CLINICAL STUDIES
Influence of a platelet GPIIb/IIIa receptor antagonist on myocardial hypoperfusion during rotational atherectomy as assessed by myocardial Tc-99m sestamibi scintigraphy
Karl-Christian Koch, MD*,
Juergen vom Dahl, MD, FESC*,
Eduard Kleinhans, MD ,
Heinrich G. Klues, MD, FESC*,
Peter W. Radke, MD*,
Susanne Ninnemann*,
Gernot Schulz, MD,
Udalrich Buell, MD and
Peter Hanrath, MD, FACC, FESC*
* Department of Cardiology, University Hospital, University of Technology, Aachen, Germany
Department of Nuclear Medicine, University Hospital, University of Technology, Aachen, Germany
Manuscript received May 13, 1998;
revised manuscript received September 3, 1998,
accepted December 4, 1998.
Reprint requests and correspondence: Dr. Juergen vom Dahl, Medizinische Klinik I, Universitätsklinikum der RWTH Aachen, Pauwelstrasse 30, D-52057, Aachen, Germany
jvda{at}pcserver.mk1.rwth-aachen.de
OBJECTIVES
This study evaluated the effect of the glycoprotein IIb/IIIa (GPIIb/IIIa) antagonist abciximab on myocardial hypoperfusion during percutaneous transluminal rotational atherectomy (PTRA).
BACKGROUND
PTRA may cause transient ischemia and periprocedural myocardial injury. A platelet-dependent risk of non-Q-wave infarctions after directional atherectomy has been described. The role of platelets for the incidence and severity of myocardial hypoperfusion during PTRA is unknown.
METHODS
Seventy-five consecutive patients with complex lesions were studied using resting Tc-99m sestamibi single-photon emission computed tomography prior to PTRA, during, and 2 days after the procedure. The last 30 patients received periprocedural abciximab (group A) and their results were compared to the remaining 45 patients (group B). For semiquantitative analysis, myocardial perfusion in 24 left ventricular regions was expressed as percentage of maximal sestamibi uptake.
RESULTS
Baseline characteristics did not differ between the groups. Transient perfusion defects were observed in 39/45 (87%) patients of group B, but only in 10/30 (33%) patients of group A (p < 0.001). Perfusion was significantly reduced during PTRA in 3.3 ± 2.5 regions in group B compared to 1.4 ± 2.5 regions in group A (p < 0.01). Perfusion in the region with maximal reduction during PTRA in groups B and A was 76 ± 15% and 76 ± 15% at baseline, decreased to 56 ± 16% (p < 0.001) and 67 ± 14%, respectively, during PTRA (p < 0.01 A vs. B), and returned to 76 ± 15% and 80 ± 13%, respectively, after PTRA. Nine patients in group B (20%) and two patients in group A (7%) had mild creatine kinase and/or troponin t elevations (p = 0.18). Patients with elevated enzymes had larger perfusion defects than did patients without myocardial injury (4.2 ± 2.7 vs. 2.3 ± 2.5 regions, p < 0.05).
CONCLUSIONS
These data indicate that GPIIb/IIIa blockade reduces incidence, extent and severity of transient hypoperfusion during PTRA. Thus, platelet aggregation may play an important role for PTRA-induced hypoperfusion.
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Abbreviations and Acronyms
| | CK | = creatine kinase | | CK-MB | = creatine kinase MB fraction | | GPIIb/IIIa | = glycoprotein IIb/IIIa | | PTCA | = percutaneous transluminal coronary angioplasty | | PTRA | = percutaneous transluminal rotational atherectomy | | SPECT | = single-photon emission computed tomography | | TrT | = troponin t |
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