In 10 anesthetized dogs, we measured high-fidelity left circumflex coronary (P(LCx)), aortic (P(Ao)), and left ventricular (P(LV)) pressures and left circumflex velocity (U(LCx); Doppler) and used wave-intensity analysis (WIA) to identify the determinants of P(LCx) and U(LCx). Dogs were paced from the right atrium (control 1) or right ventricle by use of single (control 2) and then paired pacing to evaluate the effects of left ventricular contraction on P(LCx) and U(LCx). During left ventricular isovolumic contraction, P(LCx) exceeded P(Ao), paired pacing increasing the difference. Paired pacing increased DeltaP(X) (the P(LCx)-P(Ao) difference at the P(Ao)-P(LV) crossover) and average dP(LCx)/dt (P < 0.0001 for both). During this time, WIA identified a backward-going compression wave (BCW) that increased P(LCx) and decreased U(LCx); the BCW increased during paired pacing (P < 0.0001). After the aortic valve opened, the increase in P(Ao) caused a forward-going compression wave that, when it exceeded the BCW, caused U(LCx) to increase, despite P(LV) and (presumably) elastance continuing to increase. Thus WIA identifies the contributions of upstream (aortic) and downstream (microcirculatory) effects on P(LCx) and U(LCx).

. Assessment of left ventricular diastolic suction in dogs using wave-intensity analysis. Am J Physiol Heart Circ Physiol 288: H1641-H1651, 2005. First published November 24, 2004 doi:10.1152/ajpheart.00181.2004.-Two apparently different types of mechanisms have emerged to explain diastolic suction (DS), that property of the left ventricle (LV) that tends to cause it to refill itself during early diastole independent of any force from the left atrium (LA). By means of the first mechanism, DS depends on decreased elastance [e.g., the relaxation time constant ()] and, by the second, end-systolic volume (VLVES). We used waveintensity analysis (WIA) to measure the total energy transported by the backward expansion wave (IWϪ) during LV relaxation in an attempt to reconcile these mechanisms. In six anesthetized, open-chest dogs, we measured aortic, LV (PLV), LA (PLA), and pericardial pressures and LV volume by orthogonal ultrasonic crystals. Mitral velocity was measured by Doppler echocardiography, and aortic velocity was measured by an ultrasonic flow probe. Heart rate was controlled by pacing, VLVES by volume loading, and by isoproterenol or esmolol administration. IWϪ was found to be inversely related to and VLVES. Our measure of DS, the energy remaining after mitral valve opening, IWϪDS, was also found to be inversely related to and VLVES and was ϳ10% of the total "aspirating" energy generated by LV relaxation (i.e., I WϪ). The size of the Doppler (early filling) E wave depended on IWϪDS in addition to IWϩ, the energy associated with LA decompression. We conclude that the energy of the backward-going wave generated by the LV during relaxation depends on both the rate at which elastance decreases (i.e., ) and V LVES. WIA provides a new approach for assessing DS and reconciles those two previously proposed mechanisms. The E wave depends on DS in addition to LA decompression. diastole; hemodynamics; mitral valve; ventricles DIASTOLIC SUCTION (DS) is defined as that property of the left ventricle (LV) that tends to cause it to refill itself during early diastole independent of any force from the left atrium (LA). Two apparently different types of mechanistic explanations have emerged. The first type is represented by Katz (30) and Wiggers (52), who related DS to the decrease in ventricular elastance, and by several contemporary investigators (11,12,38,47) who emphasized the importance of the rate of LV relaxation in subsequent diastolic filling. In 1957, Wiggers wrote that "During early moments of ventricular relaxation, elastic stresses created during contraction are released. . . If blood could enter the ventricular chamber during this phase of diastole, such a rapid drop in pressure would unquestionably constitute a potent aspirating force" (52).Wiggers implied that the relaxing LV generates an "aspirating force" from the moment LV pressure begins to decrease. Accordingly, as elaborated upon below, the first effect of a relaxation-generated aspirating force must be to decelerate the mass represented by the stroke v...

Wave-intensity analysis, which separates upstream from downstream events and defines their interaction, has been used to study the effects of changes in left ventricular (LV) contractility (E(max)) and left circumflex coronary artery resistance (R(LCx)) on the coronary systolic flow impediment (CSFI). In 10 anesthetized, open-chest dogs, we measured coronary, aortic, and LV pressures, coronary velocity (Flowire), and flow. E(max) was increased by paired pacing and R(LCx) was modulated by intracoronary infusions of vasodilators (adenosine and nitroglycerin) and a vasoconstrictor (phenylephrine). When both E(max) and R(LCx) were varied, CSFI and the energy of the backward-going compression wave (I(W-)) were greatest at the highest levels of E(max) and the lowest levels of R(LCx). I(W-) was proportional to the CSFI. We conclude that contractility and coronary resistance change CSFI by modulating the backward-going compression wave.

In order to explore a new approach to the analysis of diastolic dysfunction, we adapted wave-intensity analysis (WIA), a time-domain analysis that provides information regarding both upstream and downstream events, to left ventricular (LV) filling. WIA considers the pressure and flow waves as summations of successive wavelets, characterised by the direction they travel and by the sign of the pressure gradient associated with them. Wave intensity is the product, dPdU, calculated from the incremental differences in LV pressure (dP) and mitral velocity (dU) and, during the diastolic filling interval, yields up to five dPdU peaks. Peak 1 is caused by backward-travelling expansion waves that accelerate the blood while LV pressure falls, and may be related to "diastolic suction". Peak 2 is caused by forward-travelling compression waves which occur if acceleration continues after LV pressure begins to increase. Peak 3 is caused by backward compression waves and is associated with rising LV pressure and deceleration. Peak 4 is caused by forward compression waves and is associated with the increasing LV pressure and acceleration caused by atrial contraction. Peak 5 is caused by backward compression waves and is associated with increasing pressure and deceleration. These preliminary observations suggest that WIA can be useful in describing the mechanics of LV filling and, after much further work has been accomplished, it might prove useful in the detection and characterization of diastolic dysfunction.

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In native non-critical coronary artery disease or following PCI, coronary microvascular endothelial function is not improved by co-administration of Ach and BH4.

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