Angiographie morphology and the pathogenesis of unstable angina pectoris

Ambrose, John A.; Winters, Stephen L.; Stern, Audrey; Eng, Angie; Teichholz, Louis E.; Gorlin, Richard; Fuster, Valentín

doi:10.1016/s0735-1097(85)80384-3

Cited by 777 publications

(204 citation statements)

References 16 publications

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“…The coronary morphology of our 22 patients with unstable angina is comparable with that described by Ambrose et al 17 The incidence of type II lesions, thought to represent plaque hemorrhage, partially occlusive thrombus, or both, was 36%. Associated intracoronary thrombus was seen in all four of the placebotreated patients with this type of lesion but in none of the four rt-PA-treated patients.…”

Section: Resultssupporting

confidence: 86%

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

Gold¹,

Johns²,

Leinbach³

et al. 1987

Circulation

133

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Twenty-four patients with unstable angina pectoris, defined as chest pain at rest with transient ST segment deviation of at least 1 mm, were randomly assigned to blinded treatment with either placebo or intravenous recombinant human tissue-type plasminogen activator (rt-PA). Before randomization, all patients were treated with oral 13-blockers, calcium antagonists, nitrates, and continuous intravenous heparin for a monitoring period of 12 to 28 hr. After this monitoring period the 24 patients were randomly assigned to receive either placebo or 1.75 mg/kg intravenous rt-PA given over 12 hr at a rate of 0.75 mg/kg over 1 hr, 0.5 mg/kg over 4 hr, and 0.5 mg/kg over 7 hr. One patient, assigned to receive placebo, developed acute myocardial infarction after randomization but before receiving the study drug. Ischemic events were recorded during a hospital follow-up period of at least 4 days unless a further intervention was indicated or the coronary angiogram was normal. The follow-up period was 7 5 days (mean + SD) after the placebo infusion and 8 ± 4 days after the infusion of rt-PA. Unstable angina pectoris persisted after the completion of the infusion in six of 11 patients receiving placebo and only one of 12 patients receiving rt-PA (p < .03). Coronary angiography, performed 38 ± 19 hr after the infusion, demonstrated subocclusive thrombus in eight of 11 patients receiving placebo but in none of 11 patients treated with rt-PA (p < .002). One patient on rt-PA refused coronary angiography. Persistence of unstable angina pectoris correlated significantly with the presence of intracoronary thrombus (p < .003). The infusion of rt-PA caused a decrease of fibrinogen to 66 ± 19% after 1 hr, to 65 ± 21% after 5 hr, and to 64 ± 29% after 12 hr. Oozing at puncture sites was not observed in patients receiving placebo but was seen in eight of 12 patients treated with rt-PA. In three patients on rt-PA, bleeding complications necessitated termination of the infusion within 5, 8, and 11 hr after onset. Thus, in this group of patients with unstable angina pectoris, intravenous infusion of rt-PA appeared to lyse subocclusive intracoronary thrombi. The removal of intracoronary thrombus by rt-PA was associated with reduction of the severity of resting angina. The decision for further intervention could then be made on the basis of residual coronary occlusion.

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Section: Resultssupporting

confidence: 86%

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

Gold¹,

Johns²,

Leinbach³

et al. 1987

Circulation

133

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“…17 OxLDL markers and lipoprotein(a) [Lp(a)] levels were correlated with angiographic lesion characteristics.…”

Section: Patientsmentioning

confidence: 99%

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

et al. 2004

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Background-This study was performed to assess whether oxidized low-density lipoprotein (OxLDL) levels are elevated after percutaneous coronary intervention (PCI). Methods and Results-Patients (nϭ141) with stable angina pectoris undergoing PCI had serial venous blood samples drawn before PCI, after PCI, and at 6 and 24 hours, 3 days, 1 week, and 1, 3, and 6 months. Plasma levels of OxLDL-E06, a measure of oxidized phospholipid (OxPL) content on apolipoprotein B-100 detected by antibody E06, lipoprotein(a) [Lp(a)], autoantibodies to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL), and apolipoprotein B-100 -immune complexes (apoB-IC) were measured. OxLDL-E06 and Lp(a) levels significantly increased immediately after PCI by 36% (PϽ0.0001) and 64% (PϽ0.0001), respectively, and returned to baseline by 6 hours. In vitro immunoprecipitation of Lp(a) from selected plasma samples showed that almost all of the OxPL detected by E06 was bound to Lp(a) at all time points, except in the post-PCI sample, suggesting independent release and subsequent reassociation of OxPL with Lp(a) by 6 hours. Strong correlations were noted between OxLDL-E06 and Lp(a) (rϭ0.68, PϽ0.0001). MDA-LDL and Cu-OxLDL autoantibodies decreased, whereas apoB-IC levels increased after PCI, but both returned to baseline by 6 hours. Subsequently, IgM autoantibodies increased and peaked at 1 month and then returned to baseline, whereas IgG autoantibodies increased steadily over 6 months. Conclusions-PCI results in acute plasma increases of Lp(a) and OxPL and results in short-term and long-term immunologic responses to OxLDL. OxPL that are released or generated during PCI are transferred to Lp(a), suggesting that Lp(a) may contribute acutely to a protective innate immune response. In settings of enhanced oxidative stress and chronically elevated Lp(a) levels, the atherogenicity of Lp(a) may stem from its capacity as a carrier of proinflammatory oxidation byproducts.

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“…Analysis of QCA was conducted using a contour detection minimum cost algorithm (QCA-CMS Version 3.0, MEDIS, Leiden, Netherlands). When there was a coronary stenosis of >50% determined by QCA, the lesion was classified using the Ambrose classification (11,12) as either simple or complex. A stenosis with regular and smooth borders without an intraluminal filling defect was considered as a simple lesion.…”

Section: Quantitative Coronary Angiographymentioning

confidence: 99%

Association of Plasma Omega-3 to Omega-6 Polyunsaturated Fatty Acid Ratio with Complexity of Coronary Artery Lesion

et al. 2012

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Objective Eicosapentaenoic acid (EPA) of the omega-3 polyunsaturated fatty acids (ω-3 PUFA) family plays important roles in the prevention of cardiovascular disease (CVD), while, arachidonic acid (AA) of the ω-6 PUFA family promotes inflammatory and prothrombotic influences. The complexity of coronary lesions represents the vulnerability of patients. The aim of this study was to investigate the association between the plasma EPA/AA ratio and the prevalence of complex coronary lesion morphology. Methods This study consisted of 206 consecutive patients with stable angina pectoris (sAP). Each coronary lesion was determined either as complex or simple based on angiographic findings. To examine the plasma fatty acid level, blood samples were obtained. Patients were divided into three groups according to the obtained plasma EPA/AA ratio: the highest tertile, n=67, the 2nd tertile, n=70, or the lowest tertile, n=69. Results A higher incidence of complex coronary lesion was obtained from patients with a lower plasma EPA/AA ratio [43 (62%) vs. 31 (44%) vs. 25 (37%), p=0.011]. High-sensitivity CRP levels and a low plasma EPA/AA ratio could independently predict the prevalence of complex coronary lesions on multivariate logistic regression analysis [odds ratio 1.83 (95%CI 1.03-3.25), p=0.038 and odds ratio 2.10 (95%CI 1.11-3.94), p=0.02)]. Conclusion In patients with sAP, a low plasma EPA/AA ratio was significantly associated with a high prevalence of complex coronary lesions.

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Angiographie morphology and the pathogenesis of unstable angina pectoris

Cited by 777 publications

References 16 publications

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

A randomized, blinded, placebo-controlled trial of recombinant human tissue-type plasminogen activator in patients with unstable angina pectoris.

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

Association of Plasma Omega-3 to Omega-6 Polyunsaturated Fatty Acid Ratio with Complexity of Coronary Artery Lesion

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