Troponin Elevation After Percutaneous Coronary Intervention Directly Represents the Extent of Irreversible Myocardial Injury: Insights From Cardiovascular Magnetic Resonance Imaging

Background—Although troponin elevation after percutaneous coronary intervention (PCI) is common, uncertainties remain about the mechanisms of its release and its relationship to the volume of myocardial tissue loss. Delayed-enhancement MRI of the heart has been shown to reliably quantify areas of irreversible myocardial injury. To investigate the quantitative relationship between irreversible injury and cardiac troponin release, we studied the incidence and extent of new irreversible injury in patients undergoing PCI and correlated it to postprocedural changes in cardiac troponin I. Methods and Results—Fifty patients undergoing PCI were studied with preprocedural and postprocedural (24 hours) delayed-enhancement MRI for assessment of new irreversible myocardial injury. Cardiac troponin I measurements were obtained before PCI and 24 hours after PCI. Of these 50 patients, 24 underwent a further third MRI scan at a median of 8 months after the procedure. Mean patient age was 64±12 years. After the procedure, 14 patients (28%) had evidence of new myocardial hyperenhancement, with a mean mass of 6.0±5.8 g, or 5.0±4.8% of total left ventricular mass. All of these patients had raised troponin I levels (range 1.0 to 9.4 &mgr;g/L). Thirty-four patients (68%) had no elevated troponin I and no evidence of new myocardial necrosis on MRI. There was a strong correlation between the rise in troponin I measurements at 24 hours and mean mass of new myocardial hyperenhancement, both early (r=0.84; P<0.001) and late (r=0.71; P<0.001) after PCI, although there was a trend for a reduction in the size of PCI-induced myocardial injury in the late follow-up scan (P=0.07). Conclusions—In the setting of PCI, patients demonstrating postprocedural elevation in troponin I have evidence of new irreversible myocardial injury on delayed-enhancement MRI. The magnitude of this injury correlates directly with the extent of troponin elevation.

[1]  Stefan Neubauer,et al.  Value of Delayed-Enhancement Cardiovascular Magnetic Resonance Imaging in Predicting Myocardial Viability After Surgical Revascularization , 2004, Circulation.

[2]  M. Robson,et al.  Anteroseptal or apical myocardial infarction: a controversy addressed using delayed enhancement cardiovascular magnetic resonance imaging. , 2004, Journal of Cardiovascular Magnetic Resonance.

[3]  Peter Kellman,et al.  Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction. , 2004, Journal of the American College of Cardiology.

[4]  Matthew D. Robson,et al.  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 , 2004, Circulation.

[5]  T. Nageh,et al.  Cardiac troponin T and I and creatine kinase-MB as markers of myocardial injury and predictors of outcome following percutaneous coronary intervention. , 2003, International journal of cardiology.

[6]  F. Burzotta,et al.  Stenting of Culprit Lesions in Unstable Angina Leads to a Marked Reduction in Plaque Burden: A Major Role of Plaque Embolization?: A Serial Intravascular Ultrasound Study , 2003, Circulation.

[7]  R. Kim,et al.  Contrast-enhanced MRI and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study , 2003, The Lancet.

[8]  H. White.  Things ain't what they used to be: impact of a new definition of myocardial infarction. , 2002, American heart journal.

[9]  V. Hasselblad,et al.  Prognostic significance of elevated troponin I after percutaneous coronary intervention. , 2002, Journal of the American College of Cardiology.

[10]  Wolfgang G Rehwald,et al.  Myocardial Magnetic Resonance Imaging Contrast Agent Concentrations After Reversible and Irreversible Ischemic Injury , 2002, Circulation.

[11]  R. Kim,et al.  Visualization of Discrete Microinfarction After Percutaneous Coronary Intervention Associated With Mild Creatine Kinase-MB Elevation , 2001, Circulation.

[12]  J. Kao,et al.  Comparison of Abbott AxSYM, Behring Opus Plus, DPC Immulite and Ortho-Clinical Diagnostics Vitros ECi for measurement of cardiac troponin I , 2001, Annals of clinical biochemistry.

[13]  Edwin Wu,et al.  Visualisation of presence, location, and transmural extent of healed Q-wave and non-Q-wave myocardial infarction , 2001, The Lancet.

[14]  D. Atar,et al.  Cardiac Troponin I Is Modified in the Myocardium of Bypass Patients , 2001, Circulation.

[15]  J S Alpert,et al.  Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. , 2000, Journal of the American College of Cardiology.

[16]  Hugo A. Katus,et al.  Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. , 2000, European heart journal.

[17]  F. Apple.  Tissue specificity of cardiac troponin I, cardiac troponin T and creatine kinase-MB. , 1999, Clinica chimica acta; international journal of clinical chemistry.

[18]  Katherine C. Wu,et al.  Quantification and time course of microvascular obstruction by contrast-enhanced echocardiography and magnetic resonance imaging following acute myocardial infarction and reperfusion. , 1998, Journal of the American College of Cardiology.

[19]  Katherine C. Wu,et al.  Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. , 1998, Circulation.

[20]  R. Califf,et al.  Myonecrosis after revascularization procedures. , 1998, Journal of the American College of Cardiology.

[21]  V. Paul,et al.  Recruited collateral channels are not responsible for ischemic preconditioning during single vessel angioplasty , 1998 .

[22]  A. Distante,et al.  Asymmetrical effects of angiographically assessed collateral flow on vasodilator and exercise stress-induced ischemia , 1998 .

[23]  H. Arnesen,et al.  Myocardial damage during percutaneous transluminal coronary angioplasty as evidenced by troponin T measurements. , 1998, European heart journal.

[24]  S W Sharkey,et al.  Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I. , 1997, Clinical chemistry.

[25]  R. Kim,et al.  Myocardial Gd-DTPA kinetics determine MRI contrast enhancement and reflect the extent and severity of myocardial injury after acute reperfused infarction. , 1996, Circulation.

[26]  M. Jenkins,et al.  Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations. , 1996, The Annals of thoracic surgery.

[27]  J. Ravkilde,et al.  Cardiac troponin T and CK-MB mass release after visually successful percutaneous transluminal coronary angioplasty in stable angina pectoris. , 1994, American heart journal.

[28]  J. Lowe,et al.  The Wavefront Phenomenon of Ischemic Cell Death: 1. Myocardial Infarct Size vs Duration of Coronary Occlusion in Dogs , 1977, Circulation.