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Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 145 records · Page 8Linked to original sources
PubMed1998

Atherothrombosis: mechanisms and clinical therapeutic approaches.

Eroded or disrupted atherosclerotic plaques act as a substrate for thrombosis, leading to ischemic coronary artery and cerebrovascular disease. Plaques vary greatly in composition, size, and the degree of stenosis they cause. Plaques can be categorized based on these features, which helps to estimate the likelihood of rupture and subsequent thrombosis. Vascular plaques often begin at regions with low and oscillatory shear forces that cause chronic minimal endothelial damage or dysfunction. Lipoproteins enter the vessel wall, promoting the recruitment of monocytes, which imbibe lipids and become foam cells. Smooth muscle cells invade these early plaques, producing connective tissue fibrils that form a fibrous cap over the lipid center; rupture of this cap is an important cause of thrombosis. Passive plaque disruption occurs when physical forces cause cap rupture; active disruption occurs when the cap is attacked by macrophages and proteolytic enzymes. Tissue factor is one of many factors within plaque that stimulates thrombosis.

Acute Disease↗
PubMed1998

Coronary thrombolysis.

Explore the source record for details and available documents.

Angioplasty, Balloon, Coronary↗
PubMed1998

Anthropometry and strength relationship: male-female differences.

Based upon 303 students from the Complutense University at Madrid (100 males and 203 females), aged between 21 and 29 years, the results of nine anthropometric measurements and four strength tests were evaluated. Males and females were analyzed separately in order to determine whether the relationship of body typology to physical performance varies according to gender. Regarding strength, maximum gender differences were observed for pulling strength (females: 53% of male values), followed by hand grip (59%) and vertical jump (66%). In general, correlations among variables were significant (anthropometric, strength, and anthropometric/strength). Principal component analysis revealed, that for women the vertical jump could be interpretated as more dependent on trunk length than on height or body size. Body size was relevant with respect to static strength. For males the vertical jump appeared to be more related to longitudinal dimensions than for females, while static strength had more to do with body mass (weight) than with body size (height).

Adult↗
PubMed1997

Guidelines for management of left-sided prosthetic valve thrombosis: a role for thrombolytic therapy. Consensus Conference on Prosthetic Valve Thrombosis.

OBJECTIVES: We sought to form a consensus recommendation for management of prosthetic valve thrombosis (PVT) from previous case and uncontrolled reports from a consensus of international specialists. BACKGROUND: PVT and thromboembolism relate to inadequate anticoagulation and valve type and location. PVT is suspected by history (dyspnea) and auscultation (muffled valve sounds or new murmurs) and confirmed by Doppler echocardiography showing a marked valve gradient. METHODS: A consensus conference was held to recommend management of left-sided PVT. RESULTS: Transesophageal Doppler echocardiography is used to visualize abnormal leaflet motion and the size, location and mobility of thrombus. Thrombolysis is used for high risk surgical candidates with left-sided PVT (New York Heart Association functional class III or IV) because cerebral thromboembolism may occur in 12% of patients. Duration of thrombolysis depends on resolution of pressure gradients and valve areas to near normal by Doppler echocardiography performed every few hours. Lysis is stopped after 72 or 24 h if there is no hemodynamic improvement (operation indicated). Heparin infusion with frequent measurement of activated partial thromboplastin time (aPTT) begins when aPTT is more than twice control levels and can be converted to warfarin (international normalized ratio [INR] 2.5 to 3.5) plus aspirin (81 to 100 mg/day). Patients in functional class I or II have lower surgical mortality, and those with large immobile thrombi on the prosthetic valve or left atrium have responded to endogenous lysis with combined subcutaneous heparin every 12 h (aPTT 55 to 80 s) plus warfarin (INR 2.5 to 3.5) for 1 to 6 months. Operation is advised for nonresponders or patients with mobile thrombi. CONCLUSIONS: Thrombolysis, followed by heparin, warfarin and aspirin, is advised for high risk surgical candidates with left-sided PVT.

Aortic Valve↗
PubMed1997

The generalist/cardiovascular specialist: a proposal for a new training track.

The economic forces that are reshaping the delivery of health care in the United States have led to intense examination of the appropriate roles for specialists and generalists. Resolving this issue has profound implications for the future of U.S. health care and for the economic health of academic training centers and individual physicians. The issues are particularly intense in cardiovascular care, a field that has had dramatic success in the application of new diagnostic and therapeutic technology and rapid growth in specialist practitioners but is now under pressure to shrink its ranks. A new generalist/cardiovascular specialist training track and a parallel reduction in the number of standard fellowship training positions in cardiovascular disease may be a partial solution. The first 2 years of the proposed 5-year program would consist of training in internal medicine, the final 2 would consist of training in cardiovascular disease, and the middle year would be a flexible combination of the two. Graduates would be Board eligible in internal medicine but would have enhanced competency in cardiovascular disease. This plan may improve the balance between generalists and specialists, improve the quality of primary and specialized cardiovascular care, and strengthen departments of medicine and academic training centers while facing new economic realities.

Cardiology↗
PubMed1997

Human lesion studies.

We describe recent information on the atherothrombotic processes leading to the acute coronary syndromes (ACS) in humans. Then, we outline the mechanism of action and impact of lipid-lowering therapy in stabilization and secondary prevention of such processes. We start with (1) definitions of atherosclerotic lesions. In the progression of coronary atherosclerosis, eight morphologically different lesions are defined (Type I to VI) in various phases of disease. (2) Then we discuss vulnerable lipid-rich plaques and ACS. The type IV and Va lesions tend to be relatively small in size, but soft or vulnerable to disruption (with subsequent thrombosis) because of high lipid content (cholesterol esters rather than free cholesterol monohydrate crystals). The above process represents a "passive" phenomenon of plaque disruption. In addition to this "passive" phenomenon, an "active," macrophage-dependent, phenomenon of plaque disruption is evolving. (3) We then show the role of thrombosis in ACS. Monocytes/macrophages in lipid-rich plaques may play a detrimental role after plaque disruption, promoting thrombin generation and thrombosis through the tissue factor pathway, which can be prevented by tissue factor pathway inhibitor. Such thrombotic phenomena are critical in the development of ACS. (4) Finally, we discuss the effect of lipid-modifying strategies on the vulnerable lipid-rich plaques. When high LDL-cholesterol is reduced therapeutically, efflux from the plaques of the liquid or sterified cholesterol, and also its hydrolysis into cholesterol crystals depositing in the vessel wall, predominate over the influx of LDL-cholesterol. Consequently, there is a decrease in the softness of the plaque and so, presumably in the "passive" phenomenon of plaque disruption. When low HDL-cholesterol is increased experimentally, there is a partial decrease in the number and activity of the macrophages and so, presumably in the "active" phenomenon of plaque disruption.

Arteriosclerosis↗
PubMed1997

Do cardiologists do it better?

Pressure to lower the cost of health care delivery has fostered widespread efforts to limit patients' access to specialists such as cardiologists. However, there is concern that diminished specialist involvement may lead to poorer patient outcomes for specific clinical conditions. As part of a state-sponsored effort to improve the quality of health care in Pennsylvania, the Pennsylvania Health Care Cost Containment Council gathered clinical and administrative data on all 40,684 hospital admissions for acute myocardial infarction (AMI) in that state in 1993. They prepared a detailed public report that included risk-adjusted in-hospital mortality and length of hospital stay by physician group, by hospital and by region. These data demonstrate that patients cared for by cardiologists, as a group, had a lower risk-adjusted mortality than patients cared for by either internists (risk ratio 1.26, 95% confidence interval 1.17 to 1.35) or family practitioners (risk ratio 1.29, 95% confidence interval 1.18 to 1.40). The patients of cardiologists also had a shorter length of stay than the other two groups. These data suggest that there is enhanced value in the care provided by cardiologists for patients with AMI and call into question the growing trend toward reliance on generalists instead of specialists.

Cardiology↗
PubMed1997

Tissue factor modulates the thrombogenicity of human atherosclerotic plaques.

BACKGROUND: The thrombogenicity of a disrupted atherosclerotic lesion is dependent on the nature and extent of the plaque components exposed to flowing blood together with local rheology and a variety of systemic factors. We previously reported on the different thrombogenicity of the various types of human atherosclerotic lesions when exposed to flowing blood in a well-characterized perfusion system. This study examines the role of tissue factor in the thrombogenicity of different types of atherosclerotic plaques and their components. METHODS AND RESULTS: Fifty human arterial segments (5 foam cell-rich, 9 collagen-rich, and 10 lipid-rich atherosclerotic lesions and 26 normal, nonatherosclerotic segments) were exposed to heparinized blood at high shear rate conditions in the Badimon perfusion chamber. The thrombogenicity of the arterial specimens was assessed by 111In-labeled platelets. After perfusion, specimens were stained for tissue factor by use of an in situ binding assay for factor VIIa. Tissue factor in specimens was semiquantitatively assessed on a scale of 0 to 3. Platelet deposition on the lipid-rich atheromatous core was significantly higher than on all other substrates (P = .0002). The lipid-rich core also exhibited the most intense tissue factor staining (3 +/- 0.1 arbitrary units) compared with other arterial components. Comparison of all specimens showed a positive correlation between quantitative platelet deposition and tissue factor staining score (r = .35, P < .01). CONCLUSIONS: Our results show that tissue factor is present in lipid-rich human atherosclerotic plaques and suggest that it is an important determinant of the thrombogenicity of human atherosclerotic lesions after spontaneous or mechanical plaque disruption.

Animals↗
PubMed1997

Prospective Comparison of Patient Characteristics and Outcome of Non-prior Aspirin Users versus Aspirin Users with Unstable Angina or Non-Q-Wave Myocardial Infarction Treated with Combination Antithrombotic Therapy.

The objective of this study was to determine if aspirin users presenting with acute coronary syndromes are at higher risk for subsequent clinical events. In a trial evaluating combination antithrombotic therapy in resting angina or non-Q-wave myocardial infarction (MI), patients were prospectively dichotomized on admission into nonprior versus recent aspirin users. Then 105 nonprior users and 144 users were randomized to treatment with aspirin plus heparin/warfarin for 12 weeks. Recurrent myocardial ischemia occurring during the 12-week follow-up period was defined as recurrent angina (with electrocardiographic changes or prompting coronary revascularization), MI, or death. Prior aspirin users had a significantly higher incidence of previous MI, prior bypass grafting, beta-blocker use, or hypertension (p </= 0.003) and were more likely to present with unstable angina as opposed to non-Q-wave MI. (p </= 0.008). The cumulative probability of recurrent ischemic endpoints for nonprior versus recent users was 10% versus 21% at 14 days (log rank p = 0.03), and 19% versus 29%, at 12 weeks (p = 0.06). Using the Cox model, adjusting for variables significantly associated with outcome, aspirin use remained a significant predictor of 14-day outcome (p = 0.04) but not of 12-week outcome (p = 0.06). In conclusion, even after adjusting for significant differences in baseline variables, aspirin users presenting with rest angina or non-Q-infarction have a worse short-term prognosis in spite of maximal medical therapy.

Journal Article↗
PubMed1997

Thrombosis triggered by severe arterial lesions is inhibited by oral administration of a glycoprotein IIb/IIIa antagonist.

Platelet aggregation and thrombosis play an important role in the onset of acute coronary events. Regardless of the stimulus for activation, platelet thrombus formation is ultimately regulated through the IIb/IIIa receptor complex. The effects of oral administration of xemilofiban, a non-peptide mimetic of the RGDF sequence of the IIb/IIIa receptor complex, on thrombus formation were evaluated in a canine model. Xemilofiban significantly reduced platelet deposition on severely damaged arterial wall. Platelet deposition was reduced at both low (13 +/- 1 from 56 +/- 18 x 10(6) platelets cm-2; P < 0.05) and high (23 +/- 2 from 111 +/- 21 x 10(6) platelets cm-2; P < 0.01) shear rates. Platelet deposition was reduced to a monolayer as seen by electron microscopy (platelet-vessel wall interaction). Therefore, the availability of an orally active IIb/IIIa antagonist for chronic use may have significant value in preventing thrombus formation in those clinical situations associated with severe arterial injury, such as atherosclerotic plaque disruption.

Administration, Oral↗
PubMed1997

Pathogenesis of thrombosis in coronary artery disease.

Arterial thrombosis in the acute coronary syndromes is precipitated by plaque disruption. This occurs in lesions with a large lipid core, a thin fibrous cap, macrophages infiltrating the fibrous cap, and a lipid core with a high tissue-factor content. This results in acute platelet deposition and rapid growth of mural thrombus which unfavorably influences the rheology of blood flow to produce more thrombus, and propagates additional thrombosis by the high thrombogenicity of the mural thrombus overlying the disrupted culprit arterial lesion. Acute therapy in the hospital and subacute therapy beyond the hospital phase for as long as 1.5-3 months with aspirin plus anticoagulation, such as low-molecular-weight heparin, or oral anticoagulation, reduces thrombotic occlusion, myocardial infarction, death, and need for coronary revascularization.

Coronary Disease↗
PubMed1997

Water diffusion properties of human atherosclerosis and thrombosis measured by pulse field gradient nuclear magnetic resonance.

Using pulsed field gradient methods combined with magnetic resonance imaging, we calculated the apparent water diffusion coefficient D in different atherosclerotic components to probe the microstructure of normal and diseased arteries by characterizing molecular motion. D was equal to 0.26 +/- 0.13 x 10(-5) cm2.s-1 in plaque lipid core, 1.45 +/- 0.41 x 10(-5) cm2.s-1 in collagenous cap, and 1.54 +/- 0.30 x 10(-5) cm2.s-1 in normal media. Water diffuses isotropically in the atheromatous core of the plaque, suggesting the absence or destruction of confining structures. The comparable diffusion coefficients in collagenous cap and normal media are consistent with similar biophysical barriers in both components. In thrombi, D varies with the aging processes (fresh thrombus, 0.72 +/- 0.11 x 10(-5) cm2.s-1; 1-week-old thrombus, 0.36 +/- 0.08 x 10(-5) cm2.s-1; old occluding thrombus, 1.33 +/- 0.33 x 10(-5) cm2.s-1), consistent with the cross-linking of the fibrin strands occurring in the early phase and the later thrombus organization. Defining an indirect index of arterial lipid infiltration, remodeling, and aging, diffusion imaging provides a new nuclear magnetic resonance characterization of atherothrombosis.

Arteries↗