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V Fuster

Publications and source records attributed to V Fuster.

At least 217 records · Page 12Linked to original sources
PubMed1995

T2-weighted contrast for NMR characterization of human atherosclerosis.

We sought to determine whether 1H NMR images without chemical-shift selection can adequately characterize the components of human atheromatous arteries. NMR, as a nondestructive, biochemical imaging tool, has the potential to identify lipids in atherosclerotic plaques but has not yet produced detailed images of atheroma components. Using 1H NMR spectroscopy at 9.4 T, we examined microdissected components of diseased and normal arteries to determine water relaxation constants (T1 and T2) as well as the relative content of mobile lipid. Relaxation times were also measured at 1.5 and 4.7 T. Sections of arteries with atherosclerotic lesions of graded severity were imaged at 1.5 and 9.4 T. The contrast-to-noise ratio (CNR) was used to assess lesion conspicuity. In the atheromatous core, the water NMR signal predominates over that of lipid (lipid-to-water ratio, 0.11). At 9.4 T, T2 is 20.2 ms for the atheromatous core, 30.1 ms for the collagenous cap, and 29.5 ms for normal media. This results in a high CNR on T2-weighted (T2w) images for atheromatous core compared with the collagenous cap and normal media. A similar contrast was measured at lower field strength. Calcifications do not generate appreciable signal due to their low water content but can be detected on T1-weighted (T1w) images. The water T2 contrast allows discrimination of the atheromatous lipid core from collagenous regions. The combination of T1w and T2w sequences permits in vitro identification of the atheromatous core, collagenous cap, calcifications, media, adventitia, and perivascular fat. The discrimination of collagen fibers that overlie lipid deposits permits study of plaque protection and stability at all field strengths and may provide the basis for in vivo microscopy of human atherosclerosis.

Adult↗
PubMed1995

Cell biology of restenosis post-angioplasty.

PTCA is a well established intervention to reduce the severity of atherosclerotic coronary stenosis. In spite of a primary success rate of 90 - 95%, late restenosis occurs in 30 - 50% of patients within 3/6 months of the procedure. Angioplasty in swine induces similar events to those found in humans, thus providing a model for studying strategies for intervention. Blood interaction to the damaged vessel wall occurs with reperfusion after the intervention. Therefore, the in vivo characterization of the interaction of cellular elements (platelets and white cells) and blood proteins with the exposed vascular cells in the vessel wall post-angioplasty may be necessary to identify early triggers of restenosis. Angioplasty was performed simultaneously in the coronary and carotid arteries of swine by fluoroscopy assisted standard techniques. Angiography was performed acutely post-dilatation and residual lumen diameter evaluated. Dilated vessels from 30 min to 6 h postintervention were processed to prepare RNA and preserved to perform immunohistochemistry. Dilatation injury induces maximal expression of c-fos 30 min and c-myc from 2 to 4 h postdilatation. Platelet deposition is initiated immediately post-dilatation as well as infiltration of fluid phase proteins on the damaged areas.

Angioplasty, Balloon, Coronary↗
PubMed1994

Acute biological response to laser balloon angioplasty in the atherosclerotic rabbit.

Laser balloon angioplasty with Nd:YAG energy has been proposed as a method to seal intimal dissection and prevent elastic recoil after balloon angioplasty. To better define the vessel response to laser balloon angioplasty, its effects on luminal diameter, Indium-111 labelled platelet deposition, and histology were studied in 10 atherosclerotic rabbits. Balloon angioplasty was performed in both iliac arteries and was followed by laser balloon angioplasty in only one iliac artery. The nonlased artery served as a control. Single (15-35 W for 20 sec) or repetitive laser pulses (12-25 W for 20 sec x 3) were used. Platelet deposition was quantified 2 hr after the intervention. Lumen diameter (mm) increased following balloon angioplasty from 0.99 +/- 0.47 (mean +/- SD) to 1.92 +/- 0.43 and 0.89 +/- 0.46 to 1.99 +/- 0.57 in the balloon and laser-treated arteries, respectively (P < 0.001 for both groups for comparisons to baseline, P = NS for between groups comparison). Laser balloon angioplasty resulted in a further increase in luminal diameter to 2.42 +/- 0.53 (P < 0.02) when compared to the post balloon angioplasty diameter. Platelet deposition (10(6)/cm vessel) was higher following laser balloon angioplasty (26.9, 10.2-189; median range) than after balloon angioplasty (10.6, 3.4-30), P < 0.001. Histologic evidence of laser "sealing" was present in only one artery. Thus although laser balloon angioplasty results in an improved lumen diameter, it is accompanied by increased platelet deposition. In the atherosclerotic rabbit model, abolition of vascular recoil rather than "sealing" seems to be the most important advantage of laser balloon angioplasty over conventional balloon angioplasty.

Angiography↗
PubMed1994

Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture.

OBJECTIVES: The purpose of this study was to determine whether different components of human atherosclerotic plaques exposed to flowing blood resulted in different degrees of thrombus formation. BACKGROUND: It is likely that the nature of the substrate exposed after spontaneous or angioplasty-induced plaque rupture is one factor determining whether an unstable plaque proceeds rapidly to an occlusive thrombus or persists as a nonocclusive mural thrombus. Although observational data show that plaque rupture is a potent stimulus for thrombosis, and exposed collagen is suggested to have a predominant role in thrombosis, the relative thrombogenicity of different components of human atherosclerotic plaques is not well established. METHODS: We investigated thrombus formation on foam cell-rich matrix (obtained from fatty streaks), collagen-rich matrix (from sclerotic plaques), collagen-poor matrix without cholesterol crystals (from fibrolipid plaques), atheromatous core with abundant cholesterol crystals (from atheromatous plaques) and segments of normal intima derived from human aortas at necropsy. Specimens were mounted in a tubular chamber placed within an ex vivo extracorporeal perfusion system and exposed to heparinized porcine blood (mean [+/- SEM] activated partial thromboplastin time ratio 1.5 +/- 0.04) for 5 min under high shear rate conditions (1,690 s-1). Thrombus was quantitated by measurement of indium-labeled platelets and morphometric analysis. Under similar conditions, substrates were perfused with heparinized human blood (2 IU/ml) in an in vitro system, and thrombus formation was similarly evaluated. RESULTS: Thrombus formation on atheromatous core was up to sixfold greater than that on other substrates, including collagen-rich matrix (p = 0.0001) in both heterologous and homologous systems. Although the atheromatous core had a more irregular exposed surface and thrombus formation tended to increase with increasing roughness, the atheromatous core remained the most thrombogenic substrate when the substrates were normalized by the degree of irregularity as defined by the roughness index (p = 0.002). CONCLUSIONS: The atheromatous core is the most thrombogenic component of human atherosclerotic plaques. Therefore, plaques with a large atheromatous core content are at high risk of leading to acute coronary syndromes after spontaneous or mechanically induced rupture because of the increased thrombogenicity of their content.

Animals↗
PubMed1994

Synergistic action of severe wall injury and shear forces on thrombus formation in arterial stenosis: definition of a thrombotic shear rate threshold.

OBJECTIVES: This study attempted to determine the influence of progressive degrees of stenosis on platelet deposition onto a severely damaged vessel wall. BACKGROUND: The severity of wall injury and increased shear forces have been proposed as the determinants of thrombus formation and growth in arterial stenosis. METHODS: Carotid angioplasty was performed in 15 mongrel dogs to produce severe wall damage. Group I (n = 9) had arteries with damage only. In group II (n = 14), progressive degrees of stenosis were produced at the center of the dilated area. Acute thrombus formation was evaluated by angiography at the time of angioplasty and platelet deposition/cm2 quantified by indium-111 labeling 1 h after the procedure. RESULTS: Severe wall damage (group I) produced a significant increase in platelet deposition compared with control arterial segments (8.19 +/- 3.82 vs. 3.62 +/- 2.52 platelets x 10(6)/cm2 [mean +/- SD], p < 0.05), and the presence of a stenosis (group II) further increased platelet deposition (36.98 +/- 3.82 platelets x 10(6)/cm2, p < 0.05). Angiographic filling defects or total occlusion was found in seven of the arteries in group II but in none in group I (p < 0.05). A shear rate of approximately 5,000 s-1, corresponding to a critical stenosis of 70% and a 1.5- to 1.6-mm diameter, was found to identify the arteries in which thrombosis was likely to occur (p < 0.05). Four of 5 arteries < 1.5 to 1.6 mm in diameter had angiographic filling defects or occlusion compared with 1 of 13 with less severe stenosis (p < 0.01). CONCLUSIONS: In low shear rate conditions, deep arterial injury will lead to mural thrombosis without further thrombus growth. When deep arterial injury occurs under critical local shear conditions, platelet deposition will be enhanced, and thrombosis may progress to total occlusion.

Angioplasty, Balloon↗
PubMed1994

Prospective evaluation of a prostacyclin-sparing aspirin formulation and heparin/warfarin in aspirin users with unstable angina or non-Q wave myocardial infarction at rest. The Antithrombotic Therapy in Acute Coronary Syndromes Research Group.

The aim of this trial was to compare the efficacy of combination antithrombotic therapy with a prostacyclin-sparing aspirin plus anticoagulation versus conventional aspirin plus anticoagulation, when added to antianginal therapy, in patients with unstable angina or non-Q wave myocardial infarction already being treated with aspirin. In a double-blind (for the aspirin) study, 144 prior aspirin users were randomized; 72 patients received controlled-release, prostacyclin-sparing aspirin 75 mg daily plus anticoagulation (intravenous heparin followed by warfarin to maintain the international normalized ratio at 2-3), and 72 patients received conventional aspirin 75 mg daily plus the same anticoagulation. Controlled-release aspirin was formulated to preserve endothelial cell prostacyclin synthesis. Trial therapy was begun by 13.2 +/- 12.3 h of qualifying pain, and continued for 12 weeks. The frequency of recurrent angina with electrocardiographic changes, myocardial infarction, or death, was analysed by intention to treat. At 12 weeks, events were: [table: see text] Twenty-six of the 42 (62%) recurrent ischaemic events occurred within 7 days of presentation. Four of the 144 patients (3%) experienced a major bleeding complication. It is concluded that in spite of maximal antithrombotic therapy, there is a significant failure rate of medical therapy in aspirin users presenting with unstable angina or non-Q wave myocardial infarction while at rest. Prostacyclin-sparing aspirin offers no clinical benefit over conventional aspirin.

Adult↗
PubMed1994

Antithrombotic therapy in coronary artery disease.

Antithrombotic therapy has assumed a central role in the therapy of the acute coronary syndromes and chronic coronary artery disease. The theoretical rationale for antithrombotic therapy, and the established and evolving roles of antiplatelet agents and anticoagulants in coronary disease are reviewed. Emphasis is focused on new antithrombotic agents and novel combinations of existing agents.

Angioplasty↗
PubMed1994

Aortic dissection: a medical perspective.

Over the past 3 years, a greater understanding of predisposing factors and the pathology of the aortic wall has yielded more insights into the pathogenesis, as well as into more accurate diagnostic and preventive methods. This update will discuss: (1) the incidence, definition, and recent classification of aortic dissection; (2) epidemiology, medical, and recent surgical series; (3) the pathogenesis and risk factors; (4) clinical features and evolving noninvasive imaging approaches to diagnosis; and (5) management from a medical perspective.

Aortic Dissection↗
PubMed1994

13C-NMR spectroscopy of human atherosclerotic lesions. Relation between fatty acid saturation, cholesteryl ester content, and luminal obstruction.

Previous investigations have used 13C-nuclear magnetic resonance (NMR) spectroscopy to demonstrate the similarities between lipoproteins and the mobile lipids of atheroma. In this study, we tested the hypothesis that 13C-NMR changes are related to indices of histological severity. We classified 20 human arteries according to their obstruction ratio (OR), defined as the ratio of the plaque area to the area delimited by the external elastic lamina. In group A, OR was < 40%, and in group B, OR was > 40%. We analyzed at 9.4 T the resonances of unsaturated (UFA) and polyunsaturated (PUFA) carbons, the resonances of the carbons 19 and 21 (C19, C21) of cholesteryl esters (CE), the methine carbon peak of fatty acids (CH2)n, the choline peak from phospholipids (PL), and the glycerol peak from triglyceride (TG). The UFA/PUFA, UFA/(CH2)n, and PUFA/(CH2)n ratios are markers of fatty acid saturation. (C19, C21)/(CH2)n, choline/(CH2)n, and glycerol/(CH2)n are indices of CE, PL, and TG content, respectively. UFA/PUFA in group A is 1.15 +/- 0.34 versus 1.63 +/- 0.32 in group B (P = .005). PUFA/(CH2)n is 0.26 +/- 0.10 in group A versus 0.16 +/- 0.04 in group B (P = .049). C19, C21/(CH2)n in group A is 0.32 +/- 0.15 versus 0.63 +/- 0.23 for group B (P = .003). No significant difference was found in UFA/(CH2)n or in the TG or PL ratios. 13C spectral examination of human atherosclerosis demonstrates decreased resonances for polyunsaturated fatty acyl chains and cholesteryl esters with increasing obstruction.

Adult↗