TY - JOUR
T1 - Influence of increased heart rate and aortic pressure on resting indices of functional coronary stenosis severity
AU - Casadonte, Lorena
AU - Verhoeff, Bart-Jan
AU - Piek, Jan J.
AU - VanBavel, Ed
AU - Spaan, Jos A. E.
AU - Siebes, Maria
PY - 2017
Y1 - 2017
N2 - Baseline assessment of functional stenosis severity has been proposed as a practical alternative to hyperemic indices. However, intact autoregulation mechanisms may affect intracoronary hemodynamics. The aim of this study was to investigate the effect of changes in aortic pressure (Pa) and heart rate (HR) on baseline coronary hemodynamics and functional stenosis assessment. In 15 patients (55 +/- 3% diameter stenosis) Pa, intracoronary pressure (Pd) and flow velocity were obtained at control, and during atrial pacing at 120 bpm, increased Pa (+ 30 mmHg) with intravenous phenylephrine (PE), and elevated Pa while pacing at sinus heart rate (PE + sHR). We derived rate pressure product (RPP = systolic Pa 9 HR), baseline microvascular resistance (BMR = Pd/velocity), and stenosis resistance [BSR = (Pa - Pd)/velocity] as well as whole-cycle Pd/Pa. Tachycardia (120 +/- 1 bpm) raised RPP by 74% vs. control. Accordingly, BMR decreased by 27% (p <0.01) and velocity increased by 36% (p <0.05), while Pd/Pa decreased by 0.05 +/- 0.02 (p <0.05) and BSR remained similar to control. Raising Pa to 121 +/- 3 mmHg (PE) with concomitant reflex bradycardia increased BMR by 26% (p <0.001) at essentially unchanged RPP and velocity. Consequently, BSR and Pd/Pa were only marginally affected. During PE ? sHR, velocity increased by 21% (p <0.01) attributable to a 46% higher RPP (p <0.001). However, BMR, BSR, and Pd/Pa remained statistically unaffected. Nonetheless, the interventions tended to increase functional stenosis severity, causing Pd/Pa and BSR of borderline lesions to cross the diagnostic threshold. In conclusion, coronary microvascular adaptation to physiological conditions affecting metabolic demand at rest influences intracoronary hemodynamics, which may lead to altered basal stenosis indices used for clinical decision-making
AB - Baseline assessment of functional stenosis severity has been proposed as a practical alternative to hyperemic indices. However, intact autoregulation mechanisms may affect intracoronary hemodynamics. The aim of this study was to investigate the effect of changes in aortic pressure (Pa) and heart rate (HR) on baseline coronary hemodynamics and functional stenosis assessment. In 15 patients (55 +/- 3% diameter stenosis) Pa, intracoronary pressure (Pd) and flow velocity were obtained at control, and during atrial pacing at 120 bpm, increased Pa (+ 30 mmHg) with intravenous phenylephrine (PE), and elevated Pa while pacing at sinus heart rate (PE + sHR). We derived rate pressure product (RPP = systolic Pa 9 HR), baseline microvascular resistance (BMR = Pd/velocity), and stenosis resistance [BSR = (Pa - Pd)/velocity] as well as whole-cycle Pd/Pa. Tachycardia (120 +/- 1 bpm) raised RPP by 74% vs. control. Accordingly, BMR decreased by 27% (p <0.01) and velocity increased by 36% (p <0.05), while Pd/Pa decreased by 0.05 +/- 0.02 (p <0.05) and BSR remained similar to control. Raising Pa to 121 +/- 3 mmHg (PE) with concomitant reflex bradycardia increased BMR by 26% (p <0.001) at essentially unchanged RPP and velocity. Consequently, BSR and Pd/Pa were only marginally affected. During PE ? sHR, velocity increased by 21% (p <0.01) attributable to a 46% higher RPP (p <0.001). However, BMR, BSR, and Pd/Pa remained statistically unaffected. Nonetheless, the interventions tended to increase functional stenosis severity, causing Pd/Pa and BSR of borderline lesions to cross the diagnostic threshold. In conclusion, coronary microvascular adaptation to physiological conditions affecting metabolic demand at rest influences intracoronary hemodynamics, which may lead to altered basal stenosis indices used for clinical decision-making
U2 - https://doi.org/10.1007/s00395-017-0651-0
DO - https://doi.org/10.1007/s00395-017-0651-0
M3 - Article
C2 - 28905113
SN - 0300-8428
VL - 112
JO - Basic research in cardiology
JF - Basic research in cardiology
IS - 6
M1 - 61
ER -