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ABSTRACT: Acute myocardial infarction remains the leading cause of death in the United States. Following increased recognition of the role of thrombosis in the pathogenesis of myocardial infarction, both antiplatelet and anticoagulant therapy have been proven effective in preventing recurrent infarction. However, the optimal antithrombotic regimen remains undetermined. In particular, the role of combination antithrombotic therapy has not been studied. The Coumadin Aspirin Reinfarction Study (CARS) will compare the safety and efficacy of fixed-dose combination Coumadin plus aspirin versus aspirin alone among 8000 survivors of acute myocardial infarction. Patients will be followed for up to 4 years. CARS will provide important information regarding the optimal antithrombotic regimen for myocardial infarct survivors.
Journal of Thrombosis and Thrombolysis 01/1995; 2(3):171-176. · 1.48 Impact Factor
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ABSTRACT: Objectives. This study was designed to determine the blood elements responsible for spontaneous echocardiographic contrast.Background. Spontaneous contrast or “smoke” is an echocardiographic image usually found in low flow conditions. Two blood elements, erythrocytes and platelets, have been related to the generation of smoke.Methods. The echogenicity of percine blood products was assessed in static and flow conditions and was graded on a digitized videodensity computer program that assigned a score of 0 for black and 100 for white images. Blood elements were circulated from a small tube (4-mm diameter) into a larger cylindric chamber (30-mm diameter) under controlled flow rate conditions. The following blood products were studied: whole blood, platelet-depleted blood, platelet-rich plasma, platelet-poor plasma, erythrocytes suspended in saline solution, adenosine dipbosphate (ADP) added to platelet-rich plasma, and saline solution as a control medium.Results. As blood flow was increased in 30 ml/min increments from 0 to 180 ml/min, whole blood echo videodensity (scale 0 to 100) progressively decreased in the larger tube from 38 and 42 to 20, 12, 14, 16 and 14, respectively. When flow increased from 0 to 30 ml/min in the smaller tube, corresponding to a wall shear rate of 0 to 80 s−1, the blood entering the chamber was completely echolucent. The echogenicity of blood products in the larger tube was for static flow (0 ml/min) and high flow (180 ml/min), respectively: platelet-depleted blood = 36 and 14; platelet-rich plasma = 2 and 2; platelet-poor plasma = 0 and 0; erythrocytes in saline solution = 8 and 12; ADP added to platelet-rich plasma = 0 and 15; saline solution = 0 and 0. Because platelets alone were nonechogenic but platetet-depleted blood produced a flow-dependent echogenicity similar to that produced by whole blood, platelets may not be involved in the production of smoke. However, when platelets were aggregated by ADP, they were echogenic but in dense clumps and in a flow-independent pattern not typical of the smokelike images. Erythrocytes suspended in saline solution had an intermediate density image.Conclusions. Echogenic smoke appears to be due primarily to the interection of red blood cells and plasma proteins at low flow and low shear rate conditions.
Journal of the American College of Cardiology 01/1993; · 14.16 Impact Factor
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ABSTRACT: Angioplasty procedures with balloons, cutters or lasers all may greatly enlarge the arterial lumen, but luminal diameter may decrease because of mural thrombus in 70% to 80%, smooth muscle proliferation, vasoconstriction or recoil. Thrombin binds to arterial wall matrix and fibrin within a thrombus. Heparin dose-dependently decreases platelet and thrombus deposition but does not eliminate these even at high doses. Specific thrombin inhibition started before angioplasty experimentally prevents mural thrombus and limits platelet deposition to a single layer or less. Experimentally, anticoagulant and antifibrin effects occur at lower antithrombin blood levels and lower activated partial thromboplastin times (1.7 times control). Because platelets are so sensitive to thrombin, the higher level of thrombin inhibition required may occur at a specific level (activated partial thromboplastin time ≥ 2 times control); this is not defined in humans. The duration of therapy is not defined in animals or humans. Thrombus and thrombin may be related to cellular proliferation.
Journal of the American College of Cardiology 06/1991; · 14.16 Impact Factor
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ABSTRACT: Coronary angioplasty has become a successful and widely used treatment for patients with coronary artery disease since its first clinical application in 1977. The primary success rate has improved despite the increase in procedure and case complexity. However, acute reocclusion and late restenosis, which constitute the most important problems after successful angioplasty. continue to occur in about 5% and 35% of patients within 3 to 6 months, respectively, Angioscopic and pathologic observations have suggested that a multifactorial pathophysiologic process accounts for acute reocclusion, involving marked thrombosis, intimal dissection, medial and subintimal hemorrhage, vascular recoil and vasoconstriction. In contrast, chronic restenosis involves the development of fibrocellular intimal hyperplasia within a milieu created by vascular injury, platelet activation, thrombin generation and the release of mitogens. Although current pharmacologic approaches, which involve antithrombotic and anticoagulant therapy, have been largely ineffective in eliminating acute reocclusion and chronic restenosis, recent advances in the research in thrombosis, platelet receptors and smooth muscle growth regulation have allowed new therapeutic options to be tested in the experimental setting, with subsequent potential clinical applications in patients.
Journal of the American College of Cardiology 06/1991; · 14.16 Impact Factor
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ABSTRACT: Vascular injury and platelet accumulation after balloon angioplasty are two potentially important triggers of the process of restenosis that may be minimized by the use of laser energy to ablate atherosclerotic plaque. The type of laser most suitable to achieve these goals remains unknown. Accordingly, angiographic and histologic studies and quantitative platelet deposition analysis were performed on 27 atherosclerotic rabbit iliac arteries randomized to treatment with excimer laser or thermal laser angioplasty. Excimer laser angioplasty was achieved with 35 to 40 mJ/mm2 of 308 nm xenon chloride irradiation delivered through a 4.5F catheter made of 13 concentrically arranged 200 μm fiber optics, at a repetition rate of 25 to 30 Hz and a pulse duration of 135 ns; thermal laser angioplasty was achieved with a 1.7 mm metal probe heated with 10 W of continuous wave argon laser energy.The baseline and post-laser luminal diameters of excimer laser-treated vessels (0.92 ± 0.28 and 1.56 ± 0.48 mm, respectively) were similar to those observed in thermal laser-treated vessels (1.05 ± 0.44 and 1.61 ± 0.41 mm, respectively). Perforation occurred in 4 (29%) of 14 thermal laser-treated arteries and in 0 of 13 excimer laser-treated arteries (p = 0.04); spasm was observed in only 1 thermal laser-treated vessel. On the basis of a quantitative histologic grading scheme (damage scores of 0 to 4), greater degrees of injury were measured in thermal versus excimer laser-treated vessels (2.4 ± 1.0 versus 1.3 ± 0.4, p = 0.009). When arteries with vascular perforation were excluded, similar degrees of platelet deposition were seen in thermal and excimer laser-treated vessels (27 ± 22 and 17 ± 3 × 106 platelets/ cm, respectively; p = 0.37). In vessels treated with thermal laser angioplasty, platelet deposition was strongly correlated with histologie gradc (r = 0.72; p = 0.006).These results suggest that the excimer laser is able to ablate atherosclerotic plaque in vivo with fewer complications and lower levels of histologic damage than are obtained with the thermal laser; however, in atherosclerotic vessels, excimer laser angioplasty does not reduce platelet deposition. Whether these effects of the excimer laser will translate into an increased or decreased rate of restenosis after angioplasty remains to be determined.
Journal of the American College of Cardiology 04/1991; · 14.16 Impact Factor
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ABSTRACT: The relative safety and thrombogenicity of pulsed excimer and thermal laser angioplasty systems were compared in 20 normal coronary artery segments in a total of seven pigs. Using similar over the wire catheter systems and laser delivery periods of 3 to 5 s, thermal laser angioplasty was achieved with a 1.3 mm metal probe heated with 10 W of continuous argon laser energy and excimer laser angioplasty was performed with a 4.5F excimer laser catheter consisting of 13 concentrically arranged 200 μm fiber optics delivering 35 to 40 mJ/mm2 of xenon chloride (308 nm) excimer laser irradiation at a repetition rate of 25 to 30 Hz and a pulse duration of 120 ns.On angtography, the incidence of vessel perforation (1 in 10 versus 3 in 10) and abrupt vessel closure (0 in 10 versus 2 in 10) was less with excimer compared with thermal laser angioplasty. Macroscopically, there was a greater incidence of mural and occlusive thrombus formation after thermal laser than after pulsed excimer laser angioplasty. Histologic examination confirmed that this thrombogenicity was associated with greater charring and coagulation necrosis of the media.Quantitative indium-111-labeled platelet deposition was significantly increased after thermal laser angioplasty (median 87.2 × 106/cm length) compared with excimer-treated (0.4 × 106/cm length) or control (1.2 × 106/cm length) segments (p < 0.001). Thus, excimer laser angioplasty was found to result in fewer complications and, as a consequence, less thrombosis and platelet accumulation than did thermal laser angioplasty.
Journal of the American College of Cardiology 09/1990; · 14.16 Impact Factor
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ABSTRACT: 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.
Journal of the American College of Cardiology 01/1989; · 14.16 Impact Factor
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ABSTRACT: 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 cath-eterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a <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-strep-tokinase. 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 <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.
Journal of the American College of Cardiology 06/1987; · 14.16 Impact Factor
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ABSTRACT: Nitroglycerin and dipyridamole are two commonly available and well tolerated vasoactive medications. Their acute hemodynamic effects in patients with pulmonary arterial hypertension are not well defined in the current literature. The authors retrospectively analyzed the acute hemodynamic effects of IV nitroglycerin, dipyridamole, and epoprostenol in 59 patients with pulmonary arterial hypertension as determined by changes from baseline in systemic and pulmonary hemodynamic parameters. Statistical analysis was performed using the independent sample t test. A p value <0.05 was considered significant. Nitroglycerin is predominantly a vasodilator of the pulmonary vasculature with moderate systemic vasodilator effect, while dipyridamole is primarily a positive inotropic agent. Epoprostenol is a potent vasodilator of both pulmonary and systemic vessels and a strong positive inotropic agent. Nitroglycerin and dipyridamole may be useful in the acute management of pulmonary arterial hypertension.
Congestive Heart Failure 11(3):139-44; quiz 145-6.
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ABSTRACT: Thrombosis results from the activation of the hemostatic system by pathologic stimuli. It is a dynamic process that involves various blood cells and proteins, the nature of blood flow, and substrate characteristics. The classic description of the hemostatic system encompasses the coagulation and fibrinolytic systems, the platelets, and the endothelium. Thrombin plays a central role in thrombus formation, interacting with the components of the hemostatic system and vessel wall.
Trends in Cardiovascular Medicine.
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ABSTRACT: ObjectivesThe purposes of the present study were to: 1) determine whether fibrinogen (Fg) is the plasma protein responsible for spontaneous echo contrast (SEC), and 2) investigate modulators of SEC.BackgroundSpontaneous echo contrast has been linked to the development of thromboemboli. The blood products and their interaction responsible for SEC formation have not been fully elucidated.MethodsBlood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model. Human blood samples were analyzed in a manner to methodically eliminate individual blood components from whole blood to determine which components are responsible for the formation of SEC.ResultsThe videodensity (VD) of whole blood was found to be flow-dependent, with higher VD at lower flow rates, and correlated with visually dense SEC. The following blood products produced faint VD values: washed red blood cells (wRBCs), platelet-depleted plasma, Fg, defibrinated plasma, wRBCs plus defibrinated plasma, and physiologic saline. The VD of wRBCs increased incrementally as increasing concentrations of Fg were added. At each hematocrit (Hct) range, as Fg concentration increased, the SEC became denser, and the VD level also increased until a plateau level was reached that was distinct for each Hct. The addition of sialic acid, which inhibits RBC-RBC aggregation, decreased the amount of SEC, even in the presence of Fg.ConclusionsThese results demonstrated that Fg-mediated RBC aggregation may be responsible for SEC generation. Furthermore, a unique stoichiometric relationship exists between Fg and RBC concentrations that is necessary for blood echogenicity.
Journal of the American College of Cardiology.
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ABSTRACT: OBJECTIVESWe investigated the in vivo effects of tissue factor (TF) inhibition with recombinant tissue factor pathway inhibitor (rTFPI) on acute thrombus formation and intimal hyperplasia and the in vitro effects on smooth muscle cell migration and proliferation.BACKGROUNDInhibition of TF with TFPI has been shown to reduce intimal hyperplasia in experimental models. However, its effects after coronary angioplasty and the cellular mechanisms involved have not been investigated.METHODSTwenty-three swine underwent multivessel coronary angioplasty. Fifteen (n = 25 arteries) were euthanized at 72 h to assess thrombus formation and eight (n = 24 arteries) at 28 days to assess intimal hyperplasia. Animals in the 72-h time point received: 1) human rTFPI (0.5 mg bolus plus 25 μg/kg/min continuous infusion for 3 days) plus heparin (150 IU/kg intravenous bolus) plus acetyl salicylic acid (ASA) (325 mg/day); 2) rTFPI regimen plus ASA and 3) heparin (150 IU/kg intravenous bolus) plus ASA.RESULTSOn histology the control group had evidence of mural thrombus (area 0.8 ± 0.4 mm2). Treatment with TFPI plus heparin abolished thrombus formation (mean area: 0.0 ± 0.0 mm2, p < 0.05) but was associated with prolonged activated partial thromboplastin time and extravascular hemorrhage. Recombinant TFPI alone inhibited thrombosis without bleeding complications (mean area: 0.03 ± 0.02 mm2, p < 0.05 vs. control). Animals in the 28-day time point received continuous intravenous infusion of rTFPI or control solution for 14 days. Tissue factor pathway inhibitor reduced neointimal formation with mean intimal area of 1.2 ± 0.3 mm2 versus 3.2 ± 0.4 mm2 in the control group; p < 0.01. Recombinant TFPI had no effect on human aortic smooth muscle cell growth but inhibited platelet-derived growth factor BB-induced migration.CONCLUSIONSInhibition of TF with rTFPI can prevent acute thrombosis and intimal hyperplasia after injury. Tissue factor plasma inhibitor may prove useful as an adjunct to intracoronary interventions.
Journal of the American College of Cardiology.
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ABSTRACT: ObjectivesThis study tested the near-term reproducibility of 18fluorodeoxyglucose positron emission tomography (FDG-PET) imaging of atherosclerosis.BackgroundIt is known that FDG-PET can measure inflammation within the aorta, carotid, and vertebral arteries with histologic validation in humans and animal models of disease. By tracking changes in inflammation over time, PET could be used as a surrogate marker of antiatheroma drug efficacy. However, the short-term variability and reproducibility of the technique are unknown.MethodsWe imaged the carotid arteries and aorta in 11 subjects with FDG-PET/computed tomography twice, 14 days apart. We assessed interobserver and intraobserver agreement and interscan variability.ResultsInterscan plaque FDG variability over 2 weeks was very low; intraclass correlation coefficients (ICC) ranged between 0.79 and 0.92. Interobserver agreement was high across all territories imaged except aortic arch (ICC values from 0.90 to 0.97, arch 0.71). Intraobserver agreement was high, with ICC values between 0.93 and 0.98.ConclusionsSpontaneous change in plaque FDG uptake is low over 2 weeks, with favorable inter- and intraobserver agreement. Power calculations suggest that drug studies using FDG-PET imaging would require few subjects compared with other imaging modalities. This study strengthens the case for FDG-PET as a noninvasive plaque imaging technique.
Journal of the American College of Cardiology.
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ABSTRACT: Objectives. This study was designed to compare the response of unstable angina and non-Q wave myocardial infarction during treatment with antithrombotic therapy.Background. Antithrombotic therapy is beneficial in patients with these two coronary syndromes.Methods. In a multicenter trial of antithrombotic therapy in unstable angina or non-Q wave myocardial infarction, 358 patients admitted within 48 h of chest pain were randomized to antithrombotic therapy with either 1) aspirin alone, or 2) aspirin plus heparin followed by aspirin plus warfarin, and were prospeclively followed up for 12 weeks. Admission cardiac enzyme analyses revealed unstable angina in 268 patients and non-Q wave myocardial infarction in 62. Given an event rate of about 25%, this study has a power of 80% to detect a 50% difference between the two groups.Results. Patients with unstable angina and non-Q wave myocardial infarction were similar with regard to age, gender, coronary risk factors and prior antianginal medication. Primary end points at 12 weeks were recurrent ischemia, infarction and death. Recurrent AnginaMyocardial InfarctionDeathTotalUnstable angina20%4%3%27%Non-q wave infarction11%11%5%27%Full-size table In the non-Q wave group, all infarctions and death occurred within the 1st week.Conclusions. Patients with unstable angina or non-Q wave myocardial infarction on antithrombotic therapy haw a similar total number of ischemic events by 12 weeks. However, despite maximal medical therapy with antianginal and antithrombotic medication, patients with non-Q wave infarction have a significantly higher rate of reinfarction and death.
Journal of the American College of Cardiology.
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ABSTRACT: The incidence and prevention of systemic embolism in patients with chronic left ventricular aneurysm have been controversial. This retrospective study investigated the incidence of clinically evident embolic events and the effect of oral anticoagulation in patients with unequivocal angiographically defined left ventricular aneurysm. Between 1971 and 1979, 76 patients met the ventriculographic criteria and received initial medical management. The median interval from myocardial infarction to ventriculography was 11 months (range 1 month to 16 years) and subsequent median follow-up time was 5 years. Twenty patients receiving anticoagulant therapy were followed up for a total of 40 patient-years and 69 patients not on anticoagulant therapy were followed up for a total of 288 patient-years; 13 patients were included in both subsets.Twenty-eight patients died during follow-up and the 3 and 5 year survival rates were 75 and 61 %, respectively. Only one patient not receiving anticoagulant therapy had a clinical embolic event, resulting in an incidence of 0.35 per 100 patient-years. Therefore, in the absence of other predisposing conditions, the extremely low incidence of systemic emboli in these patients with chronic (first documented at least 1 month after myocardial infarction) left ventricular aneurysm does not justify the use of long-term oral anticoagulant therapy.
Journal of the American College of Cardiology.
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ABSTRACT: Inflammation of the vessel wall is involved in all stages of the course of atherothrombotic disease, from the development of early lesions to the occurrence of clinical events. Significant advances in recent years have largely improved our understanding of this phenomenon and of its influence not only on atherogenesis, but also on other intimately related disorders such as arterial hypertension or the metabolic syndrome. Emerging imaging technologies as well as measurement of serum concentrations of specific biomarkers offer the possibility to detect and, to some extent, quantify the degree of chronic vascular inflammation in vivo. In addition, many standard and novel antiatherosclerotic therapies may exert beneficial effects through anti-inflammatory actions. As a result, detection and treatment of vascular inflammation are certain to become increasingly important in the management with patients of cardiovascular disease.
Journal of the American Society of Hypertension 1(1):68-81. · 2.12 Impact Factor
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ABSTRACT: Atherothrombosis is increasingly recognized as a dynamic chronic inflammatory
process of the vessel wall, in which phases of inflammatory and thrombotic
activity underlie the clinical presentations of acute coronary syndromes (ACS).1 There is also evolving evidence that circulating monocytes
and white blood cells may be involved in a proinflammatory or prothrombotic
circulatory state.2- 3 These 2
mechanisms—inflammatory involvement of the vessel wall and of the circulating
blood—are not mutually exclusive, and both could occur within an individual
patient. Two reports in this issue of THE JOURNAL draw attention to the inflammatory
basis of coronary atherothrombotic disease.
JAMA The Journal of the American Medical Association 286(17):2154-2156. · 30.03 Impact Factor
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ABSTRACT: Today many patients admitted with an acute coronary syndrome are already taking aspirin. Because they have symptoms despite antithrombotic therapy, these patients are presumed to be at higher risk for subsequent clinical events. In a pilot trial of antithrombotic therapy in patients with unstable angina at rest or non-Q wave infarction, 93 patients admitted within 48 h of pain were prospectively followed up for 12 weeks. On admission, 29 patients (31%) were already taking daily aspirin; 64 (68%) were receiving no antiplatelet agent. After enrollment all patients received antithrombotic therapy with either aspirin or heparin according to protocol regardless of prior aspirin use.The two groups (prior users versus nonusers of aspirin) were similar with regard to age, gender, coronary risk factors, prior antianginal medication, duration of symptomatic coronary disease, presentation with non-Q wave infarction and extent of electrocardiographic changes on admission. Quantitative analysis of coronary arteriograms (on a 0 to 10 scale) showed similar myocardium-in-jeopardy scores (JS). Follow-up events (recurrent ischemia [Isch], infarction [MI] and revascularization [Revasc]) were: Prior Aspirin UseIschMIRevascJSYes27%3%44%3.7%No33%5%51%3.9%Full-size tableAspirin users experiencing rest angina are similar to other patients with ischemic rest pain. The “resistant to aspirin” group Joes not constitute a subgroup that is at higher risk for cardiac events or revascularization.
Journal of the American College of Cardiology.
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Valentin Fuster,
Lars E Rydén,
David S Cannom,
Harry J Crijns,
Anne B Curtis,
Kenneth A Ellenbogen,
Jonathan L Halperin,
Jean-Yves Le Heuzey,
G Neal Kay,
James E Lowe,
S Bertil Olsson,
Eric N Prystowsky,
Juan Luis Tamargo,
Samuel Wann
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ABSTRACT: Although it is not clear why coronary occlusion and restenosis occur after successful coronary angioplasty, factors related to the procedure may influence early and late results. The possible adverse effects of a medial tear documented histologically and produced during balloon angioplasty of the common carotid arteries were studied in 30 fully heparinized (100 U/kg body weight) normal pigs. Scanning electron microscopy showed endothelial denudation and extensive platelet deposition in all dilated arterial segments. Visible macroscopic mural thrombus was present within an hour of the procedure in 29 (91%) of the 32 arteries that had a medial tear documented by histologic study; the tear produced an indium-111-labeled platelet deposition of 116.4 ± 26.5 × 106/cm2 (mean ± SE) and total thrombotic occlusion in 2 arteries (4%). None of the 24 arteries without a medial tear had a thrombus, and the mean platelet deposition in that group was 7.0 ± 0.5 × 106/cm2 (p < 0.0008). In 12 pigs scanned with a gamma camera, visible thrombus was associated with platelet deposition in excess of 20 × 106/cm2 in 12 arteries, 9 of which had a positive indium-111-labeled platelet scintigram.Thus, arterial angioplasty causes deep arterial injury, which appears to be a major cause of mural thrombosis, heavy platelet deposition, a positive indium-lll-labeled platelet scintigram and acute arterial occlusion. A positive indium-lll-labeled platelet scintigram was always associated with macroscopic thrombus of at least 20 × 106 platelets/cm2 and underlying deep arterial injury.
Journal of the American College of Cardiology.
