Search PubMed⌕ Search

Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 361 records · Page 20Linked to original sources
PubMed1988

Radiotracers for low density lipoprotein biodistribution studies in vivo: technetium-99m low density lipoprotein versus radioiodinated low density lipoprotein preparations.

In an attempt to characterize the in vivo behavior of [99mTc] low density lipoprotein (LDL), biodistribution studies were performed in normal and hypercholesterolemic (HC) rabbits. In normal rabbits, 24 hr after the injection of [99mTc]LDL, 99mTc activity accumulated mainly in adrenal glands, spleen, liver, and kidney. In HC rabbits, however, there was a marked reduction of 99mTc activity in these organs. In both normal and HC rabbits, less than 17% of 99mTc activity appeared in the 24-hr urine following injection of [99mTc]LDL, suggesting that in vivo, [99mTc]LDL is trapped and accumulated within the tissues. Direct comparison of [99mTc]LDL, 125I-native-LDL and [131I]tyramine cellobiose-LDL (the previously validated trapped radioligand) in normal rabbits, demonstrated that the biodistribution of [99mTc]LDL was similar to that of [131I]tyramine cellobiose-LDL. The adrenal glands, liver, and spleen accumulated significantly greater quantities of 99mTc and 131I activity per gram of tissue than 125I (from native-LDL). In addition, imaging studies in monkeys, showed that the hepatic uptake and retention of [99mTc] LDL was similar to that of [131I]tyramine cellobiose LDL. In contrast, radioiodine from native-LDL was deiodinated in liver with subsequent excretion into the intestine. These results suggest that [99mTc]LDL acts as a trapped ligand in vivo and should therefore, be a good tracer for noninvasive quantitative biodistribution studies of LDL.

Animals↗
PubMed1987

Platelet/vessel wall interactions, rheologic factors and thrombogenic substrate in acute coronary syndromes: preventive strategies.

Thrombosis is an important pathogenetic factor in acute coronary syndromes, including unstable angina, myocardial infarction and sudden death. In all of these conditions, atherosclerotic plaque fissuring is a key inciting event. Minor injury to the vessel wall brings into play interactions between platelets and the wall. Platelet adhesion and aggregation ensue, modulated by a number of factors and substances. More severe injury to the vessel wall exposes the blood to other thrombogenic substances. Platelet deposition is also affected by rheologic (blood flow) factors at the site of injury, depending on the degree of stenosis and the resulting shear rates. The mechanism of unstable angina appears to be related to these factors in the following sequence: mild stenosis and minor injury with plaque fissuring, platelet responses, labile thrombosis, intermittent ischemia and pain at rest. Vasoconstriction may contribute to the symptoms. Although developing from the same origin, infarction may stem from a greater degree of vessel wall damage resulting in more permanent thrombus. Such considerations provide a focus for preventive strategies, including the optimal use of current inhibitors of platelet adhesion and aggregation and the application of peptide receptor blockers and monoclonal antibodies. Also important is control of rheologic factors by preventing stenosis or correcting it with angioplasty and thrombolytic therapy. Further elucidation of the critical role of thrombosis in coronary syndromes will facilitate progress toward the ultimate goal of primary prevention.

Blood Flow Velocity↗
PubMed1987

Restenosis after arterial angioplasty: a hemorrheologic response to injury.

Restenosis after arterial angioplasty appears to be a response to deep arterial injury, which is much more thrombogenic than superficial injury (endothelial denudation). Deep arterial injury exposes collagen, elastin and smooth muscle cells to circulating blood, releases tissue thromboplastin and causes immediate platelet-thrombus deposition as a result of activation of platelets and the clotting system, both of which mutually facilitate activation of the other. Regrowth of endothelium also is protective against platelet deposition. Platelet adherence to collagen, and thus to the arterial wall that is deeply injured, increases with shear rate (related inversely to the fourth power of luminal cross-sectional area and directly to blood flow); thus, the effect of shear rate increases the importance of adequate dilatation at the time of the procedure. Therapy that will reduce acute platelet-thrombus deposition appears to be an important factor for reduction of restenosis. Vasoconstriction occurs experimentally after arterial angioplasty in arterial segments proximal and distal to the dilated segment where there has been no necrosis of smooth muscle cells. The vasoconstriction is directly related to the severity of platelet deposition, can be reduced by reducing platelet deposition with low dose aspirin (1 mg/kg daily) and is probably mediated by vasoconstrictor substances from platelets (thromboxane A2, serotonin and other substances). Platelet-membrane receptor inhibitors to these substances reduce the vasoconstriction but do not reduce platelet deposition. Therapeutic intervention should probably involve both anticoagulation and platelet inhibition. Platelet-membrane receptor inhibition to the fibrinogen receptor, factor VIII-von Willebrand factor or both may be necessary acutely to sufficiently reduce acute platelet-thrombus deposition.

Angioplasty, Balloon↗
PubMed1987

Comparison of single plane videodensitometry-based right ventricular ejection fraction in right and left anterior oblique views to biplane geometry-based right ventricular ejection fraction.

To evaluate the reliability of the videodensitometric assessment of right ventricular ejection fraction, 38 patients were studied during diagnostic cardiac catheterization. Digital subtraction images of the right ventricle were obtained in both the right anterior oblique and the left anterior oblique views, using direct intraventricular injection of dilute contrast medium. From the end-diastolic and end-systolic images obtained in each view, analysis of the relative brightness values generated a videodensitometry-based right ventricular ejection fraction for both the right and the left anterior oblique views. These values were compared with those generated by applying the geometry-based Simpson's rule to the orthogonal images. Right ventricular ejection fraction ranged from 22 to 88%. Videodensitometric ejection fraction in the right anterior oblique view correlated well with that in the left anterior oblique view (r = 0.88) and each correlated well with geometry-based ejection fraction (r = 0.91 and 0.82, respectively). In a subset of 18 patients without significant cardiac disease, mean videodensitometric right ventricular ejection fraction was 68% (versus 61% in the abnormal subset), and it correlated closely with left ventricular ejection fraction (r = 0.82). Videodensitometric analysis of digital subtraction images provides a reliable method for calculating right ventricular ejection fraction that is independent of geometry and reliably separates normal from abnormal values. Application of videodensitometric techniques should simplify analysis of the response of the right ventricle to different interventions in patients with cardiac disease.

Adult↗
PubMed1987

Mitral valvuloplasty is superior to valve replacement for preservation of left ventricular function: an intraoperative two-dimensional echocardiographic study.

To investigate the mechanism and time of onset of ventricular dysfunction after mitral valve replacement, 18 patients with pure, severe mitral regurgitation (of whom 10 underwent mitral valve repair and 8 standard mitral valve replacement with papillary muscle excision) were studied by intraoperative two-dimensional echocardiography immediately before and immediately after the operative procedure. No patient sustained a perioperative myocardial infarction or had any residual mitral regurgitation. Although preoperative hemodynamics were similar, postoperatively the patients with valve repair had a lower pulmonary capillary wedge pressure than did the patients with valve replacement (8.6 +/- 1.9 versus 14.4 +/- 7.5 mm Hg, p less than 0.04). Although intraoperative echocardiographic ejection fraction fell significantly after mitral valve replacement (0.64 +/- 0.11 to 0.40 +/- 0.09, p less than 0.0001), it was maintained after valve repair (0.44 +/- 0.20 to 0.49 +/- 0.16, p = NS). Additionally, regional myocardial contractile abnormalities in the anterior and posterior septum were detected immediately after the procedure by intraoperative echocardiography in the patients with valve replacement, but not in those with repair. These postoperative regional contractile abnormalities after papillary muscle resection have not been described previously. Resection of the papillary muscles may disrupt the muscle bundle alignment and induce contractile abnormalities remote from the excised muscle. This study demonstrated that significant global and regional ventricular dysfunction develops immediately after removal of the papillary muscles, whereas myocardial contractility is preserved in patients undergoing mitral valve repair. Therefore, with intraoperative echocardiography to assure minimal residual regurgitation, surgeons should attempt to preserve ventricular function by performing mitral valve reconstruction in patients with mitral regurgitation.

Adult↗
PubMed1987

Quantitative and qualitative effects of intracoronary streptokinase in unstable angina and non-Q wave infarction.

Thrombolytic therapy has been shown to be effective in reopening totally occluded arteries in acute myocardial infarction. Coronary thrombus is also believed to play a role in the pathophysiology of unstable angina and non-Q wave infarction. However, few patients with these two acute coronary syndromes have been treated with intracoronary streptokinase. Therefore, 100,000 to 300,000 IU (mean 177,000 +/- 80,000 IU) of intracoronary streptokinase was infused into 36 consecutive catheterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a less than 100% occluded ischemia-producing artery could be identified. Qualitative techniques utilizing vessel magnification and quantitative analysis with digital subtraction were performed on the ischemia-producing coronary lesion before and immediately after streptokinase therapy and 3 to 10 days later in 18 patients who were restudied at the time of transluminal coronary angioplasty. Before streptokinase treatment, 24 (67%) of 36 ischemia-producing arteries contained eccentric, irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries averaged 83.8 +/- 8.3% and 94.8 +/- 3.3%, respectively. After streptokinase treatment there were 23 arteries (64%) with eccentric irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries were similar to pre-streptokinase values (82.9 +/- 5.9% and 93.8 +/- 4.0%, respectively). At restudy, there were also no significant changes in any quantitative or qualitative variable. Five individual patients showed a significant reduction in percent stenosis after streptokinase. This improvement was independent of duration of symptoms, use of heparin before angiography, streptokinase dose or reduction of fibrinogen levels post-streptokinase. Two additional patients deteriorated clinically and developed total occlusion of the ischemia-producing artery within 12 hours of streptokinase infusion. These data suggest that intracoronary streptokinase may be of limited utility in either unstable angina or recent non-Q wave infarction with a less than 100% occluded ischemia-producing artery. In these syndromes, thrombus may be organized or short infusions may be given too late to be effective. In some cases, thrombus may even be absent. Whether longer infusion of streptokinase or other thrombolytic agents will be of benefit remains to be determined.

Adult↗
PubMed1987

Is vasospasm related to platelet deposition? Relationship in a porcine preparation of arterial injury in vivo.

Although aggregating platelets can release potent vasoactive substances in vitro, the importance of platelets in mediating naturally occurring or provoked spasm in vivo is not clear. To investigate the possible role of platelets in arterial spasm following arterial injury induced by angioplasty, quantitative platelet deposition of the dilated arterial segment and the degree of vasoconstriction (average percent diameter narrowing just proximal and distal to the dilated segment) produced during angioplasty of the common carotid arteries were studied in 42 heparinized normal pigs that were killed immediately after the angioplasty procedure. Angiographic films of the carotid arteries were taken before and after the dilatation to assess the vasoconstriction. Vasoconstriction was greater (40% vs 19%, p less than .002) when platelet deposition (X 10(6)/cm2) was in excess of 10, and the severity of vasoconstriction in vivo had a close positive exponential correlation (r = .77, p less than .001) with extent of platelet deposition in 24 untreated pigs. Platelet deposition and vasoconstriction were greater with severe arterial wall injury than with mild injury (58.8 versus 6.9, p less than .0001; 37% vs 21%, p less than .001, respectively). After severe injury in 18 pigs pretreated with 1 mg/kg/day aspirin, platelet deposition decreased (from 58.8 to 19.6, p less than .02) and vasoconstriction decreased (from 37% to 21%, p less than .003) relative to control. After mild injury, platelet deposition and vasoconstriction were mild and unchanged by aspirin. Thus, local vasoconstriction is influenced by the degree of platelet deposition.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMed1987

Isolated atrial septal defect with pulmonary vascular obstructive disease--long-term follow-up and prediction of outcome after surgical correction.

UNLABELLED: We examined the cases of 702 patients found to have isolated atrial septal defect of the secundum or sinus venosus type at catheterization from 1953 to 1978. Forty patients (6%), 34 women and six men, had pulmonary vascular obstructive disease, with a total pulmonary resistance greater than 7 U/m2; of these patients 26 (mean age 47 years) underwent surgical closure and 14 (mean age 44 years) received medical treatment. All patients were followed for at least 4 years, with a median follow-up of 12 years. At the most recent follow-up, 17 of the 40 patients were dead. Of the 22 surgically treated patients with total pulmonary resistance less than 15 U/m2, 19 were alive with significant regression of symptoms. All four surgically treated patients with total pulmonary resistance greater than or equal to 15 U/m2 were dead. Of the five medically treated patients with total pulmonary resistance less than 15 U/m2, four had died, and one was alive with significant progression of symptoms. Of the nine medically treated patients with total pulmonary resistance greater than or equal to 15 U/m2, six had died and the three survivors had progression of symptoms. In the surgically treated group, the following variables correlated with survival: total pulmonary resistance (p less than .00001), pulmonary arteriolar resistance (p less than .00001), pulmonary-to-systemic resistance ratio (p = .004), systemic arterial oxygen saturation (p = .005), and pulmonary arterial oxygen saturation (p = .007). IN CONCLUSION: (1) Atrial septal defect with high total pulmonary resistance is uncommon and predominates in adult female patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Role of platelets in atherogenesis: relevance to coronary arterial restenosis after angioplasty.

There is now considerable evidence to suggest that some aspects of early lesion formation and later lesion growth are a reaction to injury. Hemodynamic factors are important in determining the site of injury and may produce injury directly. Injury can lead to atherogenesis in animal models as well as in humans. Superficial injury exposes the subendothelium, allowing platelet adhesion, which at high shear rates is dependent on vWF. Platelet adhesion and degranulation release PDGF, which stimulates smooth muscle cell proliferation, synthetic functions, and vasoconstriction. LDL stimulates smooth muscle cell growth as well as damages endothelium in some experimental systems. Thus, a link is provided between platelet and lipid involvement in atherosclerosis. Direct evidence for a role of platelets in atherogenesis comes from studies in which animals were treated to reduce platelet number or function or in which platelet function is genetically impaired (pigs with von Willebrand's disease). In these models, reduced platelet function is associated with less atherosclerosis. Deeper injury exposes collagen, with subsequent platelet aggregation, thrombin and fibrin generation. The role of reduced production of PGI2 and fibrinolytic agents following severe damage is unknown. Deep injury to the vessel occurs during plaque fissuring, the pathologic process underlying most cases of myocardial infarction, unstable angina, and some cases of sudden death. Angioplasty produces amelioration of many patients' symptoms and is safe. However, acute occlusion occurs occasionally, and restenosis in the first year occurs in some 30 percent of patients treated. Angioplasty damages the arterial wall, with endothelial denudation and intimal and medial splitting. Why does this, and plaque injury, by stimulating platelet deposition, not produce more restenosis? Changes in arterial anatomy are likely to be important: the increase in vessel diameter and in blood flow produce conditions less favorable for thrombotic or arteriosclerotic restenosis.

Angioplasty, Balloon↗
PubMed1987

Platelet-vessel wall interactions in the development of restenosis after coronary angioplasty.

Acute occlusion and restenosis of the dilated coronary segment remain serious unsolved complications that can occur after coronary angioplasty. Acute occlusion is seen in approximately 3-5% of patients and restenosis in 13-47% of patients undergoing this procedure. While the causes of these complications are incompletely understood, platelets and their interactions with the vessel wall appear to be important. The mechanism of stenosis dilatation involves a splitting or tearing of the atherosclerotic plaque as well as desquamation of the endothelial layer of the vessel wall. Therefore, superficial as well as deep arterial injury occurs as a result of angioplasty. Acute occlusion and restenosis appear to be the biological response to this injury. Following even subtle injury to the endothelial layer, platelets adhere to the vessel wall and become activated, releasing substances such as platelet derived growth factor which stimulates intimal hyperplasia and re-growth of the atherosclerotic plaque. Deeper injury results in increased platelet deposition and mural thrombus formation. Rheologic factors including oscillatory shear forces and high local shear rates resulting from residual stenosis and intimal dissection further promote platelet activation and thrombus formation. Both the rheologic factors and the thrombogenic properties of the vessel wall and circulating blood promote restenosis and acute occlusion. Studies using animal models have demonstrated that platelet inhibitor drugs used in addition to heparin can reduce the amount of platelet deposition at the time of angioplasty, and may have a favorable effect on the occurrence of acute occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMed1987

Platelet deposition on von Willebrand factor-deficient vessels. Extracorporeal perfusion studies in swine with von Willebrand's disease using native and heparinized blood.

Native (nonanticoagulated) and heparinized blood from both normal swine and swine with von Willebrand's disease was exposed to de-endothelialized thoracic aorta from normal pigs under controlled flow conditions. We have shown that these normal de-endothelialized vessel segments do not contain von Willebrand factor (vWF) in the subendothelial surface; thus, the vascular model that we are using here is representative of the conditions in severe von Willebrand's disease. The blood was recirculated for selected periods of time through an extracorporeal circuit (carotid-jugular shunt), containing a tubular perfusion chamber that held the vessel segment. Flow rates and chamber diameters were selected such that the wall shear rates at the vascular segment were 212 to 3380 sec-1. Platelets were labeled with indium 111 and their total deposition determined by a gamma counter; selected areas were also observed by electron microscopy. When native blood was perfused, the deposition of platelets depended on platelet-plasma vWF only at high wall shear rates (1690 sec-1 or greater) typical of the microcirculation, but not at the lower shear rates (212 and 424 sec-1), more characteristic of the larger arteries and veins. In contrast, when heparinized blood was perfused, platelet deposition on the vascular segments depended on the presence of vWF over the entire range of shear conditions studied. These findings demonstrate in an extracorporeal perfusion system that the defect in platelet-vessel wall interaction in swine with von Willebrand's disease is influenced by both the local flow conditions and the level of activation of the coagulation system. In the presence of an intact coagulation system a synergistic interaction between procoagulant moieties and vWF was observed at high shear rates.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

The necessity for tricuspid valve repair can be determined intraoperatively by two-dimensional echocardiography.

Residual significant tricuspid regurgitation after mitral valve operations may significantly increase postoperative morbidity and mortality. However, routine techniques to detect tricuspid regurgitation preoperatively and intraoperatively are inaccurate. Two-dimensional echocardiography was performed intraoperatively to assess its ability to evaluate and quantify the severity of tricuspid regurgitation. In 50 patients who underwent cardiac operations, 5 ml of dextrose or saline was injected into the right ventricle to generate echogenic "contrast." In patients with tricuspid regurgitation, there was systolic reflux of contrast into the right atrium, which could be semiquantified on a scale of 0 to 4+. Besides correlating well with preoperative Doppler studies for the presence or absence of tricuspid regurgitation in 18 patients (sensitivity = 0.90, specificity = 1.00), the intraoperative contrast method could quantify the severity of reflux. The 50 patients were divided into two groups on the basis of severity of tricuspid regurgitation as assessed by intraoperative two-dimensional contrast echocardiography. Group I (36 patients) had no or mild (0-2+) regurgitation, and Group II (14 patients) had moderate to severe (3-4+) tricuspid regurgitation. Patients with significant tricuspid regurgitation (Group II) had greater intraoperative preprocedure and postprocedure systolic and diastolic pulmonary pressures. Additionally, the systolic tricuspid anulus length, as measured in the intraoperative right ventricular inflow view, correlated better with severity of tricuspid regurgitation (r = 0.76, p = 0.005) than mean pulmonary pressure (r = 0.52, p less than 0.01). Therefore, intraoperative contrast two-dimensional echocardiography can accurately assess the relative severity of tricuspid regurgitation. Importantly, intraoperative measurement of tricuspid anulus diameter could predict the presence of significant echocardiographic tricuspid regurgitation before as well as immediately after the operation. Two-dimensional echocardiography may be an important intraoperative method both for evaluating the presence and severity of residual tricuspid regurgitation immediately after left heart operations as well as for determining which patients should undergo tricuspid valve repair.

Aged↗
PubMed1987

Characterization of a tubular flow chamber for studying platelet interaction with biologic and prosthetic materials: deposition of indium 111-labeled platelets on collagen, subendothelium, and expanded polytetrafluoroethylene.

A plastic (Plexiglas) chamber for evaluating platelet deposition under controlled hemodynamic conditions has been developed. The perfusion chamber has been designed to retain the cylindrical shape typical of the vasculature, to be flexible enough to accept a variety of biologic and prosthetic materials, and to simulate a broad range of physiologic flow conditions in either an ex vivo or in vitro perfusion system. Three type of surfaces were exposed to blood flowing directly from the carotid artery of a heparinized pig through the perfusion chamber: de-endothelialized pig aorta, collagen strips from rabbit Achilles tendon, and an expanded polytetrafluoroethylene material (Gore-Tex). Platelets, previously radiolabeled with indium 111 and injected into the animal, were quantified on the material surface, and the total number of deposited platelets determined for a range of blood flow rates (5 to 40 ml/min) and exposure times (0.5 to 20 minutes). The deposition rates were correlated with theory for describing the mass transport of platelets to the test surface. At the wall shear rates investigated (105 to 850 sec-1), the deposition of platelets on subendothelium was strongly dependent on the local flow conditions. Values of deposition on Gore-Tex obtained at similar flow conditions (105 to 425 sec-1) were reduced compared with that observed on subendothelium and showed a markedly weaker dependence on the shear rate. In contrast, deposition of platelets on collagen was more than an order of magnitude greater than on subendothelium and showed a dependence on flow only at the lowest flow rate studied (10 ml/min). The results indicate that collagen is much more reactive than subendothelium and Gore-Tex with respect to the growth and stability of platelet aggregates and moreover suggest that flow mechanisms for depositing platelets on various surface may be substantially different.

Animals↗
PubMed1986

Electrical aggregometry in whole blood from human, pig and rabbit.

The objective of this study was to characterize and standardize whole blood electrical aggregometry (WBEA) in the pig and rabbit, animal models extensively used in atherosclerosis research, and to compare their platelet response with that of man. Platelet aggregation was studied in blood (WBEA) and platelet rich plasma (optical aggregometry, OA). Dose response curves were obtained for ADP and collagen. The effect of hematocrit on WBEA was also evaluated. Aggregation with ADP and collagen using WBEA was more extensive with human than with pig or rabbit platelets. OA revealed similar differences among species but the time to reach maximal aggregation was markedly shorter. Using WBEA, the extent of aggregation was inversely related to the hematocrit. We conclude that WBEA is a useful technique that may be of particular importance in situations where hyperlipidemic plasma prevents the use of OA, as occurs in some atherosclerosis research animal models.

Adenosine Diphosphate↗