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

The Valsalva manoeuvre provokes strong changes in the cardiovascular system and can be used to alter parameters of cardiac mechanics for studying cardiac–coronary interaction in humans. Cardiac contraction results in coronary forward and backward travelling waves that can be quantified by wave intensity analysis. Our results show that during a Valsalva manoeuvre, combined autoregulatory vasoconstriction and decreased extravascular compression contribute to an over-compensatory reduction in coronary microvascular resistance, which yields an essentially constant coronary flow velocity despite depressed cardiac performance. The reduced energy of coronary waves during the Valsalva manoeuvre reflects the diminished compression of intramural vessels and thereby reduced extravascular resistance. These findings help us better understand the mechanisms underlying cardiac–coronary interaction and are useful to validate physiological models of the coronary circulation being developed for patient-specific diagnostic support. 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 (PLV) 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 PLV (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.