Key result
Intracoronary BH4 attenuates acetylcholine-induced vasoconstriction by ~7% but fails to prevent coronary spasm.
Why the study?
Reduced bioavailability of tetrahydrobiopterin (BH4) and decreased nitric oxide in coronary circulation may contribute to coronary spasm, but the effects of BH4 supplementation on coronary spasm have not been evaluated.
Absolute Event Rate: 6% vs -1.1%
p-value: p=0.0440
Does not support BH4 to prevent spasm in vasospastic angina; leaves open its role in milder endothelial dysfunction.
Reduced bioavailability of tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide (NO) synthase, and the resulting decrease in NO in the coronary circulation may be involved in the pathogenesis of coronary spasm. The present study investigated the effects of BH4 on the vascular response to acetylcholine (ACh) in 28 patients with vasospastic angina (VA) using quantitative angiography. After recording the vascular responses to ACh (3 and 30 microg/min), either BH4 (1 mg/min) or saline was infused into the coronary artery for 2 min before and during a subsequent infusion of ACh. With the 3 microg/min dose of ACh, BH4 attenuated the ACh-induced decrease in coronary diameter in both the nonspastic segments (-1.1 +/- 2.2% ACh vs 6.0 +/- 2.8% ACh+BH4) and spastic segments (-6.3 +/- 2.7% ACh vs 2.9 +/- 2.7% ACh+BH4), but did not influence the ACh-induced coronary spasm at 30 microg/min (-57.3 +/-2.4% ACh vs -55.3 +/- 2.4% ACh+BH4). In the control patients, saline did not influence either the spastic or nonspastic vasoconstrictor responses to ACh. Acute administration of BH4 improves coronary endothelial function, but does not prevent coronary spasm in patients with VA.
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Fukuda et al. (2002) studied Vasospastic angina (n=28). Tetrahydrobiopterin (BH4) vs. Saline (0.9%) was evaluated on Percent change in coronary diameter of nonspastic segments in response to 3 μg/min acetylcholine (p=0.0440). Intracoronary infusion of tetrahydrobiopterin (BH4) attenuated acetylcholine-induced vasoconstriction in nonspastic coronary segments (6.0% vs -1.1%, p=0.0440), but did not prevent coronary spasm at higher acetylcholine doses in patients with vasospastic angina.
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