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At least 127 records · Page 7Linked to original sources
PubMed1989

Enhancement of arterial thrombolysis with native tissue type plasminogen activator by pretreatment with heparin or batroxobin: an angioscopic study.

The enhancement of canine arterial thrombolysis with native tissue type plasminogen activator (nt-PA) obtained from human-derived normal cells by pretreatment with heparin or the defibrinogenating agent, batroxobin, was evaluated with angioscopy. The nt-PA, 0.25 mg/kg, was infused intravenously to lyse 1-hour-old thrombus (eight thrombosed arteries without medication, seven with nt-PA alone, seven with nt-PA and heparin, and seven with nt-PA plus batroxobin). Angioscopy provided a cross-sectional view of the vessel lumen with clear visualization of the thrombus. Thirty minutes after nt-PA infusion, the percent luminal obstruction decreased from 74 to 61 in nt-PA alone (p less than .025), from 77 to 37 in nt-PA plus heparin (p less than .005), and from 79 to 25 in nt-PA plus batroxobin (p less than .005). Fifteen minutes after drug infusion, plasma fibrinogen levels decreased to 89% of preinfusion value in nt-PA alone, to 84% in nt-PA plus heparin, and to less than 5% in nt-PA plus batroxobin. Thus rapid infusion of nt-PA alone provided slight thrombolytic effects. However, heparin and batroxobin showed marked enhancement of thrombolytic effects of nt-PA.

Angiography↗
PubMed1995

Angiographic, ultrasonic, and angioscopic assessment of the coronary artery wall and lumen area configuration after directional atherectomy: the mechanism revisited.

The purpose of the present study was to use the complementary information of angiography, intravascular ultrasound, and intracoronary angioscopy before and after directional atherectomy to characterize the postatherectomy appearance of vessel wall contours and the mechanism of lumen enlargement. Directional coronary atherectomy aims at debulking rather than dilating a coronary artery lesion. The selective removal of the plaque may potentially minimize the vessel wall damage and lead to subsequent better late outcome. Whether plaque removal is the main mechanism of action has only to be assessed indirectly by angiography and warrants further investigation with detailed analysis of luminal changes and vessel wall damage by ultrasound and direct visualization with angioscopy. Twenty-six patients have been investigated by quantitative angiography, intravascular ultrasound, and intracoronary angioscopy (n = 19) before and after atherectomy. In addition, all retrieved specimens were microscopically examined. Ultrasound imaging showed an increase in lumen area from 1.95 +/- 0.70 mm2 to 7.86 +/- 2.16 mm2 at atherectomy. The achieved gain mainly resulted from plaque removal because plaque plus media area decreased from 18.16 +/- 4.47 mm2 to 13.13 +/- 3.10 mm2. Vessel wall stretching (i.e., change in external elastic lamina area) accounted for only 15% of lumen area gain. Luminal gain was higher in noncalcified (6.52 +/- 2.12 mm2) lesions than in lesions containing deeply located calcium (5.19 +/- 0.99 mm2) and lowest in superficially calcified lesions (5.41 +/- 2.41 mm2). Ultrasound imaging identified an atherectomy byte in 85% of the cases, whereas angioscopy revealed such a crevice in 74%. The complementary use of the three techniques revealed an underestimation of the presence of dissection/tear and new thrombus by angiography (10% and 4%) and ultrasound imaging (12% and 0%) compared with angioscopy (26% and 21%). The combined use of angiography, ultrasound, and angioscopy reveals that the postatherectomy luminal lining is not as regular and smooth as that seen by angiography. Luminal enlargement with atherectomy is achieved by plaque excision rather than arterial expansion.

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PubMed1995

Angioscopic identification of coronary thrombus in patients with postinfarction angina.

OBJECTIVES: The purpose of this study was to determine the prevalence of intracoronary thrombus and associated anatomic abnormalities in patients with postinfarction angina using coronary angioscopy and angiography. BACKGROUND: Postinfarction angina, previously studied by angiographic methods only, identifies patients at high risk for sudden death, recurrent angina and refractory angina. The recent development of coronary angioscopy, which permits direct observation of a thrombus or atheroma and is especially used for the detection of intraluminal changes, encourages a reexamination of the pathogenesis of postinfarction angina. METHODS: Fifty-one consecutive patients with a diagnosis of acute myocardial infarction underwent cardiac catheterization. Coronary angiography followed immediately by coronary angioscopy was performed in 17 patients with and 34 without postinfarction angina during the same period of time (10.2 +/- 3.7 or 15.7 +/- 5.5 days [mean +/- SD]) after the onset of acute myocardial infarction. RESULTS: The frequency of thrombus, as observed by angioscopy, was significantly higher in patients with than without postinfarction angina (17 of 17 vs. 5 of 34, respectively, p < 0.01). There were no significant differences between groups with respect to degree of stenosis in the infarct-related artery, number of vessels with significant stenosis, presence of collateral flow, type of therapy and risk factors. CONCLUSIONS: Infarct-related artery thrombus is universally present in postinfarction angina and may be the primary pathogenic factor. Angioscopy is much more sensitive than coronary angiography for the detection of coronary thrombus.

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PubMed1995

Local treatment with antithrombotic drugs can prevent thrombus formation: an angioscopic and angiographic study.

OBJECTIVES: This study was designed to evaluate the efficacy of local versus systemic treatment of thrombosis with various antithrombotic drugs. BACKGROUND: Local use of low dose antithrombotic drugs has been proposed as being effective and safe. METHODS: Heparin (30 U/kg), an antithrombin agent (argatroban, 0.05 mg/kg body weight) or a defibrinogenating drug (batroxobin, 0.05 U/kg) was locally infused into one side of the canine iliac artery after injury by balloon inflation. The other side was injured as a control. The efficacy of systemic delivery of high dose (heparin [300 U/kg] and argatroban [0.5 mg/kg]) and low dose drugs was also assessed. RESULTS: Sixty minutes after local treatment in 22 dogs, no thrombotic stenosis was observed by angiography in locally treated arteries (p < 0.005 vs. mean thrombotic stenosis of 27% in control segments for heparin, 25.3% in control segments for argatroban and 32% in control segments for batroxobin). Angioscopy demonstrated the same trend. In locally treated arteries, thrombus weight was significantly lower in the treated than control side. In the systemic high dose group (n = 10), angiographic thrombotic stenosis was < 5% after high dose drug delivery (p < 0.05 vs. control segments, 37.4% for heparin, 43% for argatroban). In another 10 dogs, low dose systemic delivery was not effective in inhibiting thrombus formation. Activated partial thromboplastin time and fibrinogen levels did not change with local treatment. CONCLUSIONS: Compared with systemic administration of antithrombotic drugs, local treatment is a safer and more effective method of preventing thrombosis.

Angiography↗
PubMed1997

Angioscopic evaluation of angiographically complex coronary lesions.

Coronary angioscopy (CA) provides direct visualization of the endoluminal surface of coronary vessels. The usefulness of CA during coronary angioplasty of angiographically complex lesions remains to be established. This study was designed to determine the value of CA to elucidate the underlying substrate of angiographically complex lesions. Forty-seven consecutive patients with angiographically complex lesions were studied with CA before coronary intervention. Mean age of the group was 59 +/- 9 years; six patients were women. Forty (85%) patients had unstable angina. Complex angiographic lesions included coronary occlusions (n = 23) (14 with Thrombolysis in Myocardial Infarction coronary flow grade 0 and nine with flow grade 1), lesions with intraluminal filling defects suggestive of thrombus or ulceration (n = 8), and lesions that were highly eccentric (n = 16). Items analyzed with CA included red thrombus (lining or protruding) and plaque color (yellow, white, or mixed). In all patients, CA visualized the protruding material causing the angiographic appearance. At this site CA detected red thrombus in 34 (72%) patients (14 protruding, 20 lining) and atherosclerotic plaque in 45 (96%) patients. At the site of the angiographically complex lesion, plaque was classified as predominantly yellow in 24 patients, mixed in 12, and white in nine. The incidence of thrombus on CA was higher for occluded vessels (91%) or lesions with intraluminal filling defects or ulceration (87%) than in eccentric lesions (37%) (p < 0.05). However, plaque coloration was not significantly different among these three angiographic subgroups. Initial procedural success (without stent requirement) was lower in lesions showing protruding thrombus on CA (64% vs 91 %, p < 0.05). Thus most angiographically complex lesions contain thrombus. On CA red thrombus was more frequently identified on occluded vessels and lesions with filling defects or ulceration than in eccentric lesions. Yellow or mixed plaques are common in these patients, suggesting lipid-laden plaques as the underlying pathologic substrate of angiographically complex lesions.

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PubMed1997

Angioscopic assessment of coronary lesions underlying thrombus.

This study examines the characteristics of coronary lesions in which thrombus is found as assessed by angioscopy before percutaneous transluminal coronary angioplasty in patients with various coronary syndromes. Our findings demonstrate that the plaque underlying intracoronary thrombus is usually yellow and/or disrupted, and support in vitro observations that lipid-rich plaques are highly thrombogenic and that disruption of these plaques is associated with in situ thrombosis.

Angioscopy↗
PubMed2001

Extensive development of vulnerable plaques as a pan-coronary process in patients with myocardial infarction: an angioscopic study.

OBJECTIVES: To test our hypothesis that the development of vulnerable plaques is not limited to the culprit lesions, but is a pan-coronary process, we directly observed all three major coronary arteries by angioscopy and evaluated the prevalence of yellow plaques in patients with myocardial infarction (MI). BACKGROUND: Although pathologic studies have suggested that the disruption of atheromatous plaque plays a major role in the development of acute MI, the prevalence of yellow plaques in the whole coronary arteries of patients with MI has not been clarified. METHODS: Thirty-two patients undergoing follow-up catheterization one month after the onset of MI were prospectively and consecutively enrolled in this study. The prevalence of yellow plaques and thrombus in the major coronary arteries was successfully evaluated in 20 patients (58 coronary arteries, 21 culprit lesions) by coronary angioscopy. The diameter stenosis (DS) of the culprit lesions and the maximal diameter stenosis (maxDS) of nonculprit segments were angiographically measured for each coronary artery. RESULTS: The DS of the culprit lesions and maxDS were 27 +/- 17% and 19 +/- 13%, respectively. Yellow plaques and thrombus were detected in 19 (90%) and 17 (81%) of 21 culprit lesions, respectively. Yellow plaques were equally prevalent in the infarct-related and non-infarct-related coronary arteries (3.7 +/- 1.6 vs. 3.4 +/- 1.8 plaques/artery). However, thrombus was only detected in the nonculprit segments of one (2%) coronary artery. CONCLUSIONS: In patients with MI, all three major coronary arteries are widely diseased and have multiple yellow though nondisrupted plaques. Acute MI may represent the pan-coronary process of vulnerable plaque development.

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