CLINICAL RESEARCH: CARDIAC MAGNETIC RESONANCE
Infarct morphology identifies patients with substrate for sustained ventricular tachycardia
David Bello, MD,
David S. Fieno, PhD,
Raymond J. Kim, MD,
F. Scott Pereles, MD,
Rod Passman, MD, FACC,
Gina Song, BA,
Alan H. Kadish, MD, FACC and
Jeffrey J. Goldberger, MD, FACC*
Department of Medicine, Divisions of Cardiology and Radiology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois
Manuscript received July 2, 2004;
accepted December 14, 2004.
* Reprint requests and correspondence: Dr. Jeffrey J. Goldberger, Feinberg School of Medicine, Northwestern University, Division of Cardiac Electrophysiology, 251 East Huron, Feinberg Pavilion 8-542, Chicago, Illinois 60611 (Email: j-goldberger{at}northwestern.edu).
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Abstract
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OBJECTIVES: We sought to evaluate whether infarct size characterization by cardiac magnetic resonance imaging (MRI) is a better predictor of inducible ventricular tachycardia (VT) than left ventricular ejection fraction (LVEF).
BACKGROUND: Inducibility of VT at electrophysiologic study (EPS) and low LVEF can identify patients with a substrate for VT. Magnetic resonance imaging has been shown to identify, with high precision, areas of myocardial infarction and may therefore be a better tool to evaluate for a substrate for VT.
METHODS: We studied 48 patients with known coronary artery disease who were referred for EPS using cine and gadolinium-enhanced MRI. Wall motion and infarct characteristics were determined blindly and compared among patients with no inducible ventricular arrhythmias (n = 21), those with inducible monomorphic VT (MVT, n = 18), and those with either inducible polymorphic VT or ventricular fibrillation (n = 9).
RESULTS: Patients with MVT had larger infarcts than patients who did not have inducible arrhythmias (mass: 49 ± 5 g [SE] vs. 28 ± 5 g, p < 0.005; surface area: 172 ± 15 cm2 vs. 93 ± 14 cm2, p < 0.0005). Patients with polymorphic VT/fibrillation had intermediate values (mass: 36 ± 7 g; surface area: 115 ± 22 cm2). Ejection fraction was inversely related to infarct mass and surface area, with R2 values ranging from 0.21 to 0.27. Logistic regression and receiver-operating characteristic analysis demonstrated that infarct mass and surface area were better predictors of inducibility of MVT than LVEF.
CONCLUSIONS: Infarct surface area and mass, as measured by cardiac MRI, are better identifiers of patients who have a substrate for MVT than LVEF. Further evaluation of infarct size characterization by cardiac MRI as a predictor of sudden cardiac death is warranted.
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Abbreviations and Acronyms
| | CAD = coronary artery disease | | ceMRI = contrast-enhanced magnetic resonance imaging | | EPS = electrophysiologic study | | LVEF = left ventricular ejection fraction | | MRI = magnetic resonance imaging | | MVT = monomorphic ventricular tachycardia | | PVT = polymorphic ventricular tachycardia | | ROC = receiver-operating characteristic | | VF = ventricular fibrillation | | VT = ventricular tachycardia |
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Sudden cardiac death in patients with coronary artery disease (CAD) is predominantly caused by ventricular tachycardia (VT)/ventricular fibrillation (VF). Patients with a low left ventricular ejection fraction (LVEF) and inducible VT during electrophysiologic study (EPS) are at risk of sudden death and may benefit from implantable cardioverter-defibrillator (ICD) therapy (1–3). Low LVEF and VT inducibility identify a substrate for VT. Ventricular tachycardia occurs more commonly in the setting of larger infarcts (4–7), and LVEF is inversely related to infarct size (8–11). Furthermore, EPS directly establishes the presence of a substrate by the actual induction of VT. To date, there is only indirect information relating infarct size or morphology to the presence of a substrate for VT in humans. Contrast-enhanced magnetic resonance imaging (ceMRI) with a gadolinium-based contrast agent has been shown to identify, with high precision, areas of myocardial infarction in both animals (12,13) and humans (14–16). We hypothesized that infarct size and/or morphology detected by ceMRI is a better predictor of EPS inducibility of VT than LVEF.
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Methods
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Forty-eight patients with CAD referred for EPS to assess for inducibility of VT were enrolled in accordance with the policies of the Institutional Review Board. Patients underwent MRI scanning within 32 ± 6 days of EPS. Patients were placed supine in a 1.5-T Magnetom Sonata scanner (Siemens, Medical Solutions, Malvern, Pennsylvania); fiberoptic electrocardiographic (ECG) leads were placed for scanner gating and a phased-array receiver coil was placed on the chest for imaging. All images were acquired using 10- to 15-s breath-holds. Short-axis slices were acquired from the base to apex, making sure to include the entire left ventricle using methods previously described (16,17). A gadolinium-based contrast agent (0.1 to 0.2 mmol/kg, Magnevist, Berlex Pharmaceuticals, Wayne, New Jersey) was administered intravenously, and images were obtained as described previously (15).
Image data sets were scored by reviewers blinded to the EPS results. All images were reviewed off-line and arranged from base to apex using National Institutes of Health (NIH) Image Software. The presence of a ventricular aneurysm and segmental wall motion abnormalities was noted. Endocardial and epicardial borders of the myocardium were manually planimetered on the short-axis cine images for each patient. Volumes were derived by summation of the pixel areas, followed by multiplication of in-plane resolution and the effective slice thickness. The LVEF was computed as:
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Left ventricular mass was determined by subtracting endocardial volume from epicardial volume at end diastole and multiplying by a density of 1.05 g/ml (18). Infarct morphology was evaluated using the ceMRI images. The presence of myocardial infarction, its location, and the degree of transmurality were agreed upon by two observers. To measure infarct mass and surface area, the infarct region was outlined according to whether the image intensity was  2 SD that of a remote region in the same slice. From the contours, a pixel value was computed for the area and surface of each individual infarct territory. Based on the pixel values, the image resolution and slice thickness, and an assumed density of 1.05 g/ml, the pixel values were converted into actual cardiac masses and surface areas. Infarct surface area and infarct mass (absolute and percent left ventricular mass) were calculated. The surface area to volume ratio was calculated as an index of complex infarct morphology.
Electrophysiologic study was performed using standard techniques. Programmed ventricular stimulation was performed using up to three extrastimuli at two right ventricular sites during two drive-cycle lengths. Study end points were either induction of sustained VT or completion of the study protocol. Results were classified as: 1) inducible, sustained monomorphic VT (MVT); 2) inducible polymorphic VT (PVT, >15 complexes), VF, or ventricular flutter; or 3) no inducible VT/VF. Induction of MVT is highly reproducible (19,20) and typically identifies the presence of a fixed substrate for reentry (20). In contrast, induction of PVT/VF may be nonspecific due to aggressive stimulation; these arrhythmias can be induced in patients with normal hearts and normal QT intervals (21–24). Yet, PVT/VF is commonly induced in survivors of cardiac arrest (22,25). Thus, in order to evaluate the utility of infarct characteristics identified by MRI to identify patients with a substrate for VT, the main analysis of this report focuses on patients with inducible MVT versus those without inducible VT/VF.
Data are presented as the mean value ± SE. Linear and logistic regression analysis, analysis of variance, contingency analysis, and the t test or Fisher exact test were used as appropriate. The receiver-operating characteristic (ROC) curves were generated and compared for prediction of inducibility according to the method described by Metz (26). A p value <0.05 was regarded as statistically significant.
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Results
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Clinical and MRI characteristics of the study population are summarized in Table 1. Sustained MVT was induced with one (n = 1), two (n = 10), or three (n = 7) extrastimuli in 18 patients (cycle length 270 ± 11 ms), whereas PVT/VF was induced with three extrastimuli in all nine subjects. The three patients without evidence of hyperenhancement on ceMRI had LVEFs of 44% to 62%; all had CAD by angiography and had EPS for near syncope or risk stratification for nonsustained VT. Infarct mass, absolute (49 ± 5 g vs. 28 ± 5 g, p < 0.005) and as percent left ventricular mass (26 ± 3% vs. 14 ± 3%, p < 0.004), and surface area (172 ± 15 cm2 vs. 93 ± 14 cm2, p < 0.0005) were larger in patients with inducible MVT than in those without inducible VT/VF. The LVEF was lower in patients with inducible MVT versus those without inducible ventricular arrhythmias, but this difference was not statistically significant (28 ± 2% vs. 35 ± 3%, p < 0.08). In general, values for the MRI findings in patients with PVT/VF were intermediate between those noted in patients with inducible MVT and patients without inducible ventricular arrhythmias; there were no significant differences between the patients with inducible PVT/VF and those without VT/VF. Significant differences between the patients with PVT/VF and the patients with inducible MVT were noted only for infarct surface area (p < 0.04) and the number of disconnected areas of infarction (p < 0.02). When patients taking amiodarone were excluded from the analysis, the qualitative findings remained unchanged.
Figure 1 shows the relationship between infarct size parameters and LVEF. Although infarct size correlates negatively with LVEF, the strength of the correlation is weak, with R2 values from 0.21 to 0.27. Of note, the distribution of patients with inducible MVT tends to cluster above the regression line, whereas those without inducible VT/VF tend to cluster below the line, consistent with the notion that LVEF may "overstate" infarct size in patients without inducible MVT, and vice versa.
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Figure 1 Plot of infarct size characteristics versus left ventricular ejection fraction. The regression lines are based on data from all 48 subjects. However, individual data points are shown only for patients with inducible monomorphic ventricular tachycardia (circles) and those without inducible ventricular arrhythmias (squares).
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Logistic regression revealed that infarct surface area and infarct mass were significant predictors of inducible VT, whereas LVEF was not. The logistic regression models revealed chi-square and p values of 6.6 and <0.01 for infarct surface area, 0.3 and <0.6 for LVEF, 5.2 and <0.02 for infarct mass (percent left ventricular mass), 0.6 and <0.4 for LVEF, 4.5 and <0.03 for infarct mass (absolute), and 0.7 and <0.4 for LVEF, respectively. Figure 2 demonstrates ROC curves for LVEF and infarct surface area as predictors of inducible VT. The ROC curve for infarct surface area is shifted up and to the left relative to the curve for LVEF, indicating it is a better predictor of VT inducibility than LVEF (p < 0.05). Table 2 demonstrates the sensitivity and specificity for various cut-off values of LVEF, infarct surface area, and infarct mass, as well as positive and negative predictive values in this population. Finally, a sensitivity analysis was performed reclassifying patients with inducible PVT/VF as either having MVT or being not inducible; there was no significant change in the outcomes of the logistic regression models.
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Figure 2 The receiver-operating characteristic curves for infarct surface area and ejection fraction as predictors of inducibility of monomorphic ventricular tachycardia.
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Table 2. Sensitivity, Specificity, Positive Predictive Value, and Negative Predictive Value of Various Cut-Off Values for the Indicated Parameters
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Discussion
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Our findings demonstrate that infarct surface area and size, as measured by MRI, is a better identifier of patients who have a substrate for inducible MVT than LVEF. In humans, limited information suggests that infarct size, as measured by LVEF, maximum creatine kinase, and the number of fixed thallium defects, is related to induction of ventricular arrhythmias (1,27–31). Based on autopsy findings, Bolick et al. (4) reported that patients with clinical VT after myocardial infarction had larger infarcts than those without. Recently, extensive scar tissue detected by technetium-99m tetrofosmin scintigraphy was reported as an independent predictor of death or recurrent ventricular arrhythmias in survivors of aborted sudden death (32). Because improvements in ceMRI have allowed delineation of infarct regions with high precision (12–17), we were able to demonstrate that infarct size, measured in vivo, is an important predictor of induction of MVT during EPS.
The LVEF in this study and others (8–11) is inversely related to infarct size, although the strength of this relationship may be poor. Many factors affect LVEF aside from infarct size, such as preload, afterload, autonomic factors, medications, and post-infarction remodeling (33). Many of these may also influence the pathogenesis of ventricular tachyarrhythmias by affecting the substrate or by serving as triggers or modulating factors. As inducibility of VT during EPS evaluates for the presence of a fixed substrate for VT, it is not surprising that the factor most closely linked to the anatomic substrate—infarct size (surface area)—is a better discriminator of inducible VT than LVEF, which is affected by so many other variables. Interestingly, a recent study (32) found that extensive scar tissue had a higher hazard ratio for recurrent events than LVEF (2.4 vs. 2.0), although the definition of extensive scar tissue was not clearly stated.
The clinical significance of inducible PVT/VF has been the subject of controversy. Induction of PVT/VF may be a nonspecific response to aggressive stimulation, as it may be observed frequently in patients with normal hearts (21,24). Yet, the clinical significance of these arrhythmias might differ depending on the presence and severity of heart disease. These arrhythmias are inducible in a substantial percentage of patients who have survived cardiac arrest (25,34,35). Furthermore, in some patients, after treatment with anti-arrhythmic agents, MVT can be induced (36,37); it is therefore plausible that these patients have a fixed substrate for ventricular arrhythmias that, in the absence of anti-arrhythmic drugs, is polymorphic. Further studies are warranted to delineate whether infarct size/morphology may help determine whether the induction of PVT/VF is clinically significant.
The present findings demonstrate that characterization of infarct size is a better predictor than LVEF for inducibility of VT. Although inducibility of VT is not the ideal risk stratifier for prediction of sudden death, LVEF is a known strong predictor. If the role of LVEF as a predictor of sudden death is a surrogate marker for infarct size, then it is possible that measurement of infarct size by ceMRI may be a better predictor of sudden death than LVEF. Further studies comparing the roles of LVEF and infarct size for prediction of clinical events are warranted.
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Footnotes
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This study was supported in part by the ACC/MERK award (to Dr. Bello). Dr. Bello was Merck Fellow of the American College of Cardiology from 2001 to 2002.
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W P Bandettini and A E Arai
Advances in clinical applications of cardiovascular magnetic resonance imaging
Heart,
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H. R. Halperin and S. Nazarian
Damage Assessment After Ablation: Role of Cardiovascular Magnetic Resonance
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J. J. Goldberger, M. E. Cain, S. H. Hohnloser, A. H. Kadish, B. P. Knight, M. S. Lauer, B. J. Maron, R. L. Page, R. S. Passman, D. Siscovick, et al.
American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death: A Scientific Statement From the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention
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J. J. Goldberger, M. E. Cain, S. H. Hohnloser, A. H. Kadish, B. P. Knight, M. S. Lauer, B. J. Maron, R. L. Page, R. S. Passman, D. Siscovick, et al.
American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death: A Scientific Statement From the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention
Circulation,
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M. S. Maron, E. Appelbaum, C. J. Harrigan, J. Buros, C. M. Gibson, C. Hanna, J. R. Lesser, J. E. Udelson, W. J. Manning, and B. J. Maron
Clinical Profile and Significance of Delayed Enhancement in Hypertrophic Cardiomyopathy
Circ Heart Fail,
September 1, 2008;
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S. Nazarian, A. Kolandaivelu, M. M. Zviman, G. R. Meininger, R. Kato, R. C. Susil, A. Roguin, T. L. Dickfeld, H. Ashikaga, H. Calkins, et al.
Feasibility of Real-Time Magnetic Resonance Imaging for Catheter Guidance in Electrophysiology Studies
Circulation,
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B. J. Schietinger, G. M. Brammer, H. Wang, J. M. Christopher, K. W. Kwon, A. J. Mangrum, J. M. Mangrum, and C. M. Kramer
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J. Am. Coll. Cardiol. Img.,
July 1, 2008;
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A. S. Adabag, B. J. Maron, E. Appelbaum, C. J. Harrigan, J. L. Buros, C. M. Gibson, J. R. Lesser, C. A. Hanna, J. E. Udelson, W. J. Manning, et al.
Occurrence and Frequency of Arrhythmias in Hypertrophic Cardiomyopathy in Relation to Delayed Enhancement on Cardiovascular Magnetic Resonance
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S. Nazarian and J. A.C. Lima
Cardiovascular Magnetic Resonance for Risk Stratification of Arrhythmia in Hypertrophic Cardiomyopathy
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V. R. S. Fernandes, K. C. Wu, B. D. Rosen, A. Schmidt, A. C. Lardo, N. Osman, H. R. Halperin, G. Tomaselli, R. Berger, D. A. Bluemke, et al.
Enhanced Infarct Border Zone Function and Altered Mechanical Activation Predict Inducibility of Monomorphic Ventricular Tachycardia in Patients with Ischemic Cardiomyopathy
Radiology,
December 1, 2007;
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J. J. Goldberger
Letter Regarding Article by Schmidt et al, "Infarct Tissue Heterogeneity by Magnetic Resonance Imaging Identifies Enhanced Cardiac Arrhythmia Susceptibility in Patients With Left Ventricular Dysfunction"
Circulation,
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R. G Assomull, D. J Pennell, and S. K Prasad
Cardiovascular magnetic resonance in the evaluation of heart failure
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A. Schmidt, C. F. Azevedo, A. Cheng, S. N. Gupta, D. A. Bluemke, T. K. Foo, G. Gerstenblith, R. G. Weiss, E. Marban, G. F. Tomaselli, et al.
Infarct Tissue Heterogeneity by Magnetic Resonance Imaging Identifies Enhanced Cardiac Arrhythmia Susceptibility in Patients With Left Ventricular Dysfunction
Circulation,
April 17, 2007;
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E. Larose, P. Ganz, H. G. Reynolds, S. Dorbala, M. F. Di Carli, K. A. Brown, and R. Y. Kwong
Right Ventricular Dysfunction Assessed by Cardiovascular Magnetic Resonance Imaging Predicts Poor Prognosis Late After Myocardial Infarction
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February 27, 2007;
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C. M. Kramer
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R. G. Assomull, S. K. Prasad, J. Lyne, G. Smith, E. D. Burman, M. Khan, M. N. Sheppard, P. A. Poole-Wilson, and D. J. Pennell
Cardiovascular Magnetic Resonance, Fibrosis, and Prognosis in Dilated Cardiomyopathy
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November 21, 2006;
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M. Gheorghiade, G. Sopko, L. De Luca, E. J. Velazquez, J. D. Parker, P. F. Binkley, Z. Sadowski, K. S. Golba, D. L. Prior, J. L. Rouleau, et al.
Navigating the Crossroads of Coronary Artery Disease and Heart Failure
Circulation,
September 12, 2006;
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F. J. Klocke, E. Wu, and D. C. Lee
"Shades of Gray" in Cardiac Magnetic Resonance Images of Infarcted Myocardium: Can They Tell Us What We'd Like Them to?
Circulation,
July 4, 2006;
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A. T. Yan, A. J. Shayne, K. A. Brown, S. N. Gupta, C. W. Chan, T. M. Luu, M. F. Di Carli, H. G. Reynolds, W. G. Stevenson, and R. Y. Kwong
Characterization of the Peri-Infarct Zone by Contrast-Enhanced Cardiac Magnetic Resonance Imaging Is a Powerful Predictor of Post-Myocardial Infarction Mortality
Circulation,
July 4, 2006;
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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):
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S. Nazarian, D. A. Bluemke, A. C. Lardo, M. M. Zviman, S. P. Watkins, T. L. Dickfeld, G. R. Meininger, A. Roguin, H. Calkins, G. F. Tomaselli, et al.
Magnetic Resonance Assessment of the Substrate for Inducible Ventricular Tachycardia in Nonischemic Cardiomyopathy
Circulation,
November 1, 2005;
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