Automated quantitative coronary arteriography: morphologic and physiologic validation in vivo of a rapid digital angiographic method.

Mancini, G.B.John; Simon, Sandra B.; McGillem, Mark J.; LeFree, Michael T.; Friedman, H. Z.; Vogel, Robert A.

doi:10.1161/01.cir.75.2.452

Cited by 355 publications

(89 citation statements)

References 28 publications

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“…16 Similarly, analysis of interobserver variability for stenosis diameter in the human coronary artery showed high reproducibility (r= 0.97, SEE = 0.19 mm). 17 Briefly, the end-diastolic frames of the cineangiograms were projected on a Vanguard viewer that is optically coupled to a video camera.…”

Section: Quantitative Coronary Angiographymentioning

confidence: 86%

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Evidence of endothelial dysfunction in angiographically normal coronary arteries of patients with coronary artery disease.

et al. 1989

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Acetylcholine causes endothelium-dependent dilation of normal arteries in most animal species. The effect of acetylcholine on normal human coronary arteries is controversial. Pathologic studies and epicardial echocardiography have shown that diffuse atherosclerosis is often present despite angiographic evidence of discrete coronary artery disease (CAD). Therefore, we postulated that acetylcholine would cause vasoconstriction of coronary arteries that are angiographically normal in patients with CAD. Coronary artery diameter, measured by automated quantification of digitized cineangiograms, was determined before and after the intracoronary infusion of 0.2 mM acetylcholine at 0.8-1.6 ml/min. The diameter of stenotic or irregular segments of six atherosclerotic coronary arteries decreased from 1.80±0.42 mm before acetylcholine to 1.26±0.46 mm after acetylcholine (p=0.0025). Acetylcholine had a significantly diYferent effect on the diameter of two groups of coronary arteries that are angiographically normal. Acetylcholine caused a 0.16±0.09-mm increase in the diameter of 14 normal coronary arteries in patients without CAD, whereas it caused a 0.26+0.12-mm decrease in the diameter of 14 normal coronary arteries in patients with CAD (p <0.01). Thus, the normal response to intracoronary acetylcholine is vasodilation, suggesting that endotheliumderived relaxing factor is released from normal human coronary endothelium. The vasoconstrictive effect of acetylcholine in the angiographically normal coronary arteries of patients with CAD suggests the presence of a diffuse abnormality of endothelial function. (Circulation 1989;79:287-291) T here is growing evidence that acetylcholine and a number of other substances induce vasodilation by stimulating the release of an endothelium-derived relaxing factor (EDRF) from endothelial cells, whereas nitroglycerin and other endothelium-independent vasodilators induce vasodilation through the direct stimulation ofvascular smooth muscle."2,3 Thus, acetylcholine or aggregating platelets cause relaxation of arteries with an intact endothelium but cause contraction of arteries denuded of endothelium.1"2'3 An impairment of endotheliumdependent vasodilation has been observed in rabbits4 and monkeys5'6 that were fed an atherogenic diet. atherosclerosis and restored endothelium-dependent relaxation to normal.6 Conflicting data exist, however, regarding the existence of endothelium-mediated vasodilation in human coronary arteries. Several in vitro studies conclude that acetylcholine and carbachol, both muscarinic agonists, constrict human coronary arteries,7-10 whereas other studies suggest that acetylcholine dilates normal human coronary arteries.1" Similarly, a discrepancy exists regarding the effect of acetylcholine on human coronary arteries in vivo. After the intracoronary infusion of acetylcholine, Horio et al12 observed at least a 25% decrease in the diameter of normal or almost normal coronary arteries in 27 of 70 arteries, whereas Ludmer et al13 reported an 11% increase in the diame...

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Section: Quantitative Coronary Angiographymentioning

confidence: 86%

“…Several in vitro studies conclude that acetylcholine and carbachol, both muscarinic agonists, constrict human coronary arteries,7-10 whereas other studies suggest that acetylcholine dilates normal human coronary arteries. 16 patients with CAD. The group consisted of 10 men and six women ranging in age from 36 to 77 years.…”

mentioning

confidence: 99%

Evidence of endothelial dysfunction in angiographically normal coronary arteries of patients with coronary artery disease.

et al. 1989

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“…The Pharmacogenomics Journal diac catheterization, interpretable quantitative coronary angiography (QCA) measurements at baseline (prior to undergoing PTCA), immediately post-PTCA (demonstrating the initial effect of the procedure) and at follow-up cardiac catheterization 6 months later, 12,13 and the availability of a blood sample for genotype determination. Restenosis was defined as Ͼ50% reduction in the luminal diameter at the site of previous PTCA, as compared with the immediate post-PTCA angiographic record; 342 patients were classified as cases.…”

Section: Methodsmentioning

confidence: 99%

Multi-locus interactions predict risk for post-PTCA restenosis: an approach to the genetic analysis of common complex disease

et al. 2002

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The complexity of recognizing the potential contribution of a number of possible predictors of complex disorders is increasingly challenging with the application of large-scale single nucleotide polymorphism (SNP) typing. In the search for putative genetic factors predisposing to coronary artery restenosis following balloon angioplasty, we determined genotypes for 94 SNPs representing 62 candidate genes, in a prospectively assembled cohort of 342 cases and 437 controls. Using a customized coupled-logistic regression procedure accounting for both additive and interactive effects, we identified seven SNPs in seven genes that, together, showed a statistically significant association with restenosis incidence (P Ͻ0.0001), accounting for 11.6% of overall variance observed. Among them are candidate genes for cardiovascular pathophysiology (apolipoprotein-species and NOS), inflammatory response (TNF receptor and CD14), and cell-cycle control (p53 and p53-associated protein). Our results emphasize the need to account for complex multi-gene influences and interactions when assessing the molecular pathology of multifactorial medical entities.

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“…Quantitative analysis was performed using a computerized analysis system (Image Comm, Santa Clara, CA, USA) that has previously been validated. 72 …”

Section: Quantitative Angiographymentioning

confidence: 99%

Effect of percutaneous adenovirus-mediated Gax gene delivery to the arterial wall in double-injured atheromatous stented rabbit iliac arteries

et al. 2000

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Though the efficacy of intravascular gene transfer has been demonstrated in native vessels following acute injury, this methodology has not been validated in complex models of vascular injury that more closely mimic clinical angioplasty procedures. Previous studies have shown that Gax gene overexpression modulates the injury-induced remodeling of the vessel in rat carotid and normal rabbit iliac arteries. Here, we evaluated the effect of the Gax gene delivery in atheromatous stented vessels. Rabbits were fed 120 g daily of 1% cholesterol diet for 3 weeks. At 1 week they underwent initial injury on the external iliac artery, then balloon angioplasty was performed at 3 weeks at the same site with a 2.5 mm diameter channel balloon catheter (three times 1 min at 6 atm). Either saline (n = 4) or the control viral construct Ad-CMVluc (5 × 10 9 p.f.u.) (n = 5) or Ad-CMVGax (5 × 10 9 p.f.u.) (n = 4) was delivered with a poloxamer mixture via a channel balloon (6 atm, 30 min), and a 15 mm long

show abstract

Automated quantitative coronary arteriography: morphologic and physiologic validation in vivo of a rapid digital angiographic method.

Cited by 355 publications

References 28 publications

Evidence of endothelial dysfunction in angiographically normal coronary arteries of patients with coronary artery disease.

Evidence of endothelial dysfunction in angiographically normal coronary arteries of patients with coronary artery disease.

Multi-locus interactions predict risk for post-PTCA restenosis: an approach to the genetic analysis of common complex disease

Effect of percutaneous adenovirus-mediated Gax gene delivery to the arterial wall in double-injured atheromatous stented rabbit iliac arteries

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