Author + information
- Received December 10, 1985
- Revision received March 26, 1986
- Accepted April 1, 1986
- Published online October 1, 1986.
- Robert M. Knabb, PhD1,
- Thomas L. Rosamond, MD1,
- Keith A.A. Fox, MB, ChB1,
- Burton E. Sobel, MD, FACC1 and
- Steven R. Bergmann, MD, PhD1,*
- ↵*Address for reprints: Steven R. Bergmann, MD, PhD, Cardiovascular Division, Washington University School of Medicine, 660 South Euclid Avenue, Box 8086, St. Louis, Missouri 63110.
Concomitant use of pharmacologie agents may be required for maximal salvage of ischemic myocardium by reperfusion. Accordingly, in dogs with induced thrombotic coronary occlusion, the effects of intravenous dil-tiazem given 30 minutes before administration of streptokinase on myocardial blood flow and myocardial salvage were evaluated. Two independent types of end points were employed. Positron emission tomography was utilized for noninvasive assessment of myocardial perfusion and infarct extent. Direct measurements included quantification of myocardial infarction by assay of creatine kinase activity in myocardial homogenates. Infarct extent averaged 27.9 ± 11.4% of left ventricular weight in 10 control dogs in which coronary occlusion was maintained for 24 hours. In eight dogs given streptokinase alone, the infarct extent averaged 16.7 ± 10.0% of left ventricular mass (p < 0.05 versus control). In nine other dogs given diltiazem (15 μg/kg per min continuously until death was induced) beginning 30 minutes before streptokinase, infarct extent averaged 9.4 ± 6.7% of left ventricular mass (p < 0.05 compared with reperfusion alone). At the dose administered, diltiazem did not alter blood flow, heart rate or mean arterial pressure after coronary occlusion or thrombolysis.
The region at risk, determined in 16 dogs from perfusion images obtained with positron tomography and oxygen-15-labeled water after coronary occlusion, was similar in the three groups (30.6 ± 7.3% of the left ventricle in six control dogs, 31.8 ± 4.5% in five dogs with reperfusion alone and 30.5 ± 11.6% in five dogs with reperfusion plus diltiazem). Infarct size quantified in terms of the extent of myocardium exhibiting less than 50% of peak carbon-11-labeled palmitate uptake 24 hours after occlusion and expressed as the percent of the region at risk averaged 89.6 ± 11.4% in control dogs, was significantly reduced to 45.1 ± 29.8% in dogs with re-perfusion alone and was reduced further to 22.3 ± 16.4% in dogs given diltiazem and reperfusion. Thus, concomitant treatment with diltiazem markedly enhances salvage of reperfused myocardium after coronary thrombolysis.
- Received December 10, 1985.
- Revision received March 26, 1986.
- Accepted April 1, 1986.
- American College of Cardiology Foundation