Abstract
KEY POINTS: Coronary wave intensity analysis (WIA) is an emerging technique for assessing upstream and downstream influences on myocardial perfusion. It is thought that a dominant backward decompression wave (BDW(dia) ) is generated by a distal suction effect, while early-diastolic forward decompression (FDW(dia) ) and compression (FCW(dia) ) waves originate in the aorta. We show that wave reflection also makes a substantial contribution to FDW(dia) , FCW(dia) and BDW(dia) , as quantified by a novel method. In 18 sheep, wave reflection accounted for ∼70% of BDW(dia) , whereas distal suction dominated in a computer model representing a hypertensive human. Non-linear addition/subtraction of mechanistically distinct waves (e.g. wave reflection and distal suction) obfuscates the true contribution of upstream and downstream forces on measured waves (the 'smoke and mirrors' effect). The mechanisms underlying coronary WIA are more complex than previously thought and the impact of wave reflection should be considered when interpreting clinical and experimental data. ABSTRACT: Coronary arterial wave intensity analysis (WIA) is thought to provide clear insight into upstream and downstream forces on coronary flow, with a large early-diastolic surge in coronary flow accompanied by a prominent backward decompression wave (BDW(dia) ), as well as a forward decompression wave (FDW(dia) ) and forward compression wave (FCW(dia) ). The BDW(dia) is believed to arise from distal suction due to release of extravascular compression by relaxing myocardium, while FDW(dia) and FCW(dia) are thought to be transmitted from the aorta into the coronary arteries. Based on an established multi-scale computational model and high-fidelity measurements from the proximal circumflex artery (Cx) of 18 anaesthetized sheep, we present evidence that wave reflection has a major impact on each of these three waves, with a non-linear addition/subtraction of reflected waves obscuring the true influence of upstream and downstream forces through concealment and exaggeration, i.e. a 'smoke and mirrors' effect. We also describe methods, requiring additional measurement of aortic WIA, for unravelling the separate influences of wave reflection versus active upstream/downstream forces on coronary waves. Distal wave reflection accounted for ∼70% of the BDW(dia) in sheep, but had a lesser influence (∼25%) in the computer model representing a hypertensive human. Negative reflection of the BDW(dia) at the coronary-aortic junction attenuated the Cx FDW(dia) (by ∼40% in sheep) and augmented Cx FCW(dia) (∼5-fold), relative to the corresponding aortic waves. We conclude that wave reflection has a major influence on early-diastolic WIA, and thus needs to be considered when interpreting coronary WIA profiles.