(Circulation. 2001;103:2780.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
From Feinberg Cardiovascular Institute (M.J.R., C.J.D., K.M.C., F.J.K., R.O.B., R.M.J., R.J.K.) and the Departments of Medicine (M.J.R., E.W., C.J.D., K.M.C., F.J.K., R.O.B., R.M.J., R.J.K.) and Biomedical Engineering (R.M.J.), Northwestern University, Chicago, Ill.
Correspondence to Raymond J. Kim, 303 East Chicago Ave, Tarry 12-733, Chicago, IL 60611-3008. E-mail r-kim4{at}northwestern.edu
| Abstract |
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Methods and ResultsFourteen patients without prior infarction underwent cine and contrast-enhanced MRI after successful coronary stenting; 9 patients had procedure-related CK-MB elevation, and 5 did not (negative controls). The mean age of all patients was 61 years, 36% had diabetes, 43% had multivessel coronary artery disease, and all had a normal ejection fraction. Twelve patients (86%) received an intravenous glycoprotein IIb/IIIa inhibitor; none underwent atherectomy, and all had final TIMI 3 flow. Of the 9 patients with CK-MB elevation, 5 had a minor side branch occlusion during stenting, 2 had transient ECG changes, and none developed Q-waves. The median CK-MB was 21 ng/mL (range, 12 to 93 ng/mL), which is 2.3x the upper limit of normal. Contrast-enhanced MRI demonstrated discrete regions of hyperenhancement within the target vessel perfusion territory in all 9 patients. Only one developed a new wall motion abnormality. The median estimated mass of myonecrosis was 2.0 g (range, 0.7 to 12.2 g), or 1.5% of left ventricular mass (range, 0.4% to 6.0%). Hyperenhancement persisted in 5 of the 6 who underwent a repeat MRI at 3 to 12 months. No control patient had hyperenhancement.
ConclusionsContrast-enhanced MRI provides an anatomical correlate to biochemical evidence of procedure-related myocardial injury, despite the lack of ECG changes or wall motion abnormalities. Mild elevation of CK-MB after percutaneous coronary intervention is the result of discrete microinfarction.
Key Words: creatine kinase magnetic resonance imaging angioplasty
| Introduction |
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The ability to identify and quantify myocardial necrosis in vivo has recently been demonstrated using a contrast-enhanced MRI technique, in which infarcted tissue is distinguished as a hyperenhanced region.9 10 Because this technique is capable of visualizing small regions of myonecrosis that are not otherwise evident with noninvasive myocardial imaging, we hypothesized that contrast-enhanced MRI would provide a direct anatomical correlate to biochemical evidence of myocardial injury in patients undergoing successful PCI and, therefore, provide insight into the mechanism of procedure-related CK-MB elevation.
| Methods |
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MRI Protocol
Cine images were acquired on a 1.5T scanner
(Siemens Sonata) with full
ventricular
coverage.12
Contrast-enhanced images were acquired 5 to 10 minutes after
intravenous gadoteridol administration (0.1 mmol/kg)
using a breath-hold segmented gradient-echo pulse sequence, as
previously described.13 This
sequence produces strongly T1-weighted images due to the use of an
inversion pulse before image acquisition. In 2 of the 9 patients with
CK-MB elevation, MRI was performed before and after PCI. Six of the
patients with CK-MB elevation had a follow-up MRI at 3 to 12
months.
Image Analysis
Regional wall motion from the cine MRI, regional
contrast-enhancement from the contrast-enhanced MRI, and the perfusion
territory of the target vessel from the coronary angiogram were
scored by the consensus of 2 observers using a 14-segment
model.12 Each modality was
interpreted with the observer blinded to patient identity and to the
results of the other
modalities.
| Results |
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Of the 9 patients in the CK-MB elevation group, 5 had
intraprocedural occlusion of a minor side branch (
1.5 mm
diameter), one developed medial dissection (which resolved with
stenting), and 2 had transient ST-segment changes during the procedure
that resolved spontaneously. These findings were absent in the control
patients. Procedural vessel location did not differ between groups. In
those with CK-MB elevation, the median peak CK and CK-MB were 245 IU/L
(range, 146 to 709 IU/L) and 21 ng/mL (range, 12 to 93 ng/mL),
respectively. Six of the 9 peak CK-MB levels were <3x the upper limit
of normal (median, 2.3-fold elevation).
MRI Findings
All patients with procedure-related CK-MB elevation had
myocardial hyperenhancement within the target vessel perfusion
territory. Hyperenhancement was not observed in the control patients.
Hyperenhancement was present immediately adjacent to the implanted
stent in 3 patients, all of whom developed minor side-branch occlusion.
Figure 1
shows examples of this pattern of hyperenhancement
in 2 of these patients. In the remaining 6 patients, the
hyperenhancement was located more distally in the
myocardium subtended by the stented artery.
Figure 2
shows examples of this hyperenhancement pattern.
Assuming a myocardial specific gravity of 1.05
g/cm3, the median mass of infarcted tissue
based on the volume of hyperenhanced myocardium was
2.0 g (range, 0.7 to 12.2 g), or 1.5% of the mass of the
left ventricle (range, 0.4% to 6.0%). The mass of infarcted tissue
was related to the peak CK-MB level
(r=0.61,
P=0.02). Only one patient with
CK-MB elevation developed a new regional wall motion abnormality by
cine MRI. Hyperenhancement persisted in 5 of 6 patients who underwent
repeat MRI at 3 to 12 months
(Figures 1
and 2
).
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| Discussion |
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Our results are consistent with a recent consensus document on the redefinition of myocardial infarction, which states that despite the lack of complementary clinical evidence, a typical rise and fall of cardiac enzymes recovered from blood samples after PCI should be considered an acute myocardial infarction.14 One potential limitation of the present study is the lack of uniform MRI testing before PCI to rule out preexisting infarction. However, careful patient selection to limit this possibility, the lack of hyperenhancement in the control group, and the significant correlation between procedural CK-MB peak level and hyperenhancement mass (r=0.61, P=0.02) strongly suggest that the infarction occurred at the time of PCI.
Peak CK-MB level >3x the upper limit of normal has been recommended as the threshold for determining an infarction in the setting of PCI.3 5 In the current study, the majority of patients with hyperenhancement had CK-MB levels less than this threshold (6 of 9 patients). Perhaps because of the small amount of necrosis (median, 2 g), only 2 patients had transient ECG changes, none developed Q-waves, and only one developed a new wall motion abnormality. As a point of comparison, we note that, in general, >10 g of myocardial tissue must be injured before detection by radionuclide perfusion imaging.14
Myonecrosis in the setting of successful PCI may result from transient vessel closure, side-branch compromise, coronary dissection, and distal embolization.5 6 7 Interestingly, we observed 2 different patterns of myonecrosis in the current study. In 3 patients, the necrotic tissue was immediately adjacent to the implanted stent, whereas in the remaining 6 patients, the necrotic tissue was located more distally in the myocardium subtended by the stented artery. All 3 patients with myonecrosis immediately adjacent to the stent had incidental minor side-branch occlusion. No patient had angiographic evidence of transient abrupt closure, thrombus, distal embolization, or major (>1.5 mm) side-branch occlusion. The cohort studied is representative of contemporary coronary interventions with a predominance of stent use (100%) and adjunctive glycoprotein IIb/IIIa receptor blockade (86%). In this cohort, the data support 2 pathways by which myonecrosis occurs after successful PCI: (1) incidental minor side-branch occlusion and (2) microvascular obstruction from distal embolization of plaque contents (platelets, thrombus, and/or atheroma).
The process by which procedural CK-MB elevation confers increased risk for future adverse outcomes was not addressed, nor can we conclude whether the level of increased risk is the same for the 2 patterns of myonecrosis observed. This issue will require further investigation.
In summary, this study is the first to provide an anatomic correlate to biochemical evidence of myocardial injury during PCI. The findings indicate that CK-MB elevation after PCI is the result of discrete microinfarction.
| Acknowledgments |
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Received February 5, 2001; revision received April 18, 2001; accepted April 25, 2001.
| References |
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