Author + information
- Received November 1, 1988
- Revision received March 8, 1989
- Accepted April 4, 1989
- Published online October 1, 1989.
- Ryuji Nohara, MD,
- Donald W. Myears, MD,
- Burton E. Sobel, MD, FACC and
- Dana R. Abendschein, PhD∗
- ↵∗Address for reprints: Dana R. Abendschein, PhD, Washington University School of Medicine, Cardiovascular Division, Box 8086, 660 South Euclid Avenue, St. Louis, Missouri 63110.
Analysis of isoforms of MM creatine kinase (CK) in plasma is being developed as a means for rapid detection of coronary recanalization in patients given thrombolytic agents. To determine whether flow-limiting residual stenosis typical of that seen in patients affects plasma isoform profiles, stenosis sufficient to preclude reactive hyperemia was induced in dogs before coronary occlusion, followed by recanalization in 2 h. Plasma activities of the MM CK isoform released from myocardium (MM3) and its two conversion products elaborated sequentially (MM2and MM1) were assayed in serial samples with a rapid quantitative chromatofocusing procedure.
Reperfusion in 10 dogs shortened the mean intervals (±SD) to the occurrence of peak MM3activity (3.7 ± 0.9 h), peak MM3expressed as a percent of total CK activity (MM3%, 2.5 ± 0.3 h) and the maximal ratio of MM3to MM1(2.7 ± 0.3 h) compared with results in 10 control dogs without reperfusion. Nevertheless, the appearance of these peaks was delayed by 8% to 57% when residual stenosis was present. In contrast, the rate of increase of MM3% was delineated before the peak, was fivefold greater with recanalization (1.19 ± 0.46 versus 0.26 ± 0.11% min−1in control dogs) and was not attenuated by residual stenosis. Thus, this criterion appears capable of delineating recanalization early after thrombolysis whether or not high grade residual stenosis is present.
☆ This research was supported in part by Grants HL 36274 and HL 17646 SCOR in Ischemic Heart Disease from the National Institutes of Health, Bethesda, Maryland.
- Received November 1, 1988.
- Revision received March 8, 1989.
- Accepted April 4, 1989.