Coronary Angioscopy in Patients with Unstable Angina Pectoris

Sherman, Carl; Litvack, Frank; Grundfest, Warren S.; Lee, Myles; Hickey, Ann; Chaux, Aurelio; Kass, Robert M.; Blanche, Carlos; Matloff, Jack M.; Morgenstern, Leon; Ganz, William; Swan, H.J.C.; Forrester, James S.

doi:10.1056/nejm198610093151501

Cited by 840 publications

(140 citation statements)

References 24 publications

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“…[1][2][3]8,12 Thrombin is a powerful platelet proaggregant incompletely blocked by heparin26 6.2% of those studied later. However, the degree of narrowing was incompletely characterized, and the relation of spasm to the culprit lesion was not specified.…”

Section: Discussionmentioning

confidence: 99%

Vasoreactivity of the culprit lesion in unstable angina.

et al. 1994

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BACKGROUND Although abnormal vasoconstriction may be involved in the pathogenesis of the acute coronary syndromes, the vasoreactivity of the lesion responsible for unstable angina (culprit lesion) has not been directly investigated. It is also unknown if enhanced vasoreactivity is found downstream to this lesion or extends to uninvolved coronary arteries. METHODS AND RESULTS We studied seven unstable angina patients whose condition had sufficiently stabilized to allow ergometric bicycle exercise and a cold pressor test to be performed as provocative stimuli during coronary arteriography. We measured the luminal diameter of the culprit lesion, a normal-appearing distal segment, and the segment of an uninvolved coronary artery using quantitative coronary angiography. Seven stable angina patients served as controls. Antianginal medications were tapered and interrupted. The culprit lesion constricted significantly with exercise and the cold pressor test compared with a stable angina control lesion. The culprit lesion measured 1.41 +/- 0.07 mm at baseline and diminished to 1.09 +/- 0.07 mm with exercise (P = .001). It measured 1.26 +/- 0.07 mm before the cold pressor test and diminished to 1.09 +/- 0.03 mm with this test (P = .015). In contrast, the profile of the stable lesion in the stable angina control group differed significantly (P = .006). Its luminal diameter measured 1.42 +/- 0.17 mm at baseline and 1.48 +/- 0.21 mm with exercise (P = NS). It measured 1.57 +/- 0.18 mm before and 1.55 +/- 0.18 mm with the cold pressor test (P = NS). There were no significant changes to these stimuli in the uninvolved coronary artery segments in unstable angina and in the distal segments in both unstable and stable angina patients. CONCLUSIONS This study demonstrates increased vasoreactivity of the culprit lesion in unstable angina compared with a control lesion in stable angina. The lack of an effect either in the uninvolved coronary artery or downstream to the culprit lesion suggests that systemic neurohumoral or seeding mechanisms are not operative. This abnormal vasoreactivity might predispose to, or be a marker for, the recurrence of acute ischemia at this site.

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Section: Discussionmentioning

confidence: 99%

Vasoreactivity of the culprit lesion in unstable angina.

et al. 1994

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“…Thrombosis on top of an eroded or ruptured atherosclerotic plaque is the most common pathological finding in acute coronary syndromes. [1][2][3][4] In addition, there is accumulating evidence that the hemostatic system plays a part in plaque formation and plaque growth. 5 In the Northwick Park Heart Study, high plasma factor VII coagulant activity was associated with an increased risk of a subsequent fatal coronary event among middle-aged men.…”

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confidence: 99%

Factor VII Gene Polymorphism, Factor VII Levels, and Prevalent Cardiovascular Disease

Feng

Tofler

Larson

et al. 2000

ATVB

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Abstract-Elevated factor VII levels have been associated with increased cardiovascular risk in some studies. The arginine/glutamine (Arg/Gln) polymorphism of the factor VII gene has been previously shown to modify factor VII levels. However, the presence of a gene/environment interaction on factor VII levels or a link with cardiovascular disease (CVD) remains uncertain. We studied subjects from the Framingham Heart Study to determine (1) the extent to which this genetic polymorphism affects factor VII levels; (2) whether interactions exist between this polymorphism and environmental factors on factor VII levels; and (3) the association between the polymorphism and CVD. Genotype data and factor VII antigen levels were available in 1816 subjects. Factor VII levels differed significantly among genotypes in an additive fashion: Gln homozygous, 82.7Ϯ2.5%; heterozygous, 92.2Ϯ0.7%; and Arg homozygous, 100.5Ϯ0.4% (PϽ0.0001). The polymorphism was the strongest, single predictor of factor VII levels, explaining 7.7% of the total variance of factor VII levels, whereas other traditional risk factors combined explained an additional 11.5% of the variance. There was an interaction (Pϭ0.02) between the genotype and total cholesterol on factor VII levels, such that the correlation coefficient and slope (factor VII level/total cholesterol) were greatest in Gln/Gln subjects. Among 3204 subjects characterized for genotype and CVD, there was no significant relationship between the genotype and CVD (Pϭ0.12). In the Framingham Heart Study, the Arg/Gln polymorphism was significantly associated with factor VII antigen levels. The strength of the association suggests that genetic variation plays an important role in determining factor VII levels. However, despite being associated with factor VII levels, the Arg/Gln polymorphism was not associated with prevalent CVD. (Arterioscler Thromb Vasc Biol. 2000;20:593-600.)

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“…[12][13][14] They are also classified into regular (non-disrupted) and complex (disrupted) plaques. 14,15) Our angioscopic and pathologic studies revealed that glistening yellow plaques were the most vulnerable, followed by yellow. Our prospective angioscopic follow-up study also confirmed that glistening yellow plaques were vulnerable.…”

Section: )mentioning

confidence: 85%

Angioscopic Evaluation of Stabilizing Effects of an Antilipemic Agent, Bezafibrate, on Coronary Plaques in Patients with Coronary Artery Disease.

et al. 2002

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SUMMARYTo evaluate the stabilizing effects of an antilipemic agent, bezafibrate, on coronary plaques, we carried out a prospective angioscopic and angiographic open trial. From April 1997 to December 1998, 24 patients underwent coronary angioscopy of plaques in nontargeted vessels during coronary interventions and then again 6 months later. The patients were divided into control (10 patients, 14 plaques) and bezafibrate (14 patients, 21 plaques) groups. Oral administration of bezafibrate (400 mg/day) was started immediately after the intervention and was continued for 6 months. The vulnerability score was determined based on the angioscopic characteristics of plaques and compared before and 6 months later. Six months later, the vulnerability score was reduced (from 1.6 to 0.8; P<0.05) in the bezafibrate group and unchanged (from 1.4 to 1.3; NS) in the control group. In the bezafibrate group, the changes in the vulnerability score were not correlated with those in % stenosis or minimal lumen diameter. The plasma total cholesterol level (T-C) was unchanged, triglyceride level (TG) was decreased, and high density lipoprotein cholesterol level (HDL-C) was increased in the bezafibrate group, but were unchanged in the control group. In the bezafibrate group, T-C and TG were decreased and HDL-C was increased in patients with a reduced vulnerability score but were unchanged in those with an unchanged score. These results indicate that 6 month administration of bezafibrate stabilizes coronary plaques and that the stabilization is not correlated with angiographic changes. (Jpn Heart J 2002; 43: 319-331)

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Coronary Angioscopy in Patients with Unstable Angina Pectoris

Cited by 840 publications

References 24 publications

Vasoreactivity of the culprit lesion in unstable angina.

Vasoreactivity of the culprit lesion in unstable angina.

Factor VII Gene Polymorphism, Factor VII Levels, and Prevalent Cardiovascular Disease

Angioscopic Evaluation of Stabilizing Effects of an Antilipemic Agent, Bezafibrate, on Coronary Plaques in Patients with Coronary Artery Disease.

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