  
...  

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.


2006 ◽  
Vol 290 (2) ◽  
pp. H878-H885 ◽  
Author(s):  
Justin E. Davies ◽  
Zachary I. Whinnett ◽  
Darrel P. Francis ◽  
Keith Willson ◽  
Rodney A. Foale ◽  
...  

It has not been possible to measure wave speed in the human coronary artery, because the vessel is too short for the conventional two-point measurement technique used in the aorta. We present a new method derived from wave intensity analysis, which allows derivation of wave speed at a single point. We apply this method in the aorta and then use it to derive wave speed in the human coronary artery for the first time. We measured simultaneous pressure and Doppler velocity with intracoronary wires at the left main stem, left anterior descending and circumflex arteries, and aorta in 14 subjects after a normal coronary arteriogram. Then, in 10 subjects, serial measurements were made along the aorta before and after intracoronary isosorbide dinitrate. Wave speed was derived by two methods in the aorta: 1) the two-site distance/time method (foot-to-foot delay of pressure waveforms) and 2) a new single-point method using simultaneous pressure and velocity measurements. Coronary wave speed was derived by the single-point method. Wave speed derived by the two methods correlated well ( r = 0.72, P < 0.05). Coronary wave speed correlated with aortic wave speed ( r = 0.72, P = 0.002). After nitrate administration, coronary wave speed fell by 43%: from 16.4 m/s (95% confidence interval 12.6–20.1) to 9.3 m/s (95% confidence interval 6.5–12.0, P < 0.001). This single-point method allows determination of wave speed in the human coronary artery. Aortic wave speed is correlated to coronary wave speed. Finally, this technique detects the prompt fall in coronary artery wave speed with isosorbide dinitrate.


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