Cardiopulmonary Imaging Original Research

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1 Cardiopulmonary Imaging Original Research Lee et al. MDCT Detection of Myocardial Abnormalities in Patients With WPW Syndrome Cardiopulmonary Imaging Original Research Hye-Jeong Lee 1 Jae-Sun Uhm 2 Boyoung Joung 2 Yoo Jin Hong 1 Jin Hur 1 Byoung Wook Choi 1 Young Jin Kim 1 Lee HJ, Uhm JS, Joung B, et al. Keywords: cardiac CT, myocardial hypotrophy, segmental dyskinesia, ventricular preexcitation, Wolff-Parkinson-White syndrome DOI: /AJR Received June 8, 2015; accepted after revision August 29, Supported by grant from Yonsei University College of Medicine. 1 Department of Radiology, Research Institute of Radiological Science, Severance Hospital, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul , Korea. Address correspondence to Y. J. Kim (dryj@yuhs.ac). 2 Division of Cardiology, Cardiovascular Hospital, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. AJR 2016; 206: X/16/ American Roentgen Ray Society Detecting Regional Myocardial Abnormalities in Patients With Wolff-Parkinson-White Syndrome With the Use of ECG-Gated Cardiac MDCT OBJECTIVE. Myocardial dyskinesia caused by the accessory pathway and related reversible heart failure have been well documented in echocardiographic studies of pediatric patients with Wolff-Parkinson-White (WPW) syndrome. However, the long-term effects of dyskinesia on the myocardium of adult patients have not been studied in depth. The goal of the present study was to evaluate regional myocardial abnormalities on cardiac CT examinations of adult patients with WPW syndrome. MATERIALS AND METHODS. Of 74 patients with WPW syndrome who underwent cardiac CT from January 2006 through December 2013, 58 patients (mean [± SD] age, 52.2 ± 12.7 years), 36 (62.1%) of whom were men, were included in the study after the presence of combined cardiac disease was excluded. Two observers blindly evaluated myocardial thickness and attenuation on cardiac CT scans. On the basis of CT findings, patients were classified as having either normal or abnormal findings. We compared the two groups for other clinical findings, including observations from ECG, echocardiography, and electrophysiologic study. RESULTS. Of the 58 patients studied, 16 patients (27.6%) were found to have myocardial abnormalities (i.e., abnormal wall thinning with or without low attenuation). All abnormal findings corresponded with the location of the accessory pathway. Patients with abnormal findings had statistically significantly decreased left ventricular function, compared with patients with normal findings (p < 0.001). The frequency of regional wall motion abnormality was statistically significantly higher in patients with abnormal findings (p = 0.043). However, echocardiography documented structurally normal hearts in all patients. CONCLUSION. A relatively high frequency (27.6%) of regional myocardial abnormalities was observed on the cardiac CT examinations of adult patients with WPW syndrome. These abnormal findings might reflect the long-term effects of dyskinesia, suggesting irreversible myocardial injury that ultimately causes left ventricular dysfunction. Wolff-Parkinson-White (WPW) syndrome is characterized by the presence of an accessory pathway (AP) that passes through somewhere other than the atrioventricular (AV) node. This may cause an electrical stimulus to go directly from an atrium to a ventricle, resulting in the premature contraction of that ventricle [1, 2], and myocardial dyskinesia in these prematurely activated segments has been well documented through echocardiography [3, 4]. As recently hypothesized, dyskinetic segments in patients with WPW syndrome, working similar to a functional aneurysm, might induce intraventricular hemodynamics, leading to progressive ventricular dilation. This has been thought to be a direct cause of heart failure in patients with WPW syndrome, regardless of the related tachyarrhythmia [5 9]. Published reports related to these findings have almost all focused on pediatric patients observed with echocardiography. The symptoms of WPW syndrome can occur at any age. The syndrome is often first noted in childhood, but it may not be diagnosed until adulthood [10]. Because it is a type of congenital abnormality, we assumed that, in adult patients, the period of exposure to the AP would be longer than that in pediatric patients and, consequently, that the structural abnormalities at the preexcited myocardial segments might be more frequently found in adult patients than in pediatric patients. However, the long-term effects of this kinesis on myocardial impairment in adult patients are not well known. Recent advances in cardiac CT technology have greatly improved spatial and tempo- AJR:206, April

2 Lee et al. ral resolution and have expanded the potential of cardiac CT for a more comprehensive evaluation of cardiovascular disease [11]. Cardiac CT can show whole myocardial contours, compared with echocardiography, although it has lower tissue contrast when compared with cardiac MRI. Adult patients are more likely to undergo cardiac CT to rule out coronary artery disease. To our knowledge, there have been no published data on the use of MDCT to evaluate the regional myocardial abnormalities resulting from the long-term effect of premature contraction in patients with WPW syndrome, especially adult patients. Therefore, we focused on determining how much APs affected myocardial structural changes by using cardiac CT for adult patients with WPW syndrome. We then compared the CT findings to other clinical findings, including those from echocardiography, ECG, and electrophysiologic (EP) study. Materials and Methods Study Population Institutional review board approval was obtained for this retrospective study, and informed patient consent was waived. We searched our database for radiologic examinations performed at our institution from January 2006 through December A total of 39,644 consecutive patients underwent cardiac CT either for suspected coronary artery disease or for a health checkup; from this group of patients, we identified 74 patients who had WPW syndrome. Exclusion criteria were applied to patients with other combined cardiac diseases that could cause regional myocardial abnormalities. After excluding patients with combined cardiac disease (i.e., coronary artery disease [n = 9], valvular heart disease [n = 2], cardiomyopathy [n = 1], and congenital heart disease [n = 4]), a total of 58 patients (36 men [62.1%] and 22 women [37.9%]) were enrolled in the present study. To compare the frequency of regional myocardial abnormalities, we selected sex- and agematched control subjects (in a ratio of 1:4) from among those patients who had normal findings on ECG, no significant coronary artery disease, and no other history of cardiovascular disease noted in the same cardiac CT database. Clinical Characteristics of Patients With Wolff-Parkinson-White Syndrome The pertinent clinical history and all available clinical test data for each patient with WPW syndrome were collected by reviewing electronic medical records. The 12-lead ECG obtained during sinus rhythm at the time of diagnosis was reviewed. Using ECG, we confirmed ventricular preexcitation by the bundle of Kent fibers, and we measured the longest QRS complex duration of any lead with the use of a computerized analysis system. In addition, localization of the AP was also performed, especially for patients for whom an EP study was not available. All reports of patients undergoing an EP study with catheter radiofrequency ablation (RFA) for ventricular preexcitation were identified using an electronic database. Records from EP studies were reviewed to confirm the location of the APs and the presence of related tachyarrhythmia. For patients who underwent RFA, procedural details, such as approach methods and ablation sites, were also evaluated. For ECGs and EP studies, APs were reported using the traditional nomenclature presented by the Cardiac Nomenclature Study Group [12]. The traditional terminology is based on anatomic positions, rather than depiction of the position of the AV junctions, and it is defined on the basis of the AV rings and surrounding structures in one plane (Fig. 1). Transthoracic echocardiography was reviewed qualitatively. Global left ventricular function was assessed by measuring end-diastolic and endsystolic left ventricular diameters from parasternal long- and short-axis M-mode recordings. The ejection fraction was calculated using the biplane Simpson method. Regional wall motion abnormality (RWMA) and regional structural change were also evaluated qualitatively from the apical four-chamber or parasternal short-axis view at end-systole and end-diastole. Fig. 1 Illustration shows that classification of accessory pathway is based on anatomic position, defined with atrioventricular rings and surrounding structures in one plane. AV = aortic valve, MV = mitral valve, PV = pulmonary valve, TV = tricuspid valve. (Drawing by Lee HJ) Cardiac CT Contrast-enhanced cardiac CT was performed using a 64-MDCT scanner (Somatom Sensation 64, Siemens Healthcare) between 2006 and 2008, and a second-generation dual-source CT scanner (Somatom Definition Flash, Siemens Healthcare) between 2009 and In the absence of contraindications, patients with a heart rate higher than 65 beats per minute before examination received a β-blocker and a 0.3-mg sublingual dose of nitroglycerin administered just before initiation of scanning. A bolus of ml of iopamidol (Iopamiro 370, Bracco) was injected into an antecubital vein, followed by 30 ml of 30% blended iopamidol with saline and 20 ml of saline-chasing bolus administered at a flow rate of 5 ml/s. The start delay was defined by bolus tracking in the ascending aorta, and the scan start was automatically initiated 5 seconds after a threshold of 140 HU was reached. Scanning was performed using the following parameters: retrospective ECG-gated acquisitions with tube current modulation for both CT scanners or prospective ECG-gated acquisitions for the second-generation dual-source CT; tube voltage of kvp; a tube current exposure time product of mas, depending on patient size; and slice collimation of mm. Scans were performed on the area from the tracheal bifurcation to the diaphragm, and the FOV was adjusted according to the size of the heart. The cardiac CT scan was reconstructed using a slice thickness of 0.75 mm, an increment interval of 0.5 mm, and a medium-smooth convolution kernel of B36f. CT Image Analysis CT images were reviewed using software (AquarisNet Viewer, version , TeraRecon). All CT images of patients with WPW syndrome and control subjects were reconstructed at the middiastolic phase and showed good quality for myocardial evaluation. Two radiologists who had 7 and 10 years of experience in cardiac imaging and who were both blinded to clinical findings analyzed image datasets with the use of multiplanar reformatted images, such as four-chamber, longaxis, and short-axis views, in addition to axial images. First, visual assessment was independently performed to check for regional myocardial abnormalities, such as wall thinning or low attenuation. This separate assessment was performed to evaluate the interobserver agreement. Afterward, 720 AJR:206, April 2016

3 MDCT Detection of Myocardial Abnormalities in Patients With WPW Syndrome the observers identified patients with myocardial abnormalities through a consensus reading. For patients with WPW syndrome, the observers recorded abnormal findings, using traditional nomenclature for APs (Fig. 1), in the apical, mid, and basal left ventricle. The wall thickness of the abnormal myocardium was measured at its thinnest part and was compared to the remote normal myocardium from the short-axis, long-axis, or four-chamber view. For cases with suspected low attenuation, the observers drew an ROI to measure the CT number (expressed as Hounsfield units) within that area (Fig. 2). Statistical Analysis All statistical analyses were performed using statistical software (SAS, version 9.2, SAS Institute). We matched control subjects to patients with the use of the greedy matching algorithm. Interobserver agreement concerning the presence of regional myocardial abnormalities between the two observers was determined using kappa statistics, by use of a contingency table. The chi-square contingency table was used to compare the frequency of regional myocardial abnormalities between the control subjects and patients with WPW syndrome. The Wilcoxon signed rank test was performed to compare the wall thickness and CT number of the abnormal myocardium versus the remote normal myocardium in patients with abnormal findings. After confirming normality for continuous variables with the use of the Shapiro-Wilk test, comparisons between the groups with normal and abnormal findings were analyzed using the independent two-sample t tests. The chi-square contingency tables or the Fisher exact test was also used to appraise the differences in categoric variables. A difference for which p < 0.05 was considered to be statistically significant. Fig year-old man with abnormal myocardium. Measurement of wall thickness and myocardial attenuation was performed. Cardiac CT image shows that abnormal myocardium (arrows) had thin wall and low attenuation, compared with remote normal myocardium (arrowheads). Results Regional Myocardial Abnormalities on Cardiac CT For regional myocardial abnormalities, observer 1 identified 32 abnormalities in 232 control subjects and 23 abnormalities in 58 patients with WPW syndrome. Observer 2 identified 30 abnormalities in 232 control subjects and 24 abnormalities in 58 patients with WPW syndrome. Interobserver agreement was excellent (κ = 0.853). After the identification of abnormalities, the observers excluded findings of myocardial crypt (i.e., a discrete approximately V-shaped extension of blood penetrating more than 50% of the myocardial thickness) [13] and physiologic fat (i.e., fat infiltration located in the right ventricular apical walls, with small quantities occasionally found in the left ventricle) [14], and the observers also identified unexplained regional wall thinning and low attenuation through a consensus reading. Finally, among the control subjects, regional wall thinning was observed in five subjects (2.2%), and low attenuation was seen in one subject (0.4%). Of the patients with WPW syndrome, 16 (27.6%) had regional wall thinning and seven (12.1%) had low attenuation at the myocardium. For the seven patients with suspected low attenuation, all lesions were observed within the area of the abnormally thinning myocardium. The frequency of regional myocardial abnormalities was statistically significantly higher in patients with WPW syndrome than in control subjects (p < 0.001). For the 16 patients with WPW syndrome who had regional wall thinning, wall thickness was statistically significantly thinner (median, 5.05 mm; interquartile range, mm) than that of the remote myocardium (median, 7.85 mm; interquartile range, mm) (p = 0.001). The lesions with suspected attenuation were confirmed through CT number measurement, with a median attenuation of 2.70 HU (interquartile range, 6.60 to HU) noted, and they were statistically significantly different from lesions in the remote normal myocardium, which had a median attenuation of HU (interquartile range, HU) on CT (p < 0.016). These abnormal findings (i.e., regional wall thinning with or without low attenuation) were observed exclusively at the basal left ventricle in patients with WPW syndrome. Of the five control subjects with regional wall thinning, four had abnormalities observed at the inferior wall of the basal left ventricle, and one had an abnormality observed at the anterior wall of the mid left ventricle (Fig. 3). One subject with low attenuation had an abnormality observed at the lateral wall of the mid left ventricle. A B Fig year-old man who was control subject with regional myocardial abnormality noted on cardiac CT. A and B, On cardiac CT, short-axis (A) and long-axis (B) images show regional wall thinning (arrows) at inferior wall of basal left ventricle. However, ECG findings were normal, and patient had no significant coronary artery disease and no other history of cardiovascular disease. AJR:206, April

4 Lee et al. Clinical Characteristics of Patients with Wolff-Parkinson-White Syndrome The clinical characteristics of the study population are presented in Table 1. The mean (± SD) age at the time that CT was performed was 52.2 ± 12.7 years, and the mean age at the time of diagnosis of WPW syndrome was 47.1 ± 12.6 years. All patients had WPW syndrome diagnosed before CT was performed, and all patients underwent ECG at the time of diagnosis. The median interval between diagnosis and CT examination was 1.8 years (interquartile range, years), and the median interval between initial ECG and CT was the same. The mean preexcited QRS duration during sinus rhythm was ± 14.7 ms. A total of 34 of 58 patients underwent an EP study with RFA. Three of these 34 patients underwent an EP study after CT examination was performed, so they were not counted as having undergone an EP study. A total of 31 patients underwent EP study with RFA before CT, with a median interval of 4.0 years between the examinations (interquartile range, years). These 31 patients who underwent RFA had their APs successfully ablated, and no case recurred during the follow-up period. AV reentrant tachycardia was documented in 20 patients during EP studies, and atrial fibrillation was noted in 11 patients. Ablation was performed on the ventricular insertion of the AP in nine patients and on the atrial insertion in 22 patients. On the basis of the ECG and EP study results, the locations of the APs were as follows: right free wall AP in 16 patients (anterior [n = 1], lateral [n = 8], and posterior [n = 7]), septal AP in 11 patients (anteroseptal [n = 2], midseptal [n = 3], and posteroseptal [n = 6]), and left free wall AP in 31 patients (anterolateral [n = 0], lateral [n = 19], and posterior n = [12]). Multiple APs were not identified. All patients underwent echocardiography at the time of CT, and the median interval between echocardiography and CT was 3.0 days (interquartile range, days). Echocardiography documented RWMA corresponding to the AP in six patients, but a structurally normal heart was observed in all patients. The mean left ventricular ejection fraction (LVEF) was 60.9% ± 8.1%. Comparison of Clinical Characteristics Between Patients with Wolff-Parkinson-White Syndrome Who Had Abnormal Versus Normal Findings Patients with WPW syndrome were classified as having either normal or abnormal CT findings. There was no statistically significant difference in sex and age between the TABLE 1: Clinical Characteristics of Patients in the Study Population Who Had Abnormal CT Findings Versus Normal CT Findings Characteristic Abnormal Findings (n = 16) Normal Findings (n = 42) p Male sex 9 (56.3) 27 (64.3) Age at CT (y) 54.1 ± ± Age at diagnosis (y) 49.4 ± ± QRS duration (ms) a ± ± Echocardiography b Ejection fraction (%) 52.4 ± ± 3.8 < RMWA 4 (25.0) 2 (4.8) Electrophysiologic study Tachyarrhythmia 10 (62.5) 21 (50.0) AVRT 7 (43.8) 13 (31.0) Atrial fibrillation 3 (18.8) 8 (19.0) RFA site 10 (62.5) 21 (50.0) Ventricular 3 (18.8) 6 (14.3) Atrial 7 (43.8) 15 (35.7) Location of AP Right free wall 0 (0.0) 16 (38.1) Septal 6 (37.5) 5 (11.9) Left free wall 10 (62.5) 21 (50.0) Note Data are mean (± SD) values or no. (%) of patients with findings. RWMA = regional wall motion abnormality, AVRT = atrioventricular reentrant tachycardia, RFA = radiofrequency ablation, AP = accessory pathway. a QRS duration on initial ECG at the time of diagnosis. b Echocardiographic findings at the time of CT. two patient groups. At the time that CT was performed, the group with abnormal findings had a decreased LVEF (52.4% ± 10.1%), compared with the normal group (64.2% ± 3.8%), with statistical significance denoted by p < The frequency of patients with RWMA was statistically significantly higher in the group with abnormal findings (25.0%) than in the group with normal findings (4.8%) (p < 0.043). The QRS duration observed on initial ECG was statistically significantly longer in patients with abnormal findings (139.4 ± 18.3 ms) than in patients with normal findings (127.4 ± 11.8 ms; p = 0.024). Ten of the 16 patients in the group with abnormal findings and 21 of the 42 patients in the group with normal findings underwent EP studies with RFA. There were no statistically significant differences in related tachyarrhythmia (p = 0.394) or in undergoing or not undergoing RFA (p = 0.394). In addition, the ablation site was not statistically significantly different between the two patient groups. All abnormalities noted on cardiac CT corresponded with the AP location (Fig. 4); septal AP was noted in in six patients (anteroseptal [n = 1], midseptal [n = 1], and posteroseptal [n = 4]), and left free wall AP was noted in 10 patients (lateral [n = 4] and posterior [n = 6]). The left free wall AP was the most commonly found AP in this study, and there was no statistically significant difference in its location between the two patient groups (p = 0.394). No myocardial abnormalities were observed at the right free wall AP (p < 0.001), but the proportion of septal APs was statistically significantly higher in patients with abnormal findings than in those with normal findings (p = 0.026). Discussion The present study might be the first to use MDCT to assess regional myocardial abnormalities in patients with WPW syndrome, especially in adult patients. The main finding of this study was the relatively high frequency (27.6% [16/58 patients]) of abnormal myocardium noted on the cardiac CT scans of patients with WPW syndrome, compared with control subjects, and this finding was related to decreased LVEF. RWMA, as noted on echocardiography, was also related to the ab- 722 AJR:206, April 2016

5 MDCT Detection of Myocardial Abnormalities in Patients With WPW Syndrome normal myocardium, but it was observed in only four (25%) of the patients with abnormal findings. No myocardial structural abnormalities were observed on echocardiography. Manifest WPW syndrome causes premature activation of myocardial segments close to the ventricular insertion of the AP; therefore, all myocardial abnormalities might be observed at the basal left ventricle on cardiac CT. Tachycardia-induced cardiomyopathy secondary to AP-mediated supraventricular arrhythmias is well characterized [15, 16]. However, according to recent literature, ventricular dysfunction secondary to nonphysiologic activation via the AP can be considered a direct cause of heart failure, as has been reported after the implantation of pacemakers [5 8, 16 19]. In experimental studies on cardiac pacing, the myocardial workload decreases when preexcited segments experience an abnormally low local preload, which likely will induce hypotrophy [20 22]. Hypotrophy then becomes an additional reason for systolic bulging of the preexcited segment, which causes progression of ventricular dysfunction. In the present study, we observed a significant relationship between abnormal thinning myocardium on cardiac CT and decreased left ventricular function. However, RWMA, such as dyskinesia, was observed in only four of the patients with abnormal findings, and no structural abnormalities were observed on echocardiography. That is because echocardiography is operator dependent and is usually limited by the acoustic window, making it more likely that the abnormal myocardium will be missed. In addition, these previous studies showed that all cases of ventricular dysfunction in preexcitation involved septal APs. Hypothetically, this observation may be related to a relatively shorter conduction time from the sinus node to a septal AP, compared with both free-wall APs, which have more of an effect on the myocardium [6, 7, 16, 18]. Similarly, we could observe a significantly higher proportion of septal APs in patients with abnormal findings. However, abnormal myocardium in the left free wall AP was also observed to a relatively smaller extent, compared with the presence of abnormal myocardium in the septal AP. In previous studies, it was assumed that the smaller extent of abnormal myocardium did not cause notable RWMA or decreased left ventricular function on echocardiography. In comparison, no abnormalities were observed in the right free wall AP, probably because the thickness of the right ventricular wall per se is thin. C A Heart failure associated with manifest WPW syndrome has been known to be reversible, and according to most literature, it is improved after suppression of preexcitation using RFA. However, Fazio et al. [5] showed that performing RFA did not restore normal left ventricular function in three pediatric patients with left ventricle dysfunction. Low attenuation on the abnormal myocardium was observed in seven patients in our study as well. Because myocardial fat is usually defined as apparent focal low attenuation on cardiac CT [23], and because the CT number for the low attenuation observed in the present study was significantly lower than that for normal myocardium, we believed that low attenuation might indicate myocardial fat. Although the pathogenesis of myocardial fat is uncertain, it is known to result from the inability of injured myocytes to metabolize free fatty acids [24], and it usually suggests irreversible damage; therefore, in the present study, abnormal myocardium with low attenuation might signify irreversible myocardial injury, albeit with a scanty portion. Moreover, six patients with abnormal myocardium had undergone RFA more than 3 years previously, which might be evidence of irreversible myocardial injury. On D Fig year-old man who complained of palpitation. A, On initial ECG, short PR interval with delta wave was confirmed, suggesting ventricular preexcitation. QRS duration was 160 ms. Echocardiogram shows moderate global hypokinesia of left ventricle, with 40% of ejection fraction. B and C, On cardiac CT, short-axis (B) and four-chamber (C) images show regional wall thinning (arrows) at posterior septum of basal left ventricle. D, Electrophysiologic study with radiofrequency ablation was performed after 2 years of observation and posteroseptal accessory pathway was confirmed. Radiofrequency ablation was applied to right atrial side of accessory pathway (asterisk). B AJR:206, April

6 Lee et al. the other hand, we observed two patients who had RWMA noted on echocardiography but had normal myocardium noted on cardiac CT. Although RFA was not performed because there were no symptoms, we expect the RWMA to improve after RFA. We thought that performing RFA, especially for the ablation site, would be a critical determinant of abnormal myocardium. However, there was no significant difference in ablation factors between the groups with normal and abnormal findings. For patients with WPW syndrome, ablation is usually applied to a very small area near the atrioventricular annulus at either the atrial or ventricular insertion of a localized AP. Only three patients in the group with abnormal findings had ablation applied to the ventricular insertion of the AP, and those abnormalities were much larger than what would be expected with just ablation. The QRS duration on ECG is known to be related to the degree of preexcitation and relaxation abnormalities in patients with WPW syndrome [25], and the association between the longer duration of QRS and the presence of abnormal myocardium was observed in the present study. On ECG, we also localized the AP in patients without EP studies, because the combination of ECG features, such as delta wave polarity, QRS axis, and precordial R-wave transition, has been known to enable accurate identification of the anatomic region of an AP [26]. The limitations of our study are as follows. First, because this study was retrospective, the study population formed a heterogeneous group of patients with regard to CT timing. Therefore, the temporal relationship between abnormal myocardium development and patient age was difficult to evaluate. Second, cardiac CT is not a routine imaging study for WPW syndrome, and a selection bias could exist for the study population. This bias has probably introduced the relatively higher frequency of abnormal myocardium noted in the present study. Third, we performed image analysis with the middiastolic phase only, because this study was of retrospective design, and because only a few patients had additional systolic phase images. If CT data from the entire cardiac cycle had been available, wall motion at the abnormal portion might have been evaluated, and abnormal findings might have been more accurately detected as well. In conclusion, regional myocardial abnormalities were observed on cardiac CT with a relatively high frequency (27.6%), and they corresponded to the location of the AP in adult patients with WPW syndrome. These findings were not detected on echocardiography. Such abnormal findings might reflect the long-term effects of dyskinesia, suggesting irreversible myocardial injury that ultimately causes left ventricular dysfunction. In addition, patients with WPW syndrome who have left ventricular dysfunction or RWMA might have regional myocardial abnormalities, especially after catheter ablation. The next question to ask is what we should do for these patients with abnormal myocardium associated with ventricular preexcitation. Further studies involving cardiac MRI might be necessary to confirm characteristics of the abnormal myocardium, such as fibrosis indicating irreversible injury. If an irreversible myocardial injury is present, a long-term follow-up study might be needed to evaluate the clinical implications of abnormal myocardium other than the left ventricular dysfunction. These might affect future management strategies for WPW syndrome. References 1. Ticzon AR, Damato AN, Caracta AR, Russo G, Foster JR, Lau SH. Interventricular septal motion during preexcitation and normal conduction in Wolff-Parkinson-White syndrome: echocardiographic and electrophysiologic correlation. Am J Cardiol 1976; 37: Lebovitz JA, Mandel WJ, Laks MM, Kraus R, Weinstein S. Relationship between the electrical (electrocardiographic) and mechanical (echocardiographic) events in Wolff-Parkinson-White syndrome. Chest 1977; 71: Chandra MS, Kerber RE, Brown DD, Funk DC. Echocardiography in Wolff-Parkinson-White syndrome. Circulation 1976; 53: DeMaria AN, Vera Z, Neumann A, Mason DT. Alterations in ventricular contraction pattern in the Wolff-Parkinson-White syndrome: detection by echocardiography. Circulation 1976; 53: Fazio G, Mongiovi M, Sutera L, Novo G, Novo S, Pipitone S. Segmental dyskinesia in Wolff-Parkinson-White syndrome: a possible cause of dilatative cardiomyopathy. Int J Cardiol 2008; 123:e31 e34 6. Kwon BS, Bae EJ, Kim GB, Noh CI, Choi JY, Yun YS. Septal dyskinesia and global left ventricular dysfunction in pediatric Wolff-Parkinson-White syndrome with septal accessory pathway. J Cardiovasc Electrophysiol 2010; 21: Udink ten Cate FE, Kruessell MA, Wagner K, et al. Dilated cardiomyopathy in children with ventricular preexcitation: the location of the accessory pathway is predictive of this association. J Electrocardiol 2010; 43: Martí-Almor J, Bazan V, Morales M, Guerra JC. Heart failure in a patient with Wolff-Parkinson- White syndrome (in Spanish). Rev Esp Cardiol 2011; 64: Yodogawa K, Ono N, Seino Y. Rapid recovery from congestive heart failure following successful radiofrequency catheter ablation in a patient with late onset of Wolff-Parkinson-White syndrome. Intern Med 2012; 51: Kulig J, Koplan BA. Cardiology patient page: Wolff-Parkinson-White syndrome and accessory pathways. Circulation 2010; 122:e480 e Nasis A, Mottram PM, Cameron JD, Seneviratne SK. Current and evolving clinical applications of multidetector cardiac CT in assessment of structural heart disease. Radiology 2013; 267: Cosio FG, Anderson RH, Kuck KH, et al. Living anatomy of the atrioventricular junctions: a guide to electrophysiologic mapping a consensus statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE. Circulation 1999; 100:e31 e Johansson B, Maceira AM, Babu-Narayan SV, Moon JC, Pennell DJ, Kilner PJ. Clefts can be seen in the basal inferior wall of the left ventricle and the interventricular septum in healthy volunteers as well as patients by cardiovascular magnetic resonance. J Am Coll Cardiol 2007; 50: Park EA, Lee W, Na SH, Chung JW, Park JH. Left ventricular fat deposition on CT in patients without proven myocardial disease. Int J Cardiovasc Imaging 2013 Jun 25 [Epub ahead of print] PubMed 15. Soria R, Fernandez F, Heller J, et al. Wolff-Parkinson-White syndrome and cardiopathies (in French). Arch Mal Coeur Vaiss 1984; 77: Cadrin-Tourigny J, Fournier A, Andelfinger G, Khairy P. Severe left ventricular dysfunction in infants with ventricular preexcitation. Heart Rhythm 2008; 5: Emmel M, Balaji S, Sreeram N. Ventricular preexcitation associated with dilated cardiomyopathy: a causal relationship? Cardiol Young 2004; 14: Tomaske M, Janousek J, Razek V, et al. Adverse effects of Wolff-Parkinson-White syndrome with right septal or posteroseptal accessory pathways on cardiac function. Europace 2008; 10: Dai CC, Guo BJ, Li WX, et al. Dyssynchronous ventricular contraction in Wolff-Parkinson-White syndrome: a risk factor for the development of dilated cardiomyopathy. Eur J Pediatr 2013; 172: Prinzen FW, Cheriex EC, Delhaas T, et al. Asymmetric thickness of the left ventricular wall resulting from asynchronous electric activation: a study in dogs with ventricular pacing and in patients 724 AJR:206, April 2016

7 MDCT Detection of Myocardial Abnormalities in Patients With WPW Syndrome with left bundle branch block. Am Heart J 1995; 130: Vernooy K, Dijkman B, Cheriex EC, Prinzen FW, Crijns HJ. Ventricular remodeling during longterm right ventricular pacing following His bundle ablation. Am J Cardiol 2006; 97: Tsai IC, Huang JL, Ueng KC, et al. Global and regional wall motion abnormalities of pacinginduced heart failure assessed by multi-detector row CT: a patient and canine model study. Int J Cardiovasc Imaging 2010; 26: Ahn SS, Kim YJ, Hur J, et al. CT detection of subendocardial fat in myocardial infarction. AJR 2009; 192: Bilheimer DW, Buja LM, Parkey RW, Bonte FJ, Willerson JT. Fatty acid accumulation and abnormal lipid deposition in peripheral and border zones of experimental myocardial infarcts. J Nucl FOR YOUR INFORMATION Mark your calendar for the following ARRS annual meetings: April 30 May 5, 2017 Hyatt Regency New Orleans, New Orleans, LA April 22 27, 2018 Marriott Wardman Park Hotel, Washington DC May 5 10, 2019 Hawaii Convention Center, Honolulu, HI Med 1978; 19: Inaba-Sato F, Hirai M, Hayashi H, et al. Relationship between QRS duration and repolarization abnormalities in patients with Wolff-Parkinson-White syndrome. J Electrocardiol 1996; 29: Cain ME, Luke RA, Lindsay BD. Diagnosis and localization of accessory pathways. Pacing Clin Electrophysiol 1992; 15: AJR:206, April