Does pharmacologic coronary flow reserve reflect vasodilator responsiveness to increased myocardial demand in humans?

OBJECTIVE

To assess the relationship between maximal pharmacologic coronary flow reserve and metabolic coronary vasodilation in nonstenotic coronary arteries.

BACKGROUND

Evaluation of the coronary microcirculation in humans during cardiac catheterization is commonly performed by assessment of coronary hemodynamics during administration of potent coronary vasodilators. However, the relationship between maximal pharmacologic vasodilation and flow increases occurring in response to increased myocardial demand has not been evaluated.

METHODS

The coronary blood flow responses to a maximally dilating dose of intracoronary adenosine or papaverine and to a standardized atrial pacing stress were assessed in 49 patients using intracoronary Doppler velocimetry. The blood flow responses to a maximally dilating dose of intracoronary adenosine and to intravenous infusion of dobutamine were determined in 13 patients.

RESULTS

The maximal pharmacologic coronary flow reserve averaged 3.2 +/- 0.1 (mean +/- SEM). The coronary blood flow velocity increased by 32 +/- 3% during atrial pacing, and the change in coronary flow velocity was correlated with the change in the mean arterial pressure x heart rate product during pacing. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during atrial pacing or the response of the flow to pacing normalized with respect to the magnitude of stress reflected by the change in rate x pressure product. The coronary blood flow velocity increased by 135 +/- 16% during dobutamine infusion. Regression analysis revealed no relationship between the pharmacologic coronary flow reserve and the change in coronary flow velocity during dobutamine infusion.

CONCLUSIONS

Knowledge of the maximal pharmacologic coronary flow reserve is an inadequate surrogate for assessment of coronary vasodilation in response to increases in myocardial metabolic demand in nonstenotic arteries.