Abstract
Introduction Growing evidence supports ischemia-guided management of chest pain, with invasive and non-invasive tests reliant upon achieving adenosine-induced coronary hyperemia (defined as increased blood flow to an organ’s perfusion bed). In the non-invasive setting, surrogate markers of hyperemia, such as increases in heart rate, are often used, despite not being formally validated. We tested whether heart rate and other non-invasive indices are reliable markers of coronary hyperemia. Methods The first part involved Doppler flow-based validation of the best pressure-wire markers of hyperemia in 53 patients. Subsequently, using these validated pressure-derived parameters, 265 pressure-wire traces were analysed to determine whether heart rate and other non-invasive parameters correlated with hyperemia. Results In the flow derivation cohort, the best determinant of hyperemia came from having 2 out of 3 of: (1) Ventriculisation of the distal pressure waveform, (2) disappearance of distal dicrotic pressure notch, (3) separation of mean aortic and distal pressures. Within the 244 patients demonstrating hyperemia, non-invasive markers of hyperemia, such as change in heart rate (p = 0.77), blood pressure (p = 0.60) and rate-pressure product (p = 0.86), were poor correlates of coronary hyperemia, with only 37.3% demonstrating a ≥ 10% increase in heart rate that is commonly used to adjudge adenosine-induced hyperemia in the non-invasive setting. Conclusions We demonstrate, by correlation with Doppler-flow data, a validated method of identifying coronary hyperemia within the catheter laboratory using the pressure-wire. We subsequently show that non-invasive parameters, such as heart rate change, are poor predictors of coronary hyperemia during stress imaging protocols that rely upon achieving adenosine-induced hyperemia.
Highlights
Growing evidence supports ischemia-guided management of chest pain, with invasive and non-invasive tests reliant upon achieving adenosine-induced coronary hyperemia
We have shown that the time-course of heart rate (HR) change may not reflect the onset of maximal hyperemia (Fig. 5), with prolonged adenosine infusions subjecting patients to unpleasant symptoms unnecessarily
Our study has shown that there was no correlation between HR, microvasculature resistance (MR) and AIx, and highlights the likelihood of other mechanisms, beyond peripheral vasodilatation, by which HR increases in response to adenosine; such as action on the sympathetic nervous system [23]
Summary
Our study population consisted of patients who presented to a single centre for coronary angiography ± proceeding to percutaneous intervention as appropriate. 306 Consecutive patients undergoing FFR measurements between October 2013 and February 2017 were screened, where hyperemia was induced by IV adenosine infusion. A pre-defined CFR threshold of 1.2 was used to define hyperemia (defined as an increase in blood flow to an organ’s perfusion bed) to ensure that the increase in flow at hyperemia is above the margin of measurement error commonly seen with CombowireXT Doppler flow measurements In this Doppler cohort, we assessed the diagnostic performance of three commonly-used invasive pressure-waveform parameters of hyperemia, and combinations thereof by calculating their sensitivity, specificity and positive and negative predictive values. These are (1) ventricularisation of distal pressure waveform (a presystolic deflection resembling an ‘a wave’, a slower upstroke of the waveform and a steeper down-stroke than that of aortic pressure [14]), (2) separation of mean aortic and distal coronary pressure [> 10% difference in (Pa–Pd), over five consecutive heart beats, compared to the resting gradient] and (3) disappearance of dicrotic notch from the distal arterial pressure trace (see Fig. 1).
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