September 13, 2017Open Access
Influence of increased heart rate and aortic pressure on resting indices of functional coronary stenosis severity
Key Result
Tachycardia induced by atrial pacing significantly decreased the resting distal-to-aortic pressure ratio (Pd/Pa) by 0.05 compared to baseline, causing 27% of borderline lesions to cross the diagnostic threshold.
Study Design
Type
Observational (n=15)
Multicenter
No
Structured PICO
Do changes in heart rate and aortic pressure affect resting indices of functional coronary stenosis severity in patients with stable coronary artery disease?
P
Population
15 patients with stable coronary artery disease and a single de novo lesion of intermediate severity (32-74% diameter reduction, mean 55 ± 3%) scheduled for elective percutaneous coronary intervention. Mean age 57 ± 2, 87% male. Excluded: diffuse or three-vessel disease, ejection fraction <30%, recent myocardial infarction, serious valve abnormalities, prior cardiac surgery, hypertrophic cardiomyopathy, cardiac arrhythmia, abnormal clotting profiles, or severe renal failure.
I
Intervention
Hemodynamic provocations during cardiac catheterization: atrial pacing at 120 bpm, increased aortic pressure (+30 mmHg) with intravenous phenylephrine, and elevated aortic pressure while pacing at sinus heart rate.
C
Comparator
Baseline (control) resting conditions.
O
Outcome
Changes in baseline coronary hemodynamics and functional stenosis assessment indices (Pd/Pa, baseline microvascular resistance, and baseline stenosis resistance).surrogate
Physiological changes in heart rate and aortic pressure significantly alter resting intracoronary hemodynamics, potentially causing misclassification of borderline coronary lesions when using resting indices like Pd/Pa.
Main Result
Absolute Event Rate: 0.86% vs 0.91%
p-value: p=<0.01
Limitations
- Small cohort of patients limits extension of findings to a more general population
- Heterogeneous distribution of stenosis severities
- Intravenous phenylephrine may have stimulated alpha-1-adrenergic receptors in epicardial coronary vessels
- Confounding factors such as co-morbidities, medication, or microvascular disease may affect autoregulation
- Measured flow velocity rather than absolute volume flow
Abstract
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 × 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.