Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.

Egashira, Kensuke; Inou, Tetsuzi; Yamada, Akira; Hirooka, Yoshitaka; Takeshita, Akira

doi:10.1172/jci115646

Cited by 95 publications

(45 citation statements)

References 31 publications

(29 reference statements)

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“…3) In this study, we found that globally the vasodilatory response (AOD) in the nonspastic site in the ACh delayed phase was significantly greater in responders than in nonresponders and this was similar to Egashira's findings. However, it is also a fact that in some patients with VSA, dissociation between the AOD value at the spastic site and nonspastic site existed and a poor vasodilating response at the nonspastic site was found even in some responders.…”

Section: )supporting

confidence: 89%

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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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Section: )supporting

confidence: 89%

“…Five of 113 patients with an organic stenosis > 75% at the spastic site were also excluded. Eight of 93 Vol 44 No 3 patients with VSA had about 50% stenosis at the spastic site and 28 patients had about 25% stenosis. The other 57 patients with VSA had angiographically normal or nearly normal coronary arteries.…”

Section: Methodsmentioning

confidence: 95%

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

et al. 2003

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“…6,7 Coronary vasospasm has been suggested to occur as a result of reduced endotheliumdependent vasodilatation and hyperactivity of vascular smooth muscle cells. [8][9][10][11] Kugiyama et al demonstrated a deficiency in the vasodilatory activity of endothelial nitric oxide (NO) in spastic arteries. 12 NO is biosynthesized from L-arginine by a family of NO synthases (NOSs).…”

mentioning

confidence: 99%

Coronary Artery Spasm and the Polymorphisms of the Endothelial Nitric Oxide Synthase Gene

Kaneda

Taguchi

Kuwada

et al. 2006

Circ J

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oronary spasm plays an important role in the pathogenesis of vasospastic angina. It may also contribute to the development of other acute coronary syndromes. [1][2][3][4] Acute myocardial infarction can occur at the site of atherosclerotic plaques that do not narrow the coronary artery lumen. 5 Plaque rupture followed by thrombosis, and vasoconstriction at the site of the plaque, are involved in coronary artery occlusion. 6,7 Coronary vasospasm has been suggested to occur as a result of reduced endotheliumdependent vasodilatation and hyperactivity of vascular smooth muscle cells. [8][9][10][11] Kugiyama et al demonstrated a deficiency in the vasodilatory activity of endothelial nitric oxide (NO) in spastic arteries. 12 NO is biosynthesized from L-arginine by a family of NO synthases (NOSs). [13][14][15] Endothelial NOS (ecNOS), or NOS3, is constitutively expressed in the endothelium and catalyzes the synthesis of NO that regulates vascular tone. Wang et al reported that a polymorphism of intron 4 of the ecNOS gene (27-bp tandem repeats: a allele (4 repeats, rare, NOS4a), b allele (5 repeats, common)) is associated with the smoking-dependent risk for coronary artery disease. 16 The same research group also reported that these genotypes account for over 25% of the basal plasma NO production. 17 Other polymorphisms, Circulation Journal Vol.70, April 2006G894T (Glu298Asp) in exon 7 and T-786C in the 5' flanking region of the ecNOS gene, have been reported to be a risk factor for coronary artery disease, including coronary spasm. [18][19][20][21][22][23] The aim of this study is to assess the relationship between the polymorphisms of ecNOS genes, especially NOS4a, and coronary vascular behavior at spasm provocation tests in detail, by using quantitative coronary angiography (QCA). Methods Study PatientsOf 1,094 Japanese patients who underwent coronary angiography at the Cardiovascular Institute Hospital, Tokyo, Japan, 165 patients were clinically suspected of having angina and did not have fixed stenoses in their coronary arteries. Spasm provocation by serial infusions of acetylcholine (Ach) was performed on these 165 patients according to the method of Yasue et al. 24 In brief, Ach chloride (Daiichi Seiyaku) dissolved in 5 ml of warmed 0.9% saline in incremental doses of 25, 50 and 100 g was injected into the left coronary artery and then 25 and 50 g into the right coronary artery. A coronary arteriogram was obtained when ST segment changes and/or chest pain appeared or 1 min after each injection. When spasm was documented, 0.1 mg nitroglycerin (NTG) was injected into the coronary artery if the attack did not disappear within 2 min. A venous blood sample was obtained from the 165 patients. Blood samples were also obtained from 400 healthy subjects at the time of the health examination at Mitsui Memorial Hospital to determine the population incidence of polymorphisms of the ecNOS gene among Background Coronary artery spasm plays an important role in the pathogenesis of vasospastic angina, and contributes to the devel...

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“…Previous studies have shown that vasodilation caused by BK, substance P and low-dose ACh is preserved in angiographically normal spastic segments of epicardial coronary arteries in patients with CSA. [1][2][3] The 3 doses of BK also caused a similar degree of increase in CBF in the control and CSA groups, suggesting that endothelial function was preserved even in resistance coronary arteries distal to spastic arteries in patients with CSA and no apparent coronary atherosclerosis. On the other hand, the increase in CBF in response to BK in the CSA + CAD group was lower than those in the other 2 groups.…”

Section: Discussionmentioning

confidence: 69%

“…However, previous studies have demonstrated that endotheliumdependent vasodilation responses to bradykinin (BK), substance P, and low-dose ACh are preserved in epicardial spasm coronary arteries in patients with CSA. [1][2][3] These studies suggest that coronary vasospasm induced by ACh is caused primarily by direct hypercontraction of vascular smooth muscle rather than by endothelial dysfunction, but few studies have assessed endothelial function in the coronary macro-and microcirculation in patients with CSA. It is widely accepted that coronary endothelial function is abnormal in patients with coronary atherosclerosis or risk factors for atherosclerosis [4][5][6] and it must be clarified whether or not spasm coronary arteries and atherosclerotic coronary arteries result in abnormal vasomotor responses to ACh through common mechanisms.…”

mentioning

confidence: 99%

Coronary Vasomotor Responses to Bradykinin and Acetylcholine in Patients With Coronary Spastic Angina.

et al. 2001

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Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.

Cited by 95 publications

References 31 publications

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

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

Coronary Artery Spasm and the Polymorphisms of the Endothelial Nitric Oxide Synthase Gene

Coronary Vasomotor Responses to Bradykinin and Acetylcholine in Patients With Coronary Spastic Angina.

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