Background-Coronary blood flow peaks in diastole when aortic blood pressure has fallen. Current models fail to completely explain this phenomenon. We present a new approach-using wave intensity analysis-to explain this phenomenon in normal subjects and to evaluate the effects of left ventricular hypertrophy (LVH). Method and Results-We measured simultaneous pressure and Doppler velocity with intracoronary wires in the left main stem, left anterior descending, and circumflex arteries of 20 subjects after a normal coronary arteriogram. Wave intensity analysis was used to identify and quantify individual pressure and velocity waves within the coronary artery circulation.A consistent pattern of 6 predominating waves was identified. Ninety-four percent of wave energy, accelerating blood forward along the coronary artery, came from 2 waves: first a pushing wave caused by left ventricular ejection-the dominant forward-traveling pushing wave; and later a suction wave caused by relief of myocardial microcirculatory compression-the dominant backward-traveling suction wave. The dominant backward-traveling suction wave (18.2Ϯ13.7ϫ10 3 W m Ϫ2 s

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Background-In patients with chronic heart failure (CHF), periodic breathing (PB) predicts poor prognosis. Clinical studies have identified numerous risk factors for PB (which also includes Cheyne-Stokes respiration). Computer simulations have shown that oscillations can arise from delayed negative feedback. However, no simple general theory quantitatively explains PB and its mechanisms of treatment using widely-understood clinical concepts. Therefore, we introduce a new approach to the quantitative analysis of the dynamic physiology governing cardiorespiratory stability in CHF. Methods and Results-An algebraic formula was derived (presented as a simple 2D plot), enabling prediction from easily acquired clinical data to determine whether respiration will be unstable. Clinical validation was performed in 20 patients with CHF (10 with PB and 10 without) and 10 healthy normal subjects. Measurements, including chemoreflex sensitivity (S) and delay (␦), alveolar volume (V L ), and end-tidal CO 2 fraction (C ), were applied to the stability formula. The breathing pattern was correctly predicted in 28 of the 30 subjects. The principal combined parameter (C S)ϫ(␦/V L ) was higher in patients with PB (14.2Ϯ3.0) than in those without PB (3.1Ϯ0.5; Pϭ0.0005) or in normal controls (2.4Ϯ0.5; Pϭ0.0003). This was because of differences in both chemoreflex sensitivity (1749Ϯ235 versus 620Ϯ103 and 526Ϯ104 L/min per atm CO 2 ; Pϭ0.0001 and PϽ0.0001, respectively) and chemoreflex delay (0.53Ϯ0.06 vs 0.40Ϯ0.06 and 0.30Ϯ0.04 min; PϭNS and Pϭ0.02). Conclusion-This analytical approach identifies the physiological abnormalities that are important in the genesis of PB and explicitly defines the region of predicted instability. The clinical data identify chemoreflex gain and delay time (rather than hyperventilation or hypocapnia) as causes of PB.

. Use of simultaneous pressure and velocity measurements to estimate arterial wave speed at a single site in humans. Am J Physiol Heart Circ Physiol 290: H878 -H885, 2006. First published August 26, 2005 doi:10.1152/ajpheart.00751.2005.-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 ϭ 0.72, P Ͻ 0.05). Coronary wave speed correlated with aortic wave speed (r ϭ 0.72, P ϭ 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 Ͻ 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. coronary artery hemodynamics; coronary arteries; wave intensity analysis; coronary velocity; coronary flow; interventional cardiology; pulse wave velocity METHODS HAVE NOT BEEN AVAILABLE to measure wave speed in the human coronary artery, but wave speed measured in the aorta has repeatedly been shown to predict cardiac events (3,17,19). The standard approach for measuring wave speed relies on measurement of the time taken (␦t) for a pressure wave to travel between two sites a known distance apart (␦s). The pressure curves at the two sites may be acquired simultaneously with a pair of transducers or, alternatively, with one transducer moved between two positions with subsequent gating to the R wave of the ECG. The time delay (␦t) is measured between the arrival of an identifiable point on the pressure wave, such as the "foot," and wave speed (c), calculated as follows: c ϭ ␦s/␦t. This method is commonly referred to as the "foot-to-foot" method. Early work was invasive, in that catheters were used to acquire simultaneous pressure waveforms in the aorta (7). Arterial waveforms are more commonly acquired using pressure transducers, Doppler ultrasound, or applanation tonometry at peripheral sites. With ...

Continuous non-invasive arterial pressure monitoring demonstrates that even small changes in AV delay from its haemodynamic peak value have a significant effect on BP. This peak varies between individuals, is highly reproducible, and is more pronounced at higher heart rates than resting rates.

Objective: To assess the haemodynamic effect of simultaneously adjusting atrioventricular (AV) and interventricular (VV) delays. Method: 35 different combinations of AV and VV delay were tested by using digital photoplethysmography (Finometer) with repeated alternations to measure relative change in systolic blood pressure (SBP rel ) in 15 patients with cardiac resynchronisation devices for heart failure. Results: Changing AV delay had a larger effect than changing VV delay (range of SBP rel 21 v 4.2 mm Hg, p , 0.001). Each had a curvilinear effect. The curve of response to AV delay fitted extremely closely to a parabola (average R 2 = 0.99, average residual variance 0.8 mm Hg 2 ). The response to VV delay was significantly less curved (quadratic coefficient 67 v 1194 mm Hg/s 2 , p = 0.003) and therefore, although the residual variance was equally small (0.8 mm Hg 2 ), the R 2 value was 0.7. Reproducibility at two months was good, with the SD of the difference between two measurements of SBP rel being 2.5 mm Hg for AV delay (2% of mean systolic blood pressure) and 1.5 mm Hg for VV delay (1% of mean systolic blood pressure). Conclusions: Changing AV and VV delays results in a curvilinear acute blood pressure response. This shape fits very closely to a parabola, which may be valuable information in developing a streamlined clinical protocol. VV delay adjustment provides an additional, albeit smaller, haemodynamic benefit to AV optimisation.

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...

Impact of variability in the measured parameter is rarely considered in designing clinical protocols for optimization of atrioventricular (AV) or interventricular (VV) delay of cardiac resynchronization therapy (CRT). In this article, we approach this question quantitatively using mathematical simulation in which the true optimum is known and examine practical implications using some real measurements. We calculated the performance of any optimization process that selects the pacing setting which maximizes an underlying signal, such as flow or pressure, in the presence of overlying random variability (noise). If signal and noise are of equal size, for a 5-choice optimization (60, 100, 140, 180, 220 ms), replicate AV delay optima are rarely identical but rather scattered with a standard deviation of 45 ms. This scatter was overwhelmingly determined (ρ = −0.975, P < 0.001) by Information Content, \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$ {\frac{\text{Signal}}{{{\text{Signal}} + {\text{Noise}}}}} $$\end{document}, an expression of signal-to-noise ratio. Averaging multiple replicates improves information content. In real clinical data, at resting, heart rate information content is often only 0.2–0.3; elevated pacing rates can raise information content above 0.5. Low information content (e.g. <0.5) causes gross overestimation of optimization-induced increment in VTI, high false-positive appearance of change in optimum between visits and very wide confidence intervals of individual patient optimum. AV and VV optimization by selecting the setting showing maximum cardiac function can only be accurate if information content is high. Simple steps to reduce noise such as averaging multiple replicates, or to increase signal such as increasing heart rate, can improve information content, and therefore viability, of any optimization process.