(Circulation. 1997;95:1411-1416.)
© 1997 American Heart Association, Inc.
Articles |
Analysis of Coronary Ultrasound Thrombolysis Endpoints in Acute Myocardial Infarction (ACUTE Trial)
Results of the Feasibility Phase
From the Cardiac Catheterization Laboratory, Department of Cardiology, Tel Aviv Sourasky Medical Center, Tel Aviv University, Israel.
Correspondence to Uri Rosenschein, MD, Catheterization Laboratory, Department of Cardiology, Tel Aviv Sourasky Medical Center, 6 Weizman St, Tel Aviv 64239, Israel.
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Abstract |
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Background It has been demonstrated that therapeutic ultrasound effects ultrasound thrombolysis by selectively disrupting the fibrin matrix of the thrombus. This study was conducted to evaluate the clinical feasibility of percutaneous transluminal coronary ultrasound thrombolysis in acute myocardial infarction (AMI).
Methods and Results Consecutive patients (n=15) with evidence of anterior AMI and Thrombolysis In Myocardial Infarction (TIMI) grade 0 or 1 flow in the left anterior descending artery underwent coronary ultrasound thrombolysis. Angiographic follow-up was performed after 10 minutes and 12 to 24 hours. Ultrasound induced successful reperfusion (TIMI grade 3 flow) in 87% of the patients. Adjunct percutaneous transluminal coronary angioplasty (PTCA) after ultrasound thrombolysis produced a final residual stenosis of 20±12% as determined by quantitative coronary angiographic analysis. There were no adverse angiographic signs or clinical effects during the procedure. There was no change in the degree of flow in any of the patients at the 12- to 24-hour angiograms. During hospitalization, 1 patient had recurrent ischemia on the fifth day after the procedure, and emergent catheterization revealed occlusion at the treatment site. The patient was successfully treated with PTCA.
Conclusions These results suggest that ultrasound thrombolysis has the potential to be a safe and effective catheter-based therapeutic modality in reperfusion therapy for patients with AMI and other clinical conditions associated with intracoronary thrombosis.
Key Words: ultrasonics • thrombolysis • myocardial infarction
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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We have investigated the use of high-power, low-frequency ultrasound for transcatheter arterial recanalization. The data in experimental and clinical settings in the peripheral arteries suggested that thrombus-rich lesions may be the ideal type of lesion to be treated by therapeutic ultrasound.1 2 Therapeutic ultrasound was found to selectively lyse thrombi with a wide margin of safety. The ultrasound power level required to lyse thrombi is
1/20 of that required to
induce arterial wall damage.3 It has been demonstrated
that therapeutic ultrasound effects ultrasound thrombolysis by
selective disruption of the fibrin matrix of the
thrombus.2 3 Evaluation of coronary ultrasound
thrombolysis in vitro demonstrated that therapeutic ultrasound could
lyse clots rapidly, producing mostly subcapillary-sized particles and
limited heat.4 In vivo, transluminal coronary sonication
had no adverse effects.5 The purpose of the present study was to evaluate the feasibility of percutaneous transluminal coronary ultrasound thrombolysis in AMI, the archetypal clinical presentation of intracoronary thrombosis.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Population
Consecutive patients admitted to the Tel Aviv Medical Center with anterior AMI from June 1, 1995, were studied. Eligible patients showed evidence of anterior AMI defined by ischemic chest pain for <12 hours, accompanied by ST elevation
1 mm in 2
precordial leads. On angiography, there was TIMI grade 0 or 1 flow in
the LAD. Exclusion criteria included one of the following clinical or
angiographic findings: prior bypass surgery, previous intervention in
the LAD, previous Q-wave anterior infarction, significant left main
artery disease, three-vessel disease, Killip class 3, and failure to
cross the lesion with the guidewire. All patients signed a written
informed consent. The study was approved by the Institutional Review
Board at the Tel Aviv Medical Center and the Israeli Ministry of
Health.
Coronary Ultrasound Thrombolysis Protocol
The ultrasound thrombolysis device (ACULYSIS System,
Angiosonics) is a 140-cm-long, solid-metal probe, ensheathed in a
plastic catheter and connected at its proximal end to a piezoelectric
transducer. Ultrasonic energy (45 kHz) is transmitted from the
transducer as longitudinal vibrations of the probe, which direct the
energy into the arterial system. The last 18 cm of the device is a
three-wire flexible segment with a 1.6-mm tip designed to optimize the
thrombolytic effect of ultrasound. The three-wire design of the distal
segment permits the use of solid metal for optimal ultrasound
transmission while still achieving the desired flexibility. This is
similar to the way in which optic fibers enable effective transmission
of light waves through glass while maintaining flexibility. The device
fits into a 10F angioplasty guide catheter and accepts a 0.014-in
guidewire through a coaxial central lumen in a "monorail"
fashion. Power output and frequency at the hand piece (18 W) are
controlled by an integrated computer designed to ensure constant power
output at the distal tip (10-µm longitudinal displacements) under the
variable loading conditions encountered during the
procedure.4 5
Before undergoing coronary ultrasound thrombolysis, all patients were
treated with intracoronary nitroglycerin (200 µg), aspirin (250 to
325 mg chewable or IV), and heparin (15 000 U IV to obtain an ACT
>300 throughout the procedure). Guiding coronary angiograms were
obtained in standard fashion with the use of a 10F Judkins left guiding
catheter (Sherpa, Medtronics). The lesion was crossed with a 0.014-in
guidewire extra support (Advanced Cardiovascular Systems). Then, the
ultrasound probe was introduced onto the guidewire and advanced into
the LAD under fluoroscopy until the cavitation tip was positioned 1 to
2 mm past the proximal end of the occlusion. Sonication (18 W) was
performed at 60-second intervals up to a total period of 
3 minutes,
the maximal sonication time per probe. To minimize risk of
embolization, the lesion was crossed only after effective thrombus
ablation and reperfusion were established. During sonication, the probe
was either left stationary or moved slowly back and forth with a small
amplitude (3 mm).
After sonication and intracoronary nitroglycerin administration (200 µg), angiograms were taken at views identical to those of the guiding angiograms. In the event of failed coronary ultrasound thrombolysis (defined as TIMI grade 0 or 1 flow), PTCA was performed.
A third set of angiograms was obtained 10 minutes after a successful
coronary ultrasound thrombolysis and after intracoronary nitroglycerin
administration (200 µg). On the basis of the third angiogram, PTCA
was performed if there was evidence of suboptimal flow (TIMI grade 0 to
2 flow), significant residual stenosis (30%), or threatened closure.
PTCA under the same conditions was limited to other lesions on the LAD.
After 12 to 24 hours, another set of coronary angiograms was obtained
after intracoronary nitroglycerin administration (200 µg). PTCA was
performed if there was suboptimal flow (TIMI grade 0 to 2 flow),
significant residual stenosis (30%), or threatened closure. During
hospitalization, emergent catheterization was mandatory if symptomatic
recurrent ischemia occurred, to provide objective evidence of
arterial patency.
Post–Coronary Ultrasound Thrombolysis Care
After coronary ultrasound thrombolysis, patients were monitored
in the coronary care unit. All were treated by intravenous
nitroglycerin during the first 24 hours and with intravenous heparin
(adjusted to give an APTT of 50 to 70 seconds) for the first 4 days.
After the 12- to 24-hour coronary angiography, heparin was temporarily
stopped, and the sheaths were removed when the APTT decreased to 55
seconds (or when ACT was 150 seconds). Patients were ambulated
gradually, 24 hours after sheath removal.
During hospitalization, patients were treated by the attending physician. Mandatory oral therapy included aspirin (250 mg/d) and heparin (intravenous for the first 4 days followed by subcutaneous low-molecular-weight heparin for 2 weeks); other medical therapy was left to the discretion of the physician. There were no specific recommendations concerning angiograms, angioplasty, or bypass surgery. All clinical events were recorded. A predischarge clinical evaluation was performed. The ejection fraction was evaluated by nuclear ventriculography before patient discharge.
Angiographic Analysis
Cineangiograms were obtained with the use of a Philips DCI
Angiographic System. Measurements of angiograms were made with selected
cine frames at end diastole by an experienced technician using the
on-line quantitative coronary angiography system. Vessel edges were
determined with computerized algorithms, and luminal diameters were
measured with the dye-filled guide catheter used as a reference
standard. The diameters of the normal segments proximal and distal to
the treated segment were averaged to determine the reference diameter.
The MLD, reference diameter, and percentage of stenosis were calculated
by measuring the most severe stenosis using a view without
foreshortening. All angiograms were reviewed for morphological analysis
by two experienced angiographers who used the morphological
angiographic definitions provided in the Bypass Angioplasty
Revascularization Investigation (BARI Central Radiographic Laboratory
Operational Manual, unpublished data, 1989), with specific emphasis on
the TIMI grade flow and the presence of the following adverse
morphological features: dissection, spasm, perforation, distal
embolization, and side-branch occlusion. The morphological analysis was
made only by consensus.
Definitions
The flow in the infarct-related artery on the first contrast
injection was graded as follows:
TIMI grade 0 (no perfusion): No flow through the obstruction.
TIMI grade 1 (minimal perfusion): The contrast material passes beyond the area of obstruction but fails to make the entire coronary bed distal to the obstruction opaque.
TIMI grade 2 (partial perfusion): The contrast material crosses the obstruction and makes the coronary bed distal to the obstruction opaque, but the rate of entry of contrast material into the vessel distal to the obstruction or its rate of clearance is reduced relative to the nonobstructed vessel.
TIMI grade 3 (complete perfusion): Normal flow and clearance as in a normal vessel.
Dissection: Either the presence of a curvilinear filling defect parallel to the vessel lumen with contrast medium outside of the vessel lumen (but within what the operator judged to be the vessel wall) persisting after passage of contrast medium into the arterial lumen or a spiral-shaped filling defect partially or totally obstructing the coronary artery lumen.
Spasm: The presence of stenosis at the site of sonication that was relieved by intracoronary nitroglycerin.
Vessel perforation: Persistent extramural collection of contrast medium with a well-defined exit port in the absence of angiographically evident dissection.
Distal embolization: A discrete luminal filling defect seen downstream of the site of sonication with or without occlusion of the distal branch.
Threatened closure: Angiographic appearance of the vessel that predicts
imminent closure, as judged by the operator and the presence of one of
the following four criteria: (1) dissection; (2) angiographic evidence
of residual thrombus; (3) significant residual stenosis (30%); or
(4) evidence of clinical ischemia (either typical angina or ECG
changes).
Recurrent ischemia: Symptoms (eg, chest discomfort, pain in the arm and/or jaw, and nausea), ECG changes, or new hypotension, pulmonary edema, or murmur judged by the physician to represent myocardial ischemia, not relieved by sublingual nitroglycerin and lasting >15 minutes.
Reinfarction: A second myocardial infarction that occurred after the one for which the patient was hospitalized, as assessed by a physician on the basis of at least two of the following criteria: (1) recurrent ischemia; (2) occurrence of new ST-T–wave changes or new Q waves; (3) a second elevation of cardiac enzymes above the upper normal limit (or by an additional 20% if they already were above the upper normal limit); or (4) angiographic evidence of reocclusion of a documented infarct-related artery that was previously patent.
Target-vessel revascularization: A need for revascularization (PTCA or CABG) of the ultrasound-recanalized LAD within the time period between the coronary ultrasound thrombolysis and the follow-up appointment due to acute coronary syndrome. Revascularization indicated as a result of the coronary anatomy, defined before coronary ultrasound thrombolysis, would not qualify as target-vessel revascularization.
Severe bleeding: Bleeding was termed severe when it caused hemodynamic compromise—decompensation in the patient's blood pressure to <90 mm Hg systolic pressure—and required either blood or fluid replacement, surgical intervention, or CPR to maintain sufficient cardiac output. The compromise must have been due to the bleeding, which included intracranial, gastrointestinal, or retroperitoneal bleeding.
Bleeding: Bleeding requiring transfusion of blood but not extensive enough to lead to hemodynamic compromise.
Device success: Normalization of perfusion (TIMI grade 3 flow) without major clinical complications resulting from the coronary ultrasound thrombolysis procedure (death, ventricular fibrillation, cardiac arrest, pulmonary edema, or cardiogenic shock).
Angiographic success: Normalization of perfusion and final diameter stenosis <50% (irrespective of adjunct balloon use) without major clinical complications in the cardiac catheterization laboratory.
Clinical success: Normalization of perfusion, final diameter of the stenosis <50%, and absence of major complications in the cardiac catheterization laboratory and during the hospitalization period (death, cardiogenic shock, pulmonary edema, recurrent ischemia, reinfarction, target-vessel revascularization, stroke, or severe bleeding).
Data Collection and Analysis
The primary end point in the study was normalization of
perfusion (TIMI grade 3 flow) induced by coronary ultrasound
thrombolysis. Secondary end points were vessel patency (TIMI grade 3
flow) at 10 minutes and 12 to 24 hours and clinical events that
occurred in the cardiac catheterization laboratory or during
hospitalization. Continuous variables are expressed as mean±SD.
Semiquantitative variables are expressed as median and range.
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Results |
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During the recruitment phase for the study, 40 consecutive patients were found to be clinically eligible. Fifteen patients did not undergo cardiac catheterization because either the cardiac catheterization laboratory was unavailable within 1 hour (n=11), the patient had out-of-hospital thrombolytic therapy (n=3), or the patient refused to participate (n=1). Twenty-five patients underwent cardiac catheterization, and only 15 were angiographically eligible and treated by coronary ultrasound thrombolysis (Table
). Most
treated patients were middle-aged males with a high coronary risk
profile; 53% were smokers, 26% had hypercholesterolemia, 26% had
systemic hypertension, and 20% had a positive family history.
Typically, the patients were in a good hemodynamic state, with systolic
blood pressure and heart rate within the normal ranges (135±19
mm Hg, 80±13 bpm). Door-to-reperfusion time was 96±43 minutes. After
failure to induce reperfusion in the first patient, the technique and
auxiliary hardware were modified, but no change was made in ultrasound
frequency, power, or total sonication time. The modification included
changing the guiding catheter configuration from C-curve to Judkins
left. The probe was held stationary with the distal tip in the thrombus
(1 to 2 mm), whereas in the first patient it had been moved back
and forth briskly during sonication. Furthermore, sonication intervals
were extended from 30 to 60 seconds. This technique, described in
"Methods," was maintained in an identical manner in the
subsequent 14 patients. The failure in the first patient represents the
beginning of the evolutionary iterative learning process in developing
the appropriate technique for this device. The second patient failure
was a result of a defect in the software driving the device. The
software was updated accordingly.
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Angiographic Analysis
Coronary ultrasound thrombolysis induced normalization of
perfusion (TIMI grade 3 flow) in 13 (87%) of the 15 patients (Fig 1). In all the successful cases, TIMI grade 3 flow was
achieved with no adverse angiographic signs. After ultrasound
thrombolysis, only 1 patient exhibited asymptomatic reocclusion at the
10-minute angiogram, and he underwent PTCA with restoration of vessel
dimensions and a TIMI grade 2 flow. At the 12- to 24-hour angiograms,
there was no change in the degree of flow in any of the patients.
Adjunct PTCA after ultrasound thrombolysis produced excellent final
vessel dimensions (residual stenosis, 20±12% diameter; MLD,
2.4±0.6 mm) with no adverse angiographic signs (Figs 2 and 3).
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, Data from the first patient.
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Clinical Events
There were no adverse clinical events (death, ventricular
fibrillation, cardiac arrest, pulmonary edema, or cardiogenic shock)
during the procedure. Successful reperfusion was accompanied by
idioventricular rhythm in 12 (92%) of the 13 patients in whom coronary
ultrasound thrombolysis was successful. During hospitalization, 1
patient had recurrent ischemia on the fifth day after the
procedure, after abrupt discontinuation of heparin. Emergent
catheterization revealed occlusion of the LAD at the treatment site.
The patient was treated successfully with PTCA with no elevation of the
creatine kinase levels. Coronary angiography after successful coronary
ultrasound thrombolysis in another patient revealed diffuse lesions in
the LAD and in a dominant right coronary artery. His coronary status
was assessed as high risk for percutaneous treatment. The patient
underwent successful CABG surgery after an uneventful hospital course.
Three patients (20%) had severe congestive heart failure (NYHA class 3
or 4) during hospitalization.
Success
Device success was obtained in 13 (87%) of 15 patients,
angiographic success in 13 (87%), and clinical success in 12
(80%).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this study, the feasibility of coronary ultrasound thrombolysis in AMI, the archetypal clinical manifestation of thrombus-rich lesion, was investigated for the first time. Coronary ultrasound thrombolysis was found to attain device success (TIMI grade 3 flow) in 87% of patients, angiographic success in 87%, and clinical success in 80%. Final angiographic results revealed minimal residual stenosis (20%) with no adverse morphological signs on angiography. No adverse clinical side effects were observed during sonication in the coronary tree. Adverse clinical events during hospitalization were limited to reocclusion of the infarct-related artery in only one patient (7%) and severe congestive heart failure in three patients (20%). These excellent results are probably due to the ability of ultrasound to induce rapid, effective, and selective thrombolysis with no need to cross the lesion before treatment. The skills required to operate the coronary ultrasound thrombolysis system are similar to those required for coronary balloon angioplasty. The catheter was easily delivered to the target coronary arterial segment, and precise positioning or coaxiality of the catheter was not crucial. Slight operator mispositioning did not lead to damage of the ultrasound-resistant arterial wall.
Other investigators have studied the coronary application of therapeutic ultrasound. Siegel et al6 published their initial clinical experience in coronary ultrasound angioplasty. Unlike our study group, their group consisted primarily of patients with chronic atherosclerotic occlusive lesions (only 3 of 19 patients had acute coronary syndromes). Ultrasound angioplasty resulted in partial arterial recanalization, with reduction in stenosis from 80±12% to 60±18%. Similarly, only partial recanalization was observed (from 94±10% to 55±23% stenosis) when ultrasound angioplasty was attempted on atherosclerotic lesions in the peripheral arteries. Hamm and coworkers7 recently published a case report on a patient with AMI who was successfully treated with ultrasound-assisted balloon angioplasty.
Balloon angioplasty and other percutaneous coronary interventions in the presence of intracoronary thrombus are accompanied by a high rate of abrupt closure, myocardial infarction, and death.8 9 10 11 12 The use of balloon angioplasty as a primary strategy for recanalization of the infarct-related artery in AMI has been studied recently in randomized trials.13 14 Those studies suggest that PTCA might be an effective and safe method for mechanical reperfusion in AMI. Nevertheless, in those studies, PTCA was not found to induce greater myocardial salvage or to reduce infarct size, reinfarction, or overall death rate compared with chemical thrombolysis. The randomized trials of primary PTCA in AMI supply no morphological analyses of their final angiographic results. Other investigations15 found that primary PTCA in AMI is associated with a high rate of angiographic complications; distal embolization, no reflow, and residual thrombus were found in a large proportion of the treated patients (12%, 16.6%, and 3.5%, respectively). Recent analyses16 17 18 19 suggest that primary PTCA might not be the best therapeutic option in certain subgroups of patients. Furthermore, failed PTCA for AMI is associated with high mortality and emergency bypass surgery.20
The high prevalence of angiographically adverse signs and the high reocclusion rate after primary PTCA in AMI, up to 40% within the period of hospitalization,21 22 23 may explain the overall limited clinical benefit of primary PTCA in AMI despite the excellent rates of early angiographic patency.
The recently discovered limitations of thrombolytic drugs in AMI and the encouraging results from the studies on PTCA in AMI indicate the need to further explore the implementation of a device solution for reperfusion therapy in the setting of AMI.
Study Limitations
Auxiliary hardware. Currently the device requires a 10F
guiding catheter. This size requirement is due to its proximal-end
design. Next-generation devices will be compatible with a 7F guiding
catheter.
Potential embolization. A theoretical risk of distal embolization exists in treating intracoronary clots. This risk is limited with the use of this device because there is no need to cross the lesion with the device before clot lysis. Furthermore, experimental data show that most clot debris after ultrasound thrombolysis is subcapillary in size.4 Indeed, in our study, reperfusion was associated with TIMI grade 3 flow, there was no angiographically defined embolization, and the no-reflow phenomenon was not observed in this small cohort of patients.
Conclusions
The clinical data from the feasibility phase of the ACUTE trial
suggest that coronary ultrasound thrombolysis for reperfusion therapy
in AMI has the potential to be a safe and effective catheter-based
therapeutic modality in patients with AMI and other clinical conditions
associated with intracoronary thrombosis, including failed
thrombolysis, unstable angina, and degenerated vein grafts. Data from
upcoming multicenter studies are needed to better define the clinical
role for coronary ultrasound thrombolysis.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by a grant from the Israeli Ministry of Arts and Sciences and the GSF-Forschungszenter für Unwelt und Gesundheit GmbH, Neuherberg. We thank Prof L.A. Rozenszajn for his continuous advice and helpful criticism. We are grateful to Yvonne Weiden for her editorial and secretarial support.
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Footnotes |
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Dr Rosenschein is a consultant for Angiosonics (Morrisville, NC).
Received June 11, 1996; revision received December 9, 1996; accepted December 14, 1996.
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References |
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W. H. Cooke, R. Zhang, J. H. Zuckerman, J. Cui, T. E. Wilson, C. G. Crandall, and B. D. Levine Does nitric oxide buffer arterial blood pressure variability in humans? J Appl Physiol, October 1, 2002; 93(4): 1466 - 1470. [Abstract] [Full Text] [PDF]
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G. Beran, I. Lang, W. Schreiber, S. Denk, T. Stefenelli, B. Syeda, G. Maurer, D. Glogar, and P. Siostrzonek Intracoronary Thrombectomy With the X-Sizer Catheter System Improves Epicardial Flow and Accelerates ST-Segment Resolution in Patients With Acute Coronary Syndrome: A Prospective, Randomized, Controlled Study Circulation, May 21, 2002; 105(20): 2355 - 2360. [Abstract] [Full Text] [PDF]
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P. W. Armstrong and D. Collen Fibrinolysis for Acute Myocardial Infarction : Current Status and New Horizons for Pharmacological Reperfusion, Part 2 Circulation, June 19, 2001; 103(24): 2987 - 2992. [Full Text] [PDF]
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U. Rosenschein, V. Furman, E. Kerner, I. Fabian, J. Bernheim, and Y. Eshel Ultrasound Imaging-Guided Noninvasive Ultrasound Thrombolysis : Preclinical Results Circulation, July 11, 2000; 102(2): 238 - 245. [Abstract] [Full Text] [PDF]
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S. A. Strickberger, T. Tokano, J.-U. A. Kluiwstra, F. Morady, and C. Cain Extracardiac Ablation of the Canine Atrioventricular Junction by Use of High-Intensity Focused Ultrasound Circulation, July 13, 1999; 100(2): 203 - 208. [Abstract] [Full Text] [PDF]
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U. Rosenschein, G. Gaul, R. Erbel, F. Amann, D. Velasguez, H. Stoerger, R. Simon, G. Gomez, J. Troster, A. Bartorelli, et al. Percutaneous Transluminal Therapy of Occluded Saphenous Vein Grafts : Can the Challenge Be Met With Ultrasound Thrombolysis? Circulation, January 12, 1999; 99(1): 26 - 29. [Abstract] [Full Text] [PDF]
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P. G. Yock and P. J. Fitzgerald Catheter-Based Ultrasound Thrombolysis: Shake, Rattle, and Reperfuse Circulation, March 18, 1997; 95(6): 1360 - 1362. [Full Text]
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