Coronary wave intensity during the Valsalva manoeuvre in humans reflects altered intramural vessel compression responsible for extravascular resistance

Abstract

Our aim was to investigate the effect of altered cardiac-coronary interaction during the Valsalva manoeuvre (VM) on coronary wave intensity and the response of coronary microvascular resistance. In 13 patients, left ventricular (P(LV)) and aortic pressure were measured during catheterization, together with intracoronary pressure and blood flow velocity (U) via a dual-sensor guide wire advanced into an angiographically normal coronary artery. Signals were analysed for the following phases of VM: baseline (B1), onset of strain (S1), sustained strain (S2), onset of release (R1), maximal response during recovery (R2), and baseline after VM. The immediate effects of VM were most evident from diastolic P(LV) (LVDP), which increased from 11.0 ± 2.3 to 36.4 ± 2.7 mmHg between B1 and S1 and fell from 28.3 ± 3.4 to 8.3 ± 1.9 mmHg between S2 and R1. Wave intensities and rate pressure product (RPP) were only minimally affected at these transient phases, but coronary wave energies decreased by about 50% and RPP by 38% from S1 to S2, together with a 30% depression of LVdP/dt. All signals were restored to baseline values during the recovery. U did not vary significantly throughout the VM. Despite the depressed cardiac performance during VM strain, microvascular resistance, calculated with LVDP as backpressure, decreased by 31% from B1 to S2, whereas an increase via metabolically induced vasoconstriction was expected. Since coronary U remained essentially constant despite the marked reduction in oxygen consumption, microvascular vasoconstriction must have been compensated by a decrease in the contraction-mediated impediment on coronary blood flow, as confirmed by the reduced coronary wave energies.

Figure 1. Simultaneous systemic and intracoronary haemodynamic recording during the Valsalva manoeuvre

Top panel (from top to bottom): alteration in aortic (P_a), coronary (P_d) and left ventricular pressure (P_LV) as induced by the VM. Phasic and mean coronary flow velocity (U); mean coronary microvascular resistance (MR), and heart rate (HR). Shaded areas indicate cardiac cycles analysed at baseline (B1, B2) and during periods corresponding to the typical phases of strain (S1, S2) and release (R1, R2) of the VM. There is an immediate and sustained increase in left ventricular diastolic pressure during the strain period. The lower panels correspond to the boxed cycles in the top panel and illustrate the transition at the onset of strain, S1, and at the sudden release, R1, at an expanded time scale.

Figure 2. Variation in blood pressures and heart rate during the Valsalva manoeuvre

A, mean aortic pressure (P_a), coronary pressure (P_d) and left ventricular diastolic pressure (LVDP) show typical variations at different phases of the VM, with a marked elevation of LVDP during the strain. B, aortic (PP_a) and left ventricular (PP_LV) pulse pressure are depressed during S2 and R1, with an overshoot at R2. C, changes in heart rate (HR) show a reflex tachycardia during the release. #P < 0.05, *P < 0.005 compared to baseline B1; §P < 0.05, †P < 0.001 compared to the previous step.

Figure 3. Cardiac and coronary haemodynamic variables during the Valsalva manoeuvre

A, left ventricular speed of contraction (upslope) and relaxation (downslope) in terms of LVdP/dt. B, rate pressure product (RPP). C, coronary flow velocity (U). D, coronary microvascular resistance (MR). Sustained strain clearly lowers cardiac performance, oxygen consumption, and coronary resistance, while mean flow velocity stays essentially constant. #P < 0.05, *P < 0.005 compared to baseline B1; §P < 0.05, †P < 0.001 compared to the previous step.

Figure 4. Coronary wave speed during the Valsalva manoeuvre

The wave speed is reduced during the strain. *P < 0.005 compared to baseline B1; §P < 0.05, †P < 0.001 compared to the previous step.

Figure 5. Changes in coronary wave intensity pattern during the Valsalva manoeuvre

Example of ensembled coronary haemodynamic waveforms and corresponding wave intensity (dI) pattern at the different phases of the VM (same patient as shown in Fig. 1). B1, B2: baseline before and after the manoeuvre. S1, onset of strain; S2 sustained strain; R1, early release; R2, late release. Net wave intensity (dI) is indicated by a thick line and separated forward and backward components (dI_±) by thin lines; light grey fill: flow accelerating waves (FCW and BEW); darker grey fill: flow decelerating waves. The typical wave intensity pattern is depressed at maximum strain (S2) and early release of the VM (R1), and has a higher magnitude at late release (R2). Extra waves appeared in mid-systole, at S2 and R1 (arrows).

Figure 6. Energy of separated coronary waves during the Valsalva manoeuvre and their relationship with LVdP/dt

A, forward compression (FCW) and expansion waves (FEW); B, backward compression (BCW) and expansion waves (BEW). The energy of all dominant waves is reduced during the strain. C and D, energy of forward waves (C) and energy of backward waves (D) vs. LVdP/dt as a measure of the speed of cardiac contraction (compression waves) and relaxation (expansion waves). Note that flow accelerating waves (FCW and BEW) have a higher energy at the same LVdP/dt. #P < 0.05, *P < 0.005 compared to baseline B1; §P < 0.05, †P < 0.001 compared to the previous step.