Quantification of relative coronary arterial stenosis by cinevideodensitometric analysis of coronary arteriograms.

Nichols, Allen B.; Gabrieli, Christopher; Fenoglio, John J.; Esser, Peter D.

doi:10.1161/01.cir.69.3.512

Cited by 167 publications

(43 citation statements)

References 17 publications

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“…The luminal diameter was determined quantitatively by a cinevideodensitometric analysis system (Coronary Analyzer, model XR-70; Vanguard Corp., Melville, NY) (27). An end-diastolic frame ofa highquality single-plane angiogram was selected and was acquired into the analyzer.…”

Section: Methodsmentioning

confidence: 99%

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

Egashira¹,

Inou²,

Yamada³

et al. 1992

J. Clin. Invest.

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Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 ,gg/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 ,ug/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction. (J. Clin.

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Section: Methodsmentioning

confidence: 99%

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

Egashira¹,

Inou²,

Yamada³

et al. 1992

J. Clin. Invest.

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“…By using a computerassisted analysis system (Cardio 500, Kontron Elektronik, Eching, Germany), quantitative luminal diameter measurements of the coronary artery were made by an observer who was blinded to the study subjects. 8,25 The luminal diameter was measured at the middle segments between the side branches (anatomical landmarks) of the left anterior descending, left circumflex, and right coronary arteries. Both the mean diameter and the narrowest diameter of the 3 middle segments were determined before (control) and when ST segment changes and/or chest pain appeared or 1 min after Ach injection, and then after isosorbide dinitrate (ISDN) injection as shown in Fig 1. Special care was taken to measure the same coronary segment under each condition using anatomic references.…”

Section: Qcamentioning

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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“…2 1 In addition, pulsatile pressure may contribute to the periodicity of arterial measurements. In canine normal coronary arteries, a 5% variation in diameter of a 3-4 mm epicardial segment has been noted angiographically.20 Substantial tlow-dependent coronary dilatation has been recently shown in humans as even though this response is impaired in the presence of athero~clerosis.~~ In a recent report,Iy proximal left anterior descending (LAD) diameters, exposed to increased flow, were increased by 6.5% in normal arteries and by 4.6% in coronary artery disease, as measured by a previously validated border-detection method. In another flow-mediated dilation was observed in angiographically normal LAD segments but was markedly impaired in atherosclerotic vessels, probably due to impaired endothelial vasodilator function.…”

Section: Limitations Caused By Biologic Variationsmentioning

confidence: 98%

Limitations of coronary angiography: An underestimated problem?

Katritsis

Webb-Peploe

1991

Clinical Cardiology

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Summary: Angiographic imaging suffers from many limitations which may distort the diagnostic information obtained from coronary arteriograms. Radiographic features limiting precise coronary stenosis measurement are caused by the x-ray source, the image intensifier, and the chemical properties of the cinefilm. Biologic variations are introduced by fluctuations in angiographic contrast concentration and flow-or contrast-dependent coronary dilation. Random errors are also introduced by the selection of the radiographic projection and frame to be analyzed and the digitization of cineangiograms. These limitations and their significance in distorting quantitative information obtained from coronary angiograms are discussed in this review.

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Quantification of relative coronary arterial stenosis by cinevideodensitometric analysis of coronary arteriograms.

Cited by 167 publications

References 17 publications

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

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

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

Limitations of coronary angiography: An underestimated problem?

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