Dataset Information

Feasibility of cardiovascular magnetic resonance derived coronary wave intensity analysis.

ABSTRACT:

Background

Wave 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.

Methods

CMR 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).

Results

The 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%.

Conclusion

This 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.

SUBMITTER: Raphael CE

PROVIDER: S-EPMC5154155 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Publications

Feasibility of cardiovascular magnetic resonance derived coronary wave intensity analysis.

Raphael Claire E CE Keegan Jennifer J Parker Kim H KH Simpson Robin R Collinson Julian J Vassiliou Vass V Wage Ricardo R Drivas Peter P Strain Stephen S Cooper Robert R de Silva Ranil R Stables Rod H RH Di Mario Carlo C Frenneaux Michael M Pennell Dudley J DJ Davies Justin E JE Hughes Alun D AD Firmin David D Prasad Sanjay K SK

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance 20161209 1

<h4>Background</h4>Wave 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 o ...[more]

PMID: 27964736

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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.

Project description:BackgroundAngina is common in hypertrophic cardiomyopathy (HCM) and is associated with abnormal myocardial perfusion. Wave intensity analysis improves the understanding of the mechanics of myocardial ischemia.ObjectivesWave intensity analysis was used to describe the mechanisms underlying perfusion abnormalities in patients with HCM.MethodsSimultaneous pressure and flow were measured in the proximal left anterior descending artery in 33 patients with HCM and 20 control patients at rest and during hyperemia, allowing calculation of wave intensity. Patients also underwent quantitative first-pass perfusion cardiac magnetic resonance to measure myocardial perfusion reserve.ResultsPatients with HCM had a lower coronary flow reserve than control subjects (1.9 ± 0.8 vs. 2.7 ± 0.9; p = 0.01). Coronary hemodynamics in HCM were characterized by a very large backward compression wave during systole (38 ± 11% vs. 21 ± 6%; p < 0.001) and a proportionately smaller backward expansion wave (27% ± 8% vs. 33 ± 6%; p = 0.006) compared with control subjects. Patients with severe left ventricular outflow tract obstruction had a bisferiens pressure waveform resulting in an additional proximally originating deceleration wave during systole. The proportion of waves acting to accelerate coronary flow increased with hyperemia, and the magnitude of change was proportional to the myocardial perfusion reserve (rho = 0.53; p < 0.01).ConclusionsCoronary flow in patients with HCM is deranged. Distally, compressive deformation of intramyocardial blood vessels during systole results in an abnormally large backward compression wave, whereas proximally, severe left ventricular outflow tract obstruction is associated with an additional deceleration wave. Perfusion abnormalities in HCM are not simply a consequence of supply/demand mismatch or remodeling of the intramyocardial blood vessels; they represent a dynamic interaction with the mechanics of myocardial ischemia that may be amenable to treatment.

Project description:BACKGROUND:Hyperventilation with a subsequent breath-hold has been successfully used as a non-pharmacological vasoactive stimulus to induce changes in myocardial oxygenation. The purpose of this pilot study was to assess if this maneuver is feasible in patients with multi-vessel coronary artery disease (CAD), and if it is effective at detecting coronary artery stenosis >?50% determined by quantitative coronary angiography (QCA). METHODS:Twenty-six patients with coronary artery stenosis (QCA >?50% diameter stenosis) underwent a contrast-free cardiovascular magnetic resonance (CMR) exam in the time interval between their primary coronary angiography and a subsequent percutaneous coronary intervention (PCI, n?=?24) or coronary artery bypass (CABG, n?=?2) revascularization procedure. The CMR exam involved standard function imaging, myocardial strain analysis, T2 mapping, native T1 mapping and oxygenation-sensitive CMR (OS-CMR) imaging. During OS-CMR, participants performed a paced hyperventilation for 60s followed by a breath-hold to induce a vasoactive stimulus. Ten healthy subjects underwent the CMR protocol as the control group. RESULTS:All CAD patients completed the breathing maneuvers with an average breath-hold duration of 48?±?23 s following hyperventilation and without any complications or adverse effects. In comparison to healthy subjects, CAD patients had a significantly attenuated global myocardial oxygenation response to both hyperventilation (-?9.6?±?6.8% vs. -3.1?±?6.5%, p?=?0.012) and apnea (11.3?±?6.1% vs. 2.1?±?4.4%, p?<?0.001). The breath-hold maneuver unmasked regional oxygenation differences in territories subtended by a stenotic coronary artery in comparison to remote territory within the same patient (0.5?±?3.8 vs. 3.8?±?5.3%, p?=?0.011). CONCLUSION:Breathing maneuvers in conjunction with OS-CMR are clinically feasible in CAD patients. Furthermore, OS-CMR demonstrates myocardial oxygenation abnormalities in regional myocardium related to CAD without the use of pharmacologic vasodilators or contrast agents. A larger trial appears warranted for a better understanding of its diagnostic utility. TRIAL REGISTRATION:Clinical Trials Identifier: NCT02233634 , registered 8 September 2014.

Dataset Information

Feasibility of cardiovascular magnetic resonance derived coronary wave intensity analysis.

Background

Methods

Results

Conclusion

Publications

Feasibility of cardiovascular magnetic resonance derived coronary wave intensity analysis.

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