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(Circulation. 2000;101:604.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Atherosclerotic Plaque Burden and CK-MB Enzyme Elevation After Coronary Interventions
Intravascular Ultrasound Study of 2256 Patients
Presented in part at the 71st Scientific Sessions of the American Heart Association, Dallas, Tex, November 8–11, 1998, and published in abstract form (Circulation. 1998;98[suppl I]:I-496.).
From the Cardiovascular Research Foundation, New York and the Cardiac Catheterization Laboratory, Washington Hospital Center, Washington, DC.
Correspondence to George Dangas, MD, PhD, Cardiovascular Research Foundation, 55 East 59th Street, 6th Floor, New York, NY 10022.
Background—Elevation of serum creatine kinase MB fraction (CK-MB) after percutaneous coronary interventions has been associated with early and late mortality; however, the pathogenesis of CK-MB elevation is still unknown. We hypothesized that CK-MB elevation was related to atherosclerotic plaque burden as assessed by preintervention intravascular ultrasound (IVUS).
Methods and Results—We studied 2256 consecutive patients who
underwent intervention of 2780 native coronary lesions and had
complete high-quality preintervention IVUS imaging in the era before
routine use of platelet glycoprotein IIb/IIIa
inhibitors. Patients were divided into 3 groups: CK-MB
within normal range (1675 patients; 2061 lesions); CK-MB elevation 1 to
5 times upper limit of normal (292 patients; 355 lesions); and CK-MB
elevation 
5 times upper limit of normal (289 patients; 364 lesions).
Qualitative angiographic lesion morphology and quantitative
analysis were similar among the 3 groups. On preintervention
IVUS, progressively more reference segment and lesion site plaque
burden and lesion site calcium occurred in the groups with CK-MB
elevation. Positive remodeling was more common in lesions with CK-MB
elevation. As levels of CK-MB increased, cross-sectional narrowing
(percentage plaque burden) increased, both at the reference site (mean
cross-sectional narrowing values were 45.1%, <49.3%, and <52.2%
for normal CK-MB, 1 to 5 times upper limit of normal, and 5 times
upper limit of normal groups, respectively; P=0.03) and
at the lesion site (81.9%, <85.4%, and <87.1%, respectively;
P=0.04). Multivariate analysis
indicated that de novo lesions, atheroablative technique, plaque burden
at the lesion and reference segments, and final minimal lumen diameter
were independent predictors of CK-MB elevation.
Conclusions—CK-MB elevation correlates with a greater atherosclerotic plaque burden. CK-MB elevation after intervention may be a marker of diffuse atherosclerotic disease or a consequence of catheter-based intervention in more diseased arteries or both.
Key Words: necrosis, myocardial • angioplasty • stents
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