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Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 343 records · Page 19Linked to original sources
PubMed1988

Angiographic demonstration of a common link between unstable angina pectoris and non-Q-wave acute myocardial infarction.

The coronary morphology of ischemia-related arteries in unstable angina and Q-wave acute myocardial infarction (AMI) has been described. An eccentric stenosis with overhanging edges or irregular borders (type II eccentric) was seen in most lesions less than 100% occluded and probably represented plaque disruption, nonocclusive thrombus or both. The coronary morphology of non-Q AMI has not been described. Thus, the angiograms of 106 consecutive patients catheterized with either unstable angina (n = 73) or non-Q AMI (n = 33) and an identifiable ischemia-related artery were prospectively analyzed. Non-Q AMI was diagnosed by prolonged chest pain and new and persistent ST-T changes or creatine phosphokinase twice the normal level. The results showed a higher incidence of total occlusion of the ischemia-related artery in non-Q AMI (21%) compared with unstable angina (8%) (p = 0.1). The coronary morphology of nonoccluded ischemia-related arteries was similar with preponderance of type II eccentric lesions in both unstable angina and non-Q AMI. These lesions were found in 65% of ischemia-related arteries in non-Q AMI but were uncommon (3%) in nonischemia-related arteries with significant (50% to 100%) stenoses. Therefore, the type II eccentric lesion is a sensitive and specific marker of less than 100% occluded ischemia-related arteries in both unstable angina and non-Q AMI. These similarities in coronary morphology suggest a similar pathogenesis, which, as previously suggested, may relate to plaque disruption with or without thrombus. Unstable angina and non-Q AMI appear to represent part of a continuous spectrum of acute coronary artery disease. Further, the management of patients with non-Q AMI should be similar to patients with unstable angina and possibly include anticoagulation and consideration for early catheterization.

Aged↗
PubMed1988

Anticoagulation clinics and the monitoring of anticoagulant therapy.

Patients attending an anticoagulation clinic were studied to delineate predisposing risk factors for bleeding and thromboembolic episodes. Seventy-three patients were observed for a total of 921.8 patient-treatment months. The mean duration of treatment was 12.6 months (range 3-36 months). No major bleed occurred (a bleed which caused discontinuation of therapy, hospitalization or death). Thirty-two patients had minor bleeding episodes (0.42 bleeds per patient-year of treatment). The average prothrombin time ratio during the third to the sixth month of therapy was predictive of the bleeding risk. There was no association between bleeding and age, sex, indication for anticoagulation therapy or associated illnesses. Four thromboembolic episodes occurred (0.05 per patient-year of treatment), 3 arterial and 1 venous. At the time of the one venous thromboembolic event the prothrombin time ratio was subtherapeutic. In all 3 patients with arterial thromboembolism the mean 3- to 6-month prothrombin time ratio was less than or equal to the lower limit of the recommended range of 1.6-2.5. In our study prothrombin time ratios of 1.3-1.5 for venous thromboembolic disease and 1.6-2.5 for arterial thromboembolic disease were not associated with thromboembolism or major bleeding. Anticoagulation clinics facilitate the close monitoring of patients on oral anticoagulant therapy.

Aged↗
PubMed1988

Angiographic progression of coronary artery disease and the development of myocardial infarction.

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Reversal of chronic ischemic myocardial dysfunction after transluminal coronary angioplasty.

From a cohort of patients referred for elective transluminal coronary angioplasty, a subset of patients was evaluated to determine whether revascularization using coronary angioplasty could salvage chronically ischemic myocardium. Reversible chronic ischemic left ventricular dysfunction was identified by a severe wall motion abnormality at rest and at least one of the following: 1) persistent angina pectoris; 2) postextrasystolic ventricular contraction potentiation of motion in the asynergic zone on baseline ventriculogram; and 3) thallium-201 uptake in the asynergic zone. Twelve patients were identified as having reversible chronic ischemia and underwent coronary angioplasty. Their mean age was 63 +/- 11 years and duration of symptoms 8.3 +/- 9.7 weeks. Immediate pre- and postangioplasty left ventriculograms were obtained. Regional wall motion was analyzed using a radial axis model, and global ejection fraction was calculated. After angioplasty, tension development (heart rate-systolic pressure product) increased in the absence of an increase in left ventricular end-diastolic pressure. Global ejection fraction increased from 46 +/- 20 to 62 +/- 19% (p less than 0.005). The percent of left ventricular diastolic perimeter showing asynergy decreased from 29 +/- 11 to 10 +/- 13% (p less than 0.005). During follow-up ranging from 6 to 51 months, sudden death occurred in one patient who had had no improvement in wall motion after angioplasty, repeat angioplasty was performed in three patients and eight patients remained asymptomatic. Application of easily obtainable clinical data identifies a subset of patients with chronically ischemic myocardium. Coronary angioplasty in such patients is useful in salvaging hibernating myocardium.

Adult↗
PubMed1988

Antithrombotic therapy after myocardial reperfusion in acute myocardial infarction.

The problem of post-thrombolytic reocclusion can be approached in several ways. 1) Better thrombolytic agents with longer duration of effects and more powerful properties aimed at enhanced clot lysis and anticoagulation are under study. 2) The combination of high dose heparin and low dose aspirin is proposed for all patients with an acute myocardial infarction treated with thrombolytic agents. 3) Peptide inhibitors of thrombin and monoclonal antibodies against platelet glycoprotein receptors and adhesive macromolecules are potentially effective inhibitors of platelet aggregation and thrombus formation during or after thrombolytic therapy.

Coronary Disease↗
PubMed1988

Emergency thrombolysis in acute myocardial infarction.

The goal of thrombolytic treatment in acute myocardial infarction is to reestablish permanent blood flow, salvage ischemic myocardium, and reduce mortality. If patency is achieved sufficiently early and is maintained, left ventricular function is preserved and mortality decreases. The recent experience with tissue plasminogen activator and streptokinase in the TIMI I trial is reviewed with specific attention to reperfusion, reocclusion, and bleeding. Other studies concerning left ventricular preservation and mortality are also discussed. Current guidelines for antithrombotic therapy and thrombolysis are discussed. It is extremely important to adequately select patients to avoid side effects. Thorough lysis of the thrombus must be achieved to reduce the risk of rethrombosis. Simultaneous heparin should be administered to treat ongoing thrombosis. Additional antithrombotic therapy with aspirin and acute vasodilation to reduce vasoconstriction probably also decrease the likelihood of reocclusion. Because this treatment predisposes to bleeding, extreme care should be taken to avoid vascular punctures and invasive procedures in these patients. The association of immediate percutaneous transluminal coronary angioplasty has not been beneficial in preventing further events; on the contrary, adverse effects have been associated with this acute intervention.

Emergencies↗
PubMed1988

Morphologic and dynamic changes of atherosclerotic plaque at the carotid artery bifurcation: sequential imaging by real time B-mode ultrasonography.

Occurrence of new symptoms of focal cerebrovascular disease, including completed cerebral infarction, transient cerebral ischemic attack and amaurosis fugax, was correlated with changes in size and morphology of atherosclerotic plaques at the carotid artery bifurcation visualized by real time B-mode ultrasonography. Bilateral serial images of 246 plaques in 123 patients were made in a time interval of 9 to 35 months between initial and follow-up studies. There was a significantly higher incidence of symptoms ipsilateral to plaques that grew [30 (25%) of 121] than of symptoms ipsilateral to plaques that diminished or remained unchanged [8 (8%) of 98] (p less than 0.001). Plaques that became hemodynamically obstructive by causing disruption of laminar flow or reduction of distal perfusion pressure at the ophthalmic artery were associated with a higher frequency of symptoms [12 (40%) of 30] than were nonobstructive plaques [26 (13%) of 201] (p less than 0.001). There was also a strong association between symptoms and plaque configuration. Mural plaques growing in a crescentic configuration along the wall of the carotid bifurcation between the first and second examination had a higher incidence of symptoms [22 (40%) of 56] than did plaques that grew but maintained a nodular configuration [8 (12%) of 65] (p less than 0.001), although the same proportion of each became hemodynamically obstructive. Sequential visualization of atherosclerotic plaques by real time B-mode ultrasonography of the carotid bifurcation may provide a method for studying the pathogenesis of arterial thrombosis.

Aged↗
PubMed1988

Importance of adequate heparin dosage in arterial angioplasty in a porcine model.

Acute occlusion after a successful angioplasty is a severe complication that has been reported in 2-12% of patients. Therefore, to determine whether there was a relation between the dosage of heparin and the presence of mural thrombosis, we studied in a pig model the relation between the dosage of heparin and acute platelet-thrombus deposition on the site of arterial injury. We retrospectively analyzed the effect of three heparin regimens on platelet deposition in 32 normal pigs (mean weight, 32.7 kg) that underwent bilateral carotid angioplasty and were sacrificed 90 +/- 26 minutes later. Pigs in protocol 1 (n = 7) received an intravenous bolus injection of 4,000 units heparin 10 minutes before angioplasty. Pigs in protocol 2 (n = 11) received two bolus injections of 4,000 units heparin 40 minutes apart; the angioplasty was performed immediately after the second bolus. Pigs in protocol 3 (n = 14) had an initial 4,000-unit bolus injection of heparin followed immediately by an infusion of 4,000 units/hr; angioplasty was performed 20 minutes after starting the infusion. 111In-labeled platelet deposition on deeply injured (torn into the media) arterial segments were 86.3 +/- 68, 56.2 +/- 56.9, and 37.7 +/- 37.7 X 10(6)/cm2 for protocols 1, 2, and 3, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMed1988

Platelets, vasoconstriction, and nitroglycerin during arterial wall injury. A new antithrombotic role for an old drug.

Endothelial injury in vivo is associated with platelet deposition and a localized platelet-dependent vasoconstrictive response. To assess the influence of nitroglycerin on platelets and vasoconstriction, quantitative 111In-labeled platelet deposition (no platelets x 10(6)/cm2) of the injured segment and the degree of angiographic vasoconstriction (percent diameter narrowing proximal and distal to the dilated segment) produced during injury by balloon angioplasty of the common carotid arteries were studied in heparinized normal pigs that were sacrificed immediately after the procedure. In deeply injured (injury extending through the internal elastic lamina) compared with mildly injured (deendothelialization only) arteries, there was both greater platelet deposition (63.8 vs. 6.9, p = 0.04) and more vasoconstriction (30% vs. 19%, p = 0.02). In the presence of deep arterial wall injury, nitroglycerin given intravenously at a dose sufficient to lower mean arterial pressure by 9 +/- 2% significantly decreased both platelet deposition (16.2 vs. 63.8, p less than 0.008) and the vasoconstrictive response (20 vs. 30%, p less than 0.02) relative to control. However, in the presence of mild arterial wall injury, nitroglycerin decreased vasoconstriction relative to control (10% vs. 19%, p less than 0.01) without causing a significant decrease in the already low level of platelet deposition (5.6 vs. 6.9, respectively; p = NS), suggesting a direct smooth muscle relaxant effect of nitroglycerin. This is the first reported in vivo effectiveness of nitroglycerin in the reduction of platelet deposition after deep arterial injury.

Angioplasty, Balloon↗
PubMed1988

Platelet thrombus formation on collagen type I. A model of deep vessel injury. Influence of blood rheology, von Willebrand factor, and blood coagulation.

Collagen type I is a major component of atherosclerotic vessel wall that is exposed on deep vessel injury, such as in balloon angioplasty or plaque rupture. Collagen type I from pig Achilles tendon was mounted in a tubular perfusion chamber placed within an extracorporeal circuit (carotid artery to jugular vein). The material was exposed to blood from normal pigs (n = 13), severe homozygous von Willebrand factor (vWF)-deficient pigs (vWF less than 3%) (n = 6), and heterozygous vWF-deficient pigs (vWF = 24%) (n = 2). Thrombus formation was measured by autologous 111In-platelet labeling and by ultrastructural morphology. Heparinized and native blood from these pigs was perfused over the substrate for 3 and 5 minutes at local shear rates from 212 to 3,380/sec. On collagen type I exposed to nonanticoagulated blood, for all exposure times studied, thrombus formation in the absence of vWF was significantly reduced at high shear rate typical of stenotic areas but not at low shear rate typical of unobstructed medium-size arteries. A similar inhibition in thrombus formation due to vWF deficiency was observed in both heparinized and native blood; however, thrombus formation was significantly more reduced (p less than 0.05) in the presence of heparin, presumably due to the lack of stability of the accumulated platelets in the absence of fibrin formation. Intermediate levels of vWF, as in heterozygous von Willebrand's disease (vWD), support platelet deposition to extents not significantly different from normal conditions. Therefore, on collagen type I, both the activation of blood coagulation proteins and the presence of vWF contribute significantly to the platelet-platelet interactions necessary for thrombus formation. The effect of vWF occurs primarily at high shear conditions typical intravascularly of flow at the apex of advanced stenotic lesions; thus, these findings may suggest that the absence of vWF may be protective against the development of acute thrombosis in these regions.

Animals↗
PubMed1988

Thrombolysis in acute myocardial infarction.

This is an extensive review of thrombolysis in myocardial infarction with discussions of the pathophysiology of occlusion, clinical occlusion and rationale for thrombolysis, thrombolytic agents, results of thrombolysis (incidence of reperfusion, left ventricular function, and mortality), complications of thrombolytic therapy, reocclusion, and current recommendations.

Angioplasty, Balloon↗
PubMed1988

Antithrombotic therapy for patients with cardiac disease.

The use and type of antithrombotic therapy for patients with cardiac disease are described based on an understanding of the pathophysiologic mechanisms involved, the risk of thromboembolism, and the evidence from prospective and, if necessary, retrospective clinical trials. The indications and intensity of anticoagulant therapy in patients with valvular heart disease and prosthetic valves are first discussed. We recommend that the prothrombin time be reported as a ratio and standardized using the International Normalized Ratio. The pivotal role of platelets and the clotting system in the initiation and progression of atherosclerosis and the acute coronary syndromes is described. There is no evidence to date that antiplatelet therapy is of value in primary prevention or in patients with stable angina, but the value of aspirin in patients with unstable angina was clearly shown in two well-designed studies. Adequate prophylactic therapy to prevent the thrombotic complications of acute myocardial infarction (i.e., venous thrombosis and intracardiac thrombosis) is described, and the available data on the prevention of coronary reocclusion after thrombolysis reviewed. There is now convincing evidence from studies in animals and in patients that vascular injury during aortocoronary vein bypass graft surgery requires antitihrombotic therapy starting before the procedure to minimize acute platelet thrombus deposition and prevent occlusion. Restenosis after arterial angioplasty appears to be related to acute platelet thrombus deposition on the site of deep arterial injury. Therapeutic interventions should probably involve both anticoagulants and platelet inhibitor therapy. Implications derived from recent animal studies are discussed.

Antithrombins↗