P021 Wave Intensity Analysis in Patients with Coronary Artery Disease

2011 ◽  
Vol 147 ◽  
pp. S14
Author(s):  
J.W. Tian ◽  
Y. Wang ◽  
G.Q. Du
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Artery Disease

scholarly journals Wave intensity analysis and its application to the coronary circulation

2017 ◽  
Vol 2017 (1) ◽  
Author(s):  
C J Broyd ◽  
J E Davies ◽  
J E Escaned ◽  
A Hughes ◽  
K Parker
Keyword(s):  
Coronary Artery ◽  
Coronary Circulation ◽  
Spatial Location ◽  
Left Ventricular ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Decompression Wave ◽  
Artery Disease ◽  
Incident Waves

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. 

scholarly journals Differences in cardiac microcirculatory wave patterns between the proximal left mainstem and proximal right coronary artery

2008 ◽  
Vol 295 (3) ◽  
pp. H1198-H1205 ◽  
Author(s):  
Nearchos Hadjiloizou ◽  
Justin E. Davies ◽  
Iqbal S. Malik ◽  
Jazmin Aguado-Sierra ◽  
Keith Willson ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Flow Velocity ◽  
Coronary Arteries ◽  
Right Coronary Artery ◽  
Coronary Flow ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Coronary Flow Velocity ◽  
Proximal Right Coronary Artery

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.

scholarly journals Coronary wave intensity patterns in stable coronary artery disease: influence of stenosis severity and collateral circulation

Open Heart ◽  
2019 ◽  
Vol 6 (2) ◽  
pp. e000999
Author(s):  
Stefano F deMarchi ◽  
Christian Gassmann ◽  
Tobias Traupe ◽  
Steffen Gloekler ◽  
Stéphane Cook ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Stenosis ◽  
Collateral Circulation ◽  
Pulse Wave ◽  
Wave Intensity ◽  
Collateral Flow ◽  
Coronary Collaterals ◽  
Stenosis Severity ◽  
Artery Disease

ObjectiveWave intensity analysis is a method that allows separating pulse waves into components generated proximally and in the periphery of arterial trees, as well as characterising them as accelerating or decelerating. The early diastolic suction wave (eaDSW) is one of the most prominent wave events in the coronaries. The aim of this study was to determine whether (1) microvascular dilatation directly influences its energy, (2) stenosis severity can be assessed proximal to stenoses, (3) distal pulse wave entrapment exists in the presence of stenoses and (4) coronary collaterals influence wave entrapment.MethodsIn 43 coronary artery disease patients, Doppler flow velocity and pressure measurements were performed in a proximal coronary segment at rest, in a distal segment at rest, during adenosine-induced hyperaemia and during balloon occlusion. Wave energies were calculated as the area under the wave intensity curves.ResultsThe eaDSW energy showed a significant increase during hyperaemia, but did not differ between proximal and distal segments. There was no significant correlation between eaDSW energy and coronary stenosis severity. Pulse wave entrapment could not be observed consistently in the distal segments. Consequently, the effect of coronary collaterals on pulse wave entrapment could not be studied.ConclusionsMicrovascular dilation in the coronary circulation increases distal eaDSW energy. However, it does not show any diagnostically useful variation between measurement sites, various stenosis degrees and amount of collateral flow. The assessment eaDSW and its reflections were not useful for the quantification of coronary stenosis severity or the collateral circulation in clinical practice.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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