Improvement of Coronary Vasomotion With Eicosapentaenoic Acid Does Not Inhibit Acetylcholine-Induced Coronary Vasospasm in Patients With Variant Angina.

Yamamoto, Hideo; Yoshimura, Hitoshi; Noma, Mitsuru; Suzuki, Satoshi; Kai, Hisashi; Tajimi, Tsukasa; Sugihara, Masayoshi; Kikuchi, Yutaka

doi:10.1253/jcj.59.608

Cited by 24 publications

(9 citation statements)

References 18 publications

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“…Second, acute improvement in endothelial function might not prevent coronary spasm in patients with VA, as shown by 4 months of treatment with eicosapentaenoic acid, which improved coronary endothelial function, but did not prevent AChinduced coronary spasm. 12 However, the effects of longterm improvement of endothelial dysfunction have not been studied and requires further research. Third, the amount of bioavailable BH4 in this study may have been insufficient to prevent ACh-induced coronary spasm.…”

Section: Failure Of Bh4 To Prevent Coronary Artery Spasmmentioning

confidence: 99%

“…In support of this concept, recent studies have shown that supplementation of BH4 improves impaired endothelial function in humans with various pathologic states, including hypercholesterolemia, smoking and coronary artery disease. [8][9][10][11] Because coronary endothelial dysfunction is commonly observed in patients with VA, 3,12,13 the depletion of BH4 and resultant reduction in NO bioavailability in the coronary circulation may be involved in the pathogenesis of coronary spasm. However, the effects of BH4 supplementation on coronary spasm have not been evaluated and so we investigated the effects of BH4 on the coronary vasoconstrictor response to acetylcholine (ACh) in patients with VA using quantitative coronary angiography.…”

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confidence: 99%

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Tetrahydrobiopterin Improves Coronary Endothelial Function, But Does Not Prevent Coronary Spasm in Patients With Vasospastic Angina

Fukuda

Teragawa

Matsuda

et al. 2002

Circ J

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oronary spasm is believed to play an important role in the pathogenesis of vasospastic angina (VA) and can cause acute myocardial infarction or ischemic sudden death. 1 However, the precise pathophysiology of coronary spasm has yet to be elucidated, although coronary endothelial dysfunction is thought to be one of the mechanisms. 2,3 Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide (NO) synthase in both endothelial and vascular smooth muscle cells [4][5][6] and also serves as a scavenger of oxygen-derived free radicals, thereby decreasing NO breakdown. 7 Therefore, BH4 is considered essential for the regulation of NO bioavailability in endothelial cells and for the maintenance of cardiovascular homeostasis. In support of this concept, recent studies have shown that supplementation of BH4 improves impaired endothelial function in humans with various pathologic states, including hypercholesterolemia, smoking and coronary artery disease. [8][9][10][11] Because coronary endothelial dysfunction is commonly observed in patients with VA, 3,12,13 the depletion of BH4 and resultant reduction in NO bioavailability in the coronary circulation may be involved in the pathogenesis of coronary spasm. However, the effects of BH4 supplementation on coronary spasm have not been evaluated and so we investigated the effects of BH4 on the coronary vasoconstrictor response to acetylcholine (ACh) in patients with VA using quantitative coronary angiography. Methods Study PopulationWe enrolled 28 Japanese patients with VA (21 men, 7 women; mean age, 55 years; range, 38-70) who fulfilled the following inclusion criteria: (1) spontaneous chest pain associated with ST-segment elevation or depression at rest on 12-lead ECG or ambulatory ECG; (2) coronary spasm (≥50% reduction in arterial diameter during coronary angiography) in the left coronary artery associated with ST-segment changes and/or typical chest pain after intracoronary injection of ACh (Daiichi Pharmaceutical Co, Tokyo, Japan); and (3) no angiographic organic stenosis in the coronary arteries. Patients with severe left ventricular dysfunction and those with valvular heart disease were excluded. Written consent was obtained from each patient, and the protocol was approved by the Hiroshima University School of Medicine Ethics Committee. Study DesignThe study design has been described previously in detail. 14,15 Briefly, anti-anginal therapy was withheld for at least 48 h before cardiac catheterization, except for unrestricted use of sublingual nitroglycerin (NTG). Diagnostic right and left heart catheterization and coronary angiography were performed using the standard percutaneous femoral approach. A 6Fr guide catheter was introduced into the left main coronary artery, and a 5Fr temporary pacing electrode catheter (Bard, Tewksbury, MA, USA) was placed in the right ventricular apex via the right jugular vein and connected to a temporary pacemaker set at a rate of 50 beats/min. Study ProtocolAfter baseline conditions were established, incremental

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Section: Failure Of Bh4 To Prevent Coronary Artery Spasmmentioning

confidence: 99%

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confidence: 99%

Tetrahydrobiopterin Improves Coronary Endothelial Function, But Does Not Prevent Coronary Spasm in Patients With Vasospastic Angina

Fukuda

Teragawa

Matsuda

et al. 2002

Circ J

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“…18) Yamamoto, et al also reported that fish oils failed to suppress ACh-induced coronary spasm at the spastic site in patients with VSA but improved endothelial function at the nonspastic site. 19) Furthermore, one report showed that flow-mediated vasodilation of the brachial artery was preserved in patients with variant angina, 20) but these findings were in contrast to the study of Motoyama, et al 14) Thus, endothelial dysfunction in the coronary and systemic arteries in patients with VSA remains controversial.…”

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confidence: 97%

Self-vasodilating Ability at the Spastic Site of Patients with Vasospastic Angina

et al. 2003

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SUMMARYDeficient nitric oxide (NO) release is thought to be the principal mechanism of coronary spasm, however, the precise mechanisms are unknown. Although acetylcholine (ACh) is used for provocation of coronary spasm, ACh is also used for the augmentation of blood flow and flow-mediated vasodilation is induced. We estimated the self-vasodilating ability (endothelial function) at the spastic site of coronary arteries in patients with vasospastic angina (VSA) during the provocation test of coronary spasm by ACh. This study included 93 patients with VSA and 77 patients with atypical chest pain (ACP). Intracoronary injection of ACh (20, 50, and 100 µg) was performed over 30 seconds and the coronary artery diameter of the spastic site was measured 3 to 4 minutes after ACh injection (delayed phase). The ability of dilation (AOD) was calculated as : ([diameter of delayed phase-baseline diameter]/[diameter after isosorbide dinitrate-baseline diameter]) ×100 (%).No significant difference was noted between the AOD in patients with ACP and VSA (28 ± 36 vs 15 ± 60%, respectively). The AOD values of 49% of patients with VSA were greater than the mean value of AOD of patients with ACP. At least almost half of the patients with VSA may have preserved self-vasodilating ability at the spastic site, and an abnormality other than endothelial dysfunction is involved in the mechanism of coronary spasm in these patients. (Jpn Heart J 2003; 44: 299-311)

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“…First, NO-dependent coronary dilatation, as tested with intracoronary acetylcholine, bradykinin, and substance-P, is well preserved at the spastic segment to the degree comparable with that of the non-spastic segment (Egashira et al 1992;Kuga et al 1995;Yamamoto et al 1992;Okumura et al 1992). Second, long-term treatment with fish oil (eicosapentaenoic acid) improved endothelial dysfunction but failed to prevent coronary artery spasm (Yamamoto et al 1995). Third, basal release of NO as estimated by constrictor response to intracoronary administration of NO synthase inhibitor (N G -monomethyl-L-arginine) was actually preserved between spastic and non-spastic arteries (Egashira et al 1996).…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Coronary Artery Spasm: Part I Clinical Aspect

Shimokawa

2014

PanVascular Medicine

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Improvement of Coronary Vasomotion With Eicosapentaenoic Acid Does Not Inhibit Acetylcholine-Induced Coronary Vasospasm in Patients With Variant Angina.

Cited by 24 publications

References 18 publications

Tetrahydrobiopterin Improves Coronary Endothelial Function, But Does Not Prevent Coronary Spasm in Patients With Vasospastic Angina

Tetrahydrobiopterin Improves Coronary Endothelial Function, But Does Not Prevent Coronary Spasm in Patients With Vasospastic Angina

Self-vasodilating Ability at the Spastic Site of Patients with Vasospastic Angina

Coronary Artery Spasm: Part I Clinical Aspect

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