doi: 10.1161/hc2301.092121
(Circulation. 2001;103:2780.)
© 2001 American Heart Association, Inc.
Brief Rapid Communications |
Visualization of Discrete Microinfarction After Percutaneous Coronary Intervention Associated With Mild Creatine Kinase-MB Elevation
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
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Abstract |
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Background—Mild elevations in creatine kinase-MB (CK-MB) are common after successful percutaneous coronary interventions and are associated with future adverse cardiac events. The mechanism for CK-MB release remains unclear. A new contrast-enhanced MRI technique allows direct visualization of myonecrosis.
Methods and Results—Fourteen 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.
Conclusions—Contrast-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
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Creatine kinase-MB (CK-MB) elevation occurs in 5% to 30% of patients after percutaneous coronary intervention (PCI)1 2 3 4 5 and is associated with increased mortality.3 4 6 7 Importantly, even patients with minimal CK-MB elevation (<3x upper limit of normal) and otherwise successful PCI seem to be at an increased risk for adverse outcomes.4 6 7 The mechanism responsible for procedure-related CK-MB elevation is unclear. Because the majority of patients have no other clinical evidence of myocardial infarction, there is debate regarding whether myonecrosis has actually occurred.2 5 6 8
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.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Population
All 14 patients without evidence of prior myocardial infarction by history and noninvasive testing who underwent a successful elective PCI at Northwestern Memorial Hospital between August 1999 and August 2000 and who had a cardiac MRI within 4 weeks of PCI (median, 2 days) were investigated. Blood samples for CK and CK-MB were obtained at 4 and at 12 to 24 hours after PCI or until a peak level was established. CK-MB was quantified if the total CK was >100 IU/L. Study patients included 9 with procedure-related CK-MB elevation (>9 ng/mL) and 5 negative controls (no elevation). Four patients (2 in the index group and 2 controls) had rest or prolonged angina and were enrolled only after myocardial infarction was ruled out by serial CK-MB and troponin I determinations to limit the possibility that myocardial necrosis was present before PCI. All patients gave informed consent to the study protocol, which was approved by the Northwestern Institutional Review Board. The safety of performing MRI soon after coronary stent placement has been previously confirmed.11
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.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Characteristics and Procedural Variables
The 14 patients ranged in age from 40 to 77 years (mean, 61 years); 5 (36%) had diabetes mellitus, and 6 (43%) had multivessel coronary disease (Table
).
All had normal left ventricular systolic function
on contrast ventriculography or echocardiography,
and all underwent angiographically successful coronary stent
placement. Twelve (86%) received periprocedural
intravenous glycoprotein IIb/IIIa receptor
blockade. None underwent atherectomy. No patient had angiographic
evidence of distal embolization, thrombus, transient abrupt closure, or
transient slow flow. All had normal TIMI 3 flow at procedure
completion. No patient developed Q-waves. There were no
procedure-related major (>1.5 mm diameter) side-branch
occlusions.
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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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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The mechanism of cardiac enzyme release after otherwise successful PCI has been disputed. Although myocellular necrosis has been implicated, severe ischemia without infarction has also been invoked.5 8 In the current study, all patients with CK-MB elevation had discrete hyperenhancement in the target vessel perfusion territory. None of the CK-MB negative controls had hyperenhancement. Because hyperenhancement is known to occur after irreversible myocellular injury but not after severe but reversible injury, such as myocardial stunning,9 10 the data provide evidence that PCI-related CK-MB elevation is due to new myonecrosis.
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.
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Acknowledgments |
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Supported in part by AHA Scientist Development grant 0030280N (R.J.K.), grant R01-HL64726 (R.J.K.), and grant R01-HL63268 (R.M.J.).
Received February 5, 2001; revision received April 18, 2001; accepted April 25, 2001.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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I. Porto, J. B. Selvanayagam, W. J. Van Gaal, F. Prati, A. Cheng, K. Channon, S. Neubauer, and A. P. Banning Plaque Volume and Occurrence and Location of Periprocedural Myocardial Necrosis After Percutaneous Coronary Intervention: Insights From Delayed-Enhancement Magnetic Resonance Imaging, Thrombolysis in Myocardial Infarction Myocardial Perfusion Grade Analysis, and Intravascular Ultrasound Circulation, August 15, 2006; 114(7): 662 - 669. [Abstract] [Full Text] [PDF]
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S. Mandapaka, R. D'Agostino Jr, and W. G. Hundley Does Late Gadolinium Enhancement Predict Cardiac Events in Patients With Ischemic Cardiomyopathy? Circulation, June 13, 2006; 113(23): 2676 - 2678. [Full Text] [PDF]
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R. Y. Kwong, A. K. Chan, K. A. Brown, C. W. Chan, H. G. Reynolds, S. Tsang, and R. B. Davis Impact of Unrecognized Myocardial Scar Detected by Cardiac Magnetic Resonance Imaging on Event-Free Survival in Patients Presenting With Signs or Symptoms of Coronary Artery Disease Circulation, June 13, 2006; 113(23): 2733 - 2743. [Abstract] [Full Text] [PDF]
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 W. J. Gomes and E. Buffolo Coronary stenting and inflammation: implications for further surgical and medical treatment. Ann. Thorac. Surg., May 1, 2006; 81(5): 1918 - 1925. [Abstract] [Full Text] [PDF]
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H. Thiele, M. J.E. Kappl, S. Conradi, J. Niebauer, R. Hambrecht, and G. Schuler Reproducibility of Chronic and Acute Infarct Size Measurement by Delayed Enhancement-Magnetic Resonance Imaging J. Am. Coll. Cardiol., April 18, 2006; 47(8): 1641 - 1645. [Abstract] [Full Text] [PDF]
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I. Atar, M. E. Korkmaz, I. A. Atar, O. Gulmez, B. Ozin, H. Bozbas, T. Erol, A. Aydinalp, A. Yildirir, M. Yucel, et al. Effects of metoprolol therapy on cardiac troponin-I levels after elective percutaneous coronary interventions Eur. Heart J., March 1, 2006; 27(5): 547 - 552. [Abstract] [Full Text] [PDF]
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J. Herrmann Peri-procedural myocardial injury: 2005 update Eur. Heart J., December 1, 2005; 26(23): 2493 - 2519. [Abstract] [Full Text] [PDF]
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D. L. Bhatt and E. J. Topol Periprocedural Cardiac Enzyme Elevation Predicts Adverse Outcomes Circulation, August 9, 2005; 112(6): 906 - 922. [Full Text] [PDF]
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D. E. Cutlip and R. E. Kuntz Cardiac Enzyme Elevation After Successful Percutaneous Coronary Intervention Is Not an Independent Predictor of Adverse Outcomes Circulation, August 9, 2005; 112(6): 916 - 923. [Full Text] [PDF]
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C. Cavallini, S. Savonitto, R. Violini, G. Arraiz, M. Plebani, Z. Olivari, P. Rubartelli, S. Battaglia, L. Niccoli, G. Steffenino, et al. Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study Eur. Heart J., August 1, 2005; 26(15): 1494 - 1498. [Abstract] [Full Text] [PDF]
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H. Mahrholdt, A. Wagner, R. M. Judd, U. Sechtem, and R. J. Kim Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies Eur. Heart J., August 1, 2005; 26(15): 1461 - 1474. [Abstract] [Full Text] [PDF]
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V. Fuster and R. J. Kim Frontiers in Cardiovascular Magnetic Resonance Circulation, July 5, 2005; 112(1): 135 - 144. [Full Text] [PDF]
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D. Bello, D. S. Fieno, R. J. Kim, F. S. Pereles, R. Passman, G. Song, A. H. Kadish, and J. J. Goldberger Infarct morphology identifies patients with substrate for sustained ventricular tachycardia J. Am. Coll. Cardiol., April 5, 2005; 45(7): 1104 - 1108. [Abstract] [Full Text] [PDF]
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M. J. Claeys, M. G. Van der Planken, J. M. Bosmans, J. J. Michiels, F. Vertessen, P. Van Der Goten, F. L. Wuyts, and C. J. Vrints Does pre-treatment with aspirin and loading dose clopidogrel obviate the need for glycoprotein IIb/IIIa antagonists during elective coronary stenting? A focus on peri-procedural myonecrosis Eur. Heart J., March 2, 2005; 26(6): 567 - 575. [Abstract] [Full Text] [PDF]
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J. B. Selvanayagam, I. Porto, K. Channon, S. E. Petersen, J. M. Francis, S. Neubauer, and A. P. Banning Troponin Elevation After Percutaneous Coronary Intervention Directly Represents the Extent of Irreversible Myocardial Injury: Insights From Cardiovascular Magnetic Resonance Imaging Circulation, March 1, 2005; 111(8): 1027 - 1032. [Abstract] [Full Text] [PDF]
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R. Y. Kwong and R. H. Falk Cardiovascular Magnetic Resonance in Cardiac Amyloidosis Circulation, January 18, 2005; 111(2): 122 - 124. [Full Text] [PDF]
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J. B. Selvanayagam, S. Neubauer, and D. P. Taggart Quantification of peri-operative myocardial infarction after coronary artery bypass surgery Eur. Heart J., December 1, 2004; 25(23): 2171 - 2171. [Full Text] [PDF]
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V. Pasceri, G. Patti, A. Nusca, C. Pristipino, G. Richichi, G. Di Sciascio, and on behalf of the ARMYDA Investigators Randomized Trial of Atorvastatin for Reduction of Myocardial Damage During Coronary Intervention: Results From the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) Study Circulation, August 10, 2004; 110(6): 674 - 678. [Abstract] [Full Text] [PDF]
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J. C. C. Moon, D. Perez De Arenaza, A. G. Elkington, A. K. Taneja, A. S. John, D. Wang, R. Janardhanan, R. Senior, A. Lahiri, P. A. Poole-Wilson, et al. The pathologic basis of Q-wave and non-Q-wave myocardial infarction: A cardiovascular magnetic resonance study J. Am. Coll. Cardiol., August 4, 2004; 44(3): 554 - 560. [Abstract] [Full Text] [PDF]
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A. E. Arai and G. A. Hirsch Q-wave and non-q-wave myocardial infarctions through the eyes of cardiac magnetic resonance imaging J. Am. Coll. Cardiol., August 4, 2004; 44(3): 561 - 563. [Full Text] [PDF]
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P. Schoenhagen The emerging role of delayed contrast-enhanced magnetic resonance imaging in the peri-operative evaluation of patients undergoing coronary revascularisation Eur. Heart J., August 1, 2004; 25(15): 1279 - 1280. [Full Text] [PDF]
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J. Steuer, T. Bjerner, O. Duvernoy, L. Jideus, L. Johansson, H. Ahlstrom, E. Stahle, and B. Lindahl Visualisation and quantification of peri-operative myocardial infarction after coronary artery bypass surgery with contrast-enhanced magnetic resonance imaging Eur. Heart J., August 1, 2004; 25(15): 1293 - 1299. [Abstract] [Full Text] [PDF]
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W. P. Ingkanisorn, K. L. Rhoads, A. H. Aletras, P. Kellman, and A. E. Arai Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2253 - 2259. [Abstract] [Full Text] [PDF]
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K. Shan, G. Constantine, M. Sivananthan, and S. D. Flamm Role of Cardiac Magnetic Resonance Imaging in the Assessment of Myocardial Viability Circulation, March 23, 2004; 109(11): 1328 - 1334. [Full Text] [PDF]
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M.T. Roe, K.W. Mahaffey, R. Kilaru, J.H. Alexander, K.M. Akkerhuis, M.L. Simoons, R.A. Harrington, B.E. Tardiff, C.B. Granger, E.M. Ohman, et al. Creatine kinase-MB elevation after percutaneous coronary intervention predicts adverse outcomes in patients with acute coronary syndromes Eur. Heart J., February 2, 2004; 25(4): 313 - 321. [Abstract] [Full Text] [PDF]
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H. P. Kuhl, T. S. Papavasiliu, A. M. Beek, M. B. M. Hofman, N. S. Heusen, and A. C. van Rossum Myocardial Viability: Rapid Assessment with Delayed Contrast-enhanced MR Imaging with Three-dimensional Inversion-Recovery Prepared Pulse Sequence Radiology, February 1, 2004; 230(2): 576 - 582. [Abstract] [Full Text] [PDF]
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J. B. Selvanayagam, S. E. Petersen, J. M. Francis, M. D. Robson, A. Kardos, S. Neubauer, and D. P. Taggart Effects of Off-Pump Versus On-Pump Coronary Surgery on Reversible and Irreversible Myocardial Injury: A Randomized Trial Using Cardiovascular Magnetic Resonance Imaging and Biochemical Markers Circulation, January 27, 2004; 109(3): 345 - 350. [Abstract] [Full Text] [PDF]
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W. G. van Dockum, F. J. ten Cate, J. M. ten Berg, A. M. Beek, J. W. R. Twisk, J. Vos, M. B. M. Hofman, C. A. Visser, and A. C. van Rossum Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging J. Am. Coll. Cardiol., January 7, 2004; 43(1): 27 - 34. [Abstract] [Full Text] [PDF]
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D. O. Williams A twist in our understanding of enzyme elevation after coronary intervention J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1906 - 1908. [Full Text] [PDF]
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B. K. Nallamothu and E. R. Bates Periprocedural myocardial infarction and mortality: Causality versus association J. Am. Coll. Cardiol., October 15, 2003; 42(8): 1412 - 1414. [Full Text] [PDF]
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C. J. White Angiographic predictors of adverse outcomes in the modern interventional era J. Am. Coll. Cardiol., September 17, 2003; 42(6): 989 - 990. [Full Text] [PDF]
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R. Y. Kwong, A. E. Schussheim, S. Rekhraj, A. H. Aletras, N. Geller, J. Davis, T. F. Christian, R. S. Balaban, and A. E. Arai Detecting Acute Coronary Syndrome in the Emergency Department With Cardiac Magnetic Resonance Imaging Circulation, February 4, 2003; 107(4): 531 - 537. [Abstract] [Full Text] [PDF]
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A. S. Kini, P. Lee, C. A. Mitre, M. E. Duffy, and S. K. Sharma Postprocedure chest pain after coronary stenting: implications on clinical restenosis J. Am. Coll. Cardiol., January 1, 2003; 41(1): 33 - 38. [Abstract] [Full Text] [PDF]
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L. Choudhury, H. Mahrholdt, A. Wagner, K. M. Choi, M. D. Elliott, F. J. Klocke, R. O. Bonow, R. M. Judd, and R. J. Kim Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., December 18, 2002; 40(12): 2156 - 2164. [Abstract] [Full Text] [PDF]
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S. J. Brener, B. W. Lytle, J. P. Schneider, S. G. Ellis, and E. J. Topol Association between CK-MB elevation after percutaneous or surgical revascularization and three-year mortality J. Am. Coll. Cardiol., December 4, 2002; 40(11): 1961 - 1967. [Abstract] [Full Text] [PDF]
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J. R. Guyton Clinical Assessment of Atherosclerotic Lesions: Emerging From Angiographic Shadows Circulation, September 10, 2002; 106(11): 1308 - 1309. [Full Text] [PDF]
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E. C. Perin, G. V. Silva, R. Sarmento-Leite, A. L.S. Sousa, M. Howell, R. Muthupillai, B. Lambert, W. K. Vaughn, and S. D. Flamm Assessing Myocardial Viability and Infarct Transmurality With Left Ventricular Electromechanical Mapping in Patients With Stable Coronary Artery Disease: Validation by Delayed-Enhancement Magnetic Resonance Imaging Circulation, August 20, 2002; 106(8): 957 - 961. [Abstract] [Full Text] [PDF]
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