Key result
Intracoronary aspirin reduced resting coronary blood flow by 27% (P=0.008) and attenuated pacing-induced hyperemia (32.6 vs 45.0 mL/min, P=0.005), highlighting the role of vasodilator prostanoids.
Why the study?
Does inhibition of vasodilator prostanoids and NO with intracoronary ASA and L-NMMA alter resting flow, metabolic vasodilation, and flow-mediated dilation in patients with normal coronary flow reserve?
Population
25 patients undergoing clinically indicated procedures, with angiographically smooth or mildly irregular…
Comparison
Intracoronary aspirin and N-monomethyl-L-arginine vs Baseline
Design
Other
Authors
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Endothelial prostanoid contribution to coronary tone may matter in ischemia; leaves open clinical relevance of systemic inhibition.
Does inhibition of vasodilator prostanoids and NO with intracoronary ASA and L-NMMA alter resting flow, metabolic vasodilation, and flow-mediated dilation in patients with normal coronary flow reserve?
Absolute Event Rate: 32.6% vs 45%
p-value: p=0.005
Tonic release of vasodilator prostanoids and nitric oxide contributes significantly to resting coronary tone and metabolic vasodilation, highlighting the importance of normal endothelial function in preventing myocardial ischemia.
Duffy et al. (1999) studied Coronary artery disease (n=25). Intracoronary aspirin (ASA) and N(G)-monomethyl-L-arginine (L-NMMA) vs. Baseline (before inhibition) was evaluated on Pacing-induced hyperemia (mL/min) before and after ASA (p=0.005). Intracoronary aspirin reduced resting coronary blood flow by 27% (P=0.008) and attenuated pacing-induced hyperemia (32.6 vs 45.0 mL/min, P=0.005), highlighting the role of vasodilator prostanoids.
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