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Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 163 records · Page 9Linked to original sources
PubMed1997

Management of stable coronary artery disease.

Options for the treatment of multivessel coronary artery disease include medical therapy and revascularization with either coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA). CABG has been shown to prolong survival in patients with left main coronary disease or when at least two of the following factors are present: extensive coronary artery disease, significant ischemia as shown on stress testing and left ventricular dysfunction. In patients with extensive coronary artery disease but normal left ventricular function, either PTCA or CABG may be used initially without adversely affecting rates of survival. However, patients undergoing angioplasty have a higher rate of repeat revascularization procedures than those treated with bypass. The complex interplay of the various risks and benefits of medical therapy, angioplasty or bypass in the treatment of coronary artery disease requires an individualized approach to therapy and careful patient education.

Angioplasty, Balloon, Coronary↗
PubMed1997

Atherosclerosis: imaging techniques and the evolving role of nuclear medicine.

UNLABELLED: Quantitative assessment of atherosclerotic or atherothrombotic disease during its natural history and following therapeutic interventions is important for understanding the progression and stabilization of the disease and for selecting appropriate medical or surgical interventions. A number of invasive and noninvasive imaging techniques are available to detect and display different characteristics of vascular lesions of clinical and/or research interest. METHODS: Angiography, the traditional "gold standard," detects advanced lesions and measures the degree of stenosis. Angioscopy clearly identifies thrombus. In carotid arteries and arteries in lower extremities, duplex ultrasonography is useful for providing the degree of stenosis, as well as plaque morphology, and assessing changes in wall thickness. RESULTS: Magnetic resonance angiography, being noninvasive, may replace conventional angiography for anatomical imaging of the vasculature. Ultrafast electron beam CT measures the calcium content in the atherosclerotic lesions. Intravascular ultrasound is the only technique that appears to be clinically useful in imaging the unstable, vulnerable plaques in coronary arteries. Magnetic resonance imaging techniques may be able to image vulnerable plaques and characterize plaques in terms of lipid and fibrous content and identify the presence of thrombus associated with the plaques. In regard to the nuclear scientigraphic imaging techniques, radiolabeled lipoproteins, platelets and immunoglobulins have shown some clinical potential as imaging agents, but due to poor target-to-background and target-to-blood ratios these agents are not ideal for imaging coronary or even carotid lesions. Technetium-99m-labeled peptides and monoclonal antibody fragments that clear from circulation rapidly and bind specifically to different components of the atherosclerotic lesion showed significant potential in animal models and in limited clinical studies. FRE Peptides capable of binding to GPIIb/IIIA receptors on activated platelets appear to offer significant diagnostic potential for imaging intra-arterial thrombus. Positron emission tomography with metabolic tracers like [18F]-fluorodeoxyglucose (FDG) also appears to offer new opportunities for noninvasive imaging of atherosclerosis and atherothrombosis.

Arteriosclerosis↗
PubMed1997

Red-green colour blindness in the Tormes-Alberche Valley (Avila-Central Spain).

A population from a Central Spanish region (Tormes-Alberche Valley) has been investigated for the presence of red-green colour vision defects. A sample of 998 subjects (469 male and 529 female) was analyzed. To identify colour vision defects, Ishihara test plates were used. The red-green colour blindness percentage obtained was 4.69 +/- 0.976% for males (2.13% protan and 2.56% deutan types) and none of the females tested were found to be colour blind. These results are within the variation range of Mediterranean populations and lower than the usual frequencies among non-Mediterranean European samples.

Color Vision Defects↗
PubMed1997

Present concepts of coronary atherosclerosis-thrombosis, therapeutic implications and perspectives.

Our knowledge of the pathophysiology of coronary atherosclerosis has remarkably changed in the last few years. The types of atherosclerotic lesions, the mechanisms of progression of coronary atherosclerosis with plaque instability and disruption, and the subsequent thrombotic phenomenon leading to acute coronary syndromes are now better understood. Therapeutic strategies leading to atherosclerotic lesion stabilization and even regression, as well as new antithrombotic strategies to alleviate or prevent the thrombotic complications are being pursued. This review focuses on the coronary unstable atherosclerotic plaque and complicating thrombosis.

Acute Disease↗
PubMed1996

Macrophages, smooth muscle cells, and tissue factor in unstable angina. Implications for cell-mediated thrombogenicity in acute coronary syndromes.

BACKGROUND: Macrophage expression of tissue factor may be responsible for coronary thrombogenicity in patients with plaque rupture. In patients without plaque rupture, smooth muscle cells may be the thrombogenic substrate. This study was designed to identify the cellular correlations of tissue factor in patients with unstable angina. METHODS AND RESULTS: Tissue from 50 coronary specimens (1560 pieces) from patients with unstable angina and 15 specimens from patients with stable angina were analyzed. Total and segmental areas (in square millimeters) were identified with trichrome staining. Macrophages, smooth muscle cells, and tissue factor were identified by immunostaining. Tissue factor content was larger in unstable angina (42 +/- 3%) than in stable angina (18 +/- 4%) (P = .0001). Macrophage content was also larger in unstable angina (16 +/- 2%) than in stable angina (5 +/- 2%) (P = .002). The percentage of tissue factor located in cellular areas was larger in coronary samples from patients with unstable angina (67 +/- 8%) than in samples from patients with stable angina (40 +/- 5%) (P = .00007). Multiple linear stepwise regression analysis showed that coronary tissue factor content correlated significantly (r = .83, P < .0001) with macrophage and smooth muscle cell areas only in tissue from patients with unstable angina, with a strong relationship between tissue factor content and macrophages in the atheromatous gruel (r = .98, P < .0001). CONCLUSIONS: Tissue factor content is increased in unstable angina and correlates with areas of macrophages and smooth muscle cells, suggesting a cell-mediated thrombogenicity in patients with acute coronary syndromes.

Adult↗
PubMed1996

Macrophage infiltration predicts restenosis after coronary intervention in patients with unstable angina.

BACKGROUND: Restenosis remains the major limitation of percutaneous coronary revascularization. Macrophages release cytokines, metalloproteinases, and growth factors that may induce smooth muscle cell migration and proliferation. We tested the hypothesis that primary lesions that develop restenosis after coronary atherectomy have more macrophages and smooth muscle cells than primary lesions that do not develop restenosis. METHODS AND RESULTS: Fifty patients with unstable angina were identified. Total and segmental areas were quantified on trichrome-stained sections of coronary atherectomy tissue. Macrophages and smooth muscle cells were identified by immunohistochemical staining. Restenosis, defined as > 50% stenosis diameter by quantitative cineangiography, was present in 30 patients. The other 20 patients (< 50% stenosis) constitute the "no restenosis" group. The percentages of smooth muscle cell areas were similar in specimens from patients with and without restenosis (57 +/- 5% and 52 +/- 6%) (P = NS). However, macrophage-rich areas were larger in plaque tissue from patients with restenosis (20.4 +/- 2%) than in tissue from patients without restenosis (9.3 +/- 2%) (P = .0007). Multiple stepwise logistic regression analysis identified macrophages as the only independent predictor for restenosis (P = .006). CONCLUSIONS: Macrophages are increased in coronary atherectomy tissue from primary lesions that develop restenosis, suggesting a possible role for macrophages in the restenotic process after percutaneous coronary intervention.

Adult↗
PubMed1996

Distinct effects of recombinant desulfatohirudin (Revasc) and heparin on plasma levels of fibrinopeptide A and prothrombin fragment F1.2 in unstable angina. A multicenter trial.

BACKGROUND: Thrombin plays an important role in the pathogenesis of acute coronary thrombosis. We studied the effects of a direct thrombin inhibitor, recombinant desulfatohirudin, and heparin on plasma levels (at 0, 4, 12, and 24 hours) of fibrinopeptide A (FPA), which reflects thrombin action, and prothrombin fragment F1.2, which reflects thrombin generation, in patients with unstable angina. METHODS AND RESULTS: Patients were randomized to one of two doses of heparin (n = 50) (target activated partial thromboplastin time, 65 to 90 seconds or 90 to 110 seconds) or one of four doses of r-hirudin (n = 113) (0.05, 0.10, 0.20, or 0.30 mg.kg-1.h-1 by infusion). r-Hirudin induced a dose-dependent decline in plasma FPA. At 24 hours, FPA levels with 0.1- to 0.3-mg.kg-1.h-1 r-hirudin regimens were significantly lower than with 0.05 mg.kg-1.h-1 r-hirudin; levels with 0.1- to 0.2-mg.kg-1.h-1 r-hirudin regimens were lower than with both heparin regimens. Plasma F1.2 did not decline significantly during therapy with heparin or hirudin except at 0.3 mg.kg-1.h-1 hirudin. At 24 hours, they were higher with the 0.05-mg.kg-1.h-1 r-hirudin regimen than with other regimens. For comparable levels of thrombin generation (F1.2 levels), FPA levels were higher in heparin patients than in hirudin patients. For the same FPA values, the corresponding F1.2 values were higher in the hirudin group. CONCLUSIONS: Our findings provide evidence for distinct in vivo effects of the two agents and suggest that r-hirudin is a relatively more potent inhibitor of thrombin action but a less effective inhibitor of thrombin generation than heparin. The lower FPA levels in hirudin patients may reflect its ability to inactivate clot-bound thrombin. The relative clinical efficacies of the two agents need to be defined by clinical trials in progress.

Angina, Unstable↗
PubMed1996

Magnetic resonance images lipid, fibrous, calcified, hemorrhagic, and thrombotic components of human atherosclerosis in vivo.

BACKGROUND: Although MRI can discriminate the lipid core from the collagenous cap of atherosclerotic lesions in vitro with T2 contrast, it has not yet produced detailed in vivo images of these human plaque components. METHODS AND RESULTS: We imaged seven lesions from six patients who required surgical carotid endarterectomy and calculated T2 in vivo before surgery in various plaque regions. Using the same acquisition parameters, we repeated these measurements in vitro on the resected fragment and compared MR images with histology. T2 values calculated in vivo correlate with in vitro measurements for each plaque component; the in vitro discrimination we demonstrated previously with T2 contrast can therefore be performed similarly in vivo. CONCLUSIONS: MRI is the first noninvasive imaging technique that allows the discrimination of lipid cores, fibrous caps, calcifications, normal media, and adventitia in human atheromatous plaques in vivo. This technique also characterizes intraplaque hemorrhage and acute thrombosis. This result may support further investigations that include MRI of plaque progression, stabilization, and rupture in human atherosclerosis.

Aged↗
PubMed1996

Does antithrombotic therapy influence residual thrombus after thrombolysis of platelet-rich thrombus? Effects of recombinant hirudin, heparin, or aspirin.

BACKGROUND: Thrombolysis to normal flow in patients with acute myocardial infarction preserves left ventricular function and decreases mortality. Failure of early reperfusion, reocclusion, or residual thrombus may be due to concurrent activation of the platelet-coagulation system. Thus, we hypothesized that the best concomitant antithrombotic therapy (recombinant [r]-hirudin, heparin, or aspirin) will maximally accelerate thrombolysis by r-tissue-type plasminogen activator (rTPA) and reduce residual thrombus. METHODS AND RESULTS: Occlusive thrombi were formed in the carotid arteries of 29 pigs (by balloon dilatation followed by endarterectomy at the site of injury-induced vasospasm) and matured for 30 minutes before rTPA was started, with or without antithrombotic therapy. Thrombolysis was assessed with the use of angiography and measurement of residual thrombus. Pigs were allocated to one of five treatments: placebo, rTPA, rTPA plus r-hirudin, rTPA plus heparin, or rTPA plus intravenous aspirin. No placebo-treated pig reperfused. Two of six animals treated with rTPA alone reperfused compared with seven of seven animals treated with rTPA plus r-hirudin (reperfusion time, 33 +/- 10 minutes), six of seven animals treated with rTPA plus heparin (reperfusion time, 110 +/- 31 minutes), and two of six animals with rTPA plus aspirin. The activated partial thromboplastin time was prolonged in only the rTPA plus r-hirudin group (25 +/- 0.1 times baseline) and the rTPA plus heparin group (5.3 +/- 0.2 times baseline). Residual 111In-platelet and 125I-fibrin(ogen) depositions were lower in the heparin-treated group and lowest in the r-hirudin-treated group (heparin versus hirudin, respectively; incidence of residual macroscopic thrombus was six of six animals versus two of seven [P = .01]; 125I-fibrin(ogen), 170 +/- 76 versus 48 +/- 6 x 10(6) molecules/cm2 [P = .02]; 111In-platelets, 47 +/- 15 versus 13 +/- 2 x 10(6)/cm2, P = .10). No pigs developed spontaneous bleeding. CONCLUSIONS: Thrombin inhibition with heparin or r-hirudin significantly accelerated thrombolysis of occlusive platelet-rich thrombosis, but only the best antithrombotic therapy (r-hirudin) eliminated or nearly eliminated residual thrombus.

Animals↗
PubMed1996

Management of restenosis after coronary intervention.

Coronary restenosis has proven to be the "Achilles heel" of percutaneous coronary interventions, frequently leading to repeated procedures. The pathogenesis of restenosis can be divided into four phases: early elasic recoil (hours to days), mural thrombus formation (hours to days), neointimal proliferation and extracellular matrix formation (weeks), and chronic geometric arterial changes (months). Restenosis is device nonspecific except for intravascular stents, which can eliminate elastic recoil and prevent geometric vessel changes, leading to decreased restenosis. Of all antithrombotics tried so far, only an inhibitor of the platelet IIb/IIIa integrin, which may lead to early vessel wall passivation, has shown reduction of clinical restenosis. Trapidil (antiproliferative agent) and angiopeptin (somatostatin analog) have also resulted in improved restenosis rates. The field of local drug delivery is currently under investigation in association with radiation or molecular therapy. The current specific target of these approaches is the neointimal proliferation, especially because this is the most dominant mechanism of restenosis after stent placement. Evaluation of these novel methods is complex and interrelates the delivery system with the therapeutic agent administered. However, they provide the means for very specific and timely interruption of the pathogenic process that may lead to better understanding and, ultimately, elimination of restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1996

Transient thrombotic state after abrupt discontinuation of heparin in percutaneous coronary angioplasty.

Clinical and biochemical evidence of a rebound phenomenon after discontinuing thrombin inhibitors has been reported in patients with unstable angina. To investigate if a similar phenomenon occurs in patients undergoing coronary angioplasty, 14 patients were prospectively studied during and after discontinuation of heparin infusion. A transient thrombotic state identified by a significant increase in a polypeptide fragment and fibrinopeptide A was observed 3 hours after abruptly discontinuing heparin infusion. This observation may be clinically important in managing patients after coronary angioplasty.

Adult↗