SummaryBackground Symptomatic relief is the primary goal of percutaneous coronary intervention (PCI) in stable angina and is commonly observed clinically. However, there is no evidence from blinded, placebocontrolled randomised trials to show its efficacy.
iFR and FFR had equivalent agreement with classification of coronary stenosis severity by HSR. Further reduction in resistance by the administration of adenosine did not improve diagnostic categorization, indicating that iFR can be used as an adenosine-free alternative to FFR.
The augmentation index predicts cardiovascular mortality and is usually explained as a distally reflected wave adding to the forward wave generated by systole. We propose that the capacitative properties of the aorta (the arterial reservoir) also contribute significantly to the augmentation index and have calculated the contribution of the arterial reservoir, independently of wave reflection, and assessed how these contributions change with aging. In 15 subjects (aged 53 ± 10 yr), we measured pressure and Doppler velocity simultaneously in the proximal aorta using intra-arterial wires. We calculated the components of augmentation pressure in two ways: 1) into forward and backward (reflected) components by established separation methods, and 2) using an approach that accounts for an additional reservoir component. When the reservoir was ignored, augmentation pressure (22.7 ± 13.9 mmHg) comprised a small forward wave (peak pressure = 6.5 ± 9.4 mmHg) and a larger backward wave (peak pressure = 16.2 ± 7.6 mmHg). After we took account of the reservoir, the contribution to augmentation pressure of the backward wave was reduced by 64% to 5.8 ± 4.4 mmHg (P < 0.001), forward pressure was negligible, and reservoir pressure was the largest component (peak pressure = 19.8 ± 9.3 mmHg). With age, reservoir pressure increased progressively (9.9 mmHg/decade, r = 0.69, P < 0.001). In conclusion, the augmentation index is principally determined by aortic reservoir function and other elastic arteries and only to a minor extent by reflected waves. Reservoir function rather than wave reflection changes markedly with aging, which accounts for the age-related changes in the aortic pressure waveform.
Abstract-Wave reflection is thought to be important in the augmentation of blood pressure. However, identification of distal reflections sites remains unclear. One possible explanation for this is that wave reflection is predominately determined by an amalgamation of multiple proximal small reflections rather than large discrete reflections originating from the distal peripheries. In 19 subjects (age, 35-73 years), sensor-tipped intra-arterial wires were used to measure pressure and Doppler velocity at 10-cm intervals along the aorta, starting at the aortic root. Incident and reflected waves were identified and timings and magnitudes quantified using wave intensity analysis. Mean wave speed increased along the length of the aorta (proximal, 6.8Ϯ0.9 m/s; distal, 10.7Ϯ1.5 m/s). The incident wave was tracked moving along the aorta, taking 55Ϯ4 ms to travel from the aortic root to the distal aorta. However, the timing to the refection site distance did not differ between proximal and distal aortic measurement sites (proximal aorta, 48Ϯ5 ms versus distal aorta, 42Ϯ4 ms; Pϭ0.3). We performed a second analysis using aortic waveforms in a nonlinear model of pulse-wave propagation. This demonstrated very similar results to those observed in vivo and also an exponential attenuation in reflection magnitude. There is no single dominant refection site in or near the distal aorta. Rather, there are multiple reflection sites along the aorta, for which the contributions are attenuated with distance. We hypothesize that rereflection of reflected waves leads to wave entrapment, preventing distal waves being seen in the proximal aorta. Key Words: pressure augmentation Ⅲ pulse wave propagation Ⅲ wave reflection Ⅲ aging and disease Ⅲ 1D modeling Ⅲ wave tracking Ⅲ pulse wave velocity Ⅲ augmentation index W ave reflection is thought to be an important mechanism of augmentation of blood pressure with aging and in disease. This hypothesis assumes that the forward-traveling (incident) wave from cardiac ejection is reflected back toward the heart at sites of impedance mismatch. Several investigators have tried to identify the principal reflection locations, based on estimates of wave speed and time of return of the reflected wave, usually arriving at differing conclusions. [1][2][3][4] Others have taken an alternative approach, instead, identifying changes in aortic composition or aortic diameter as being most important in the determination of reflection sites. Furthermore, a recent meta-analysis has found that reflection timing changes little with aging (despite the expected increases in pulse wave velocity), supporting the findings from the Framingham Study, which showed a lengthening of distance to an apparent reflection site with aging. 5,6 One explanation for these findings is that the reflection site is not fixed but is dynamically determined by sites of impedance mismatch, tapering, and composition of the aorta.We set out to explore this by measuring incident and reflected waves along the aorta to quantify how the reflected wave ti...
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