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Delayed-enhancement cardiac MRI (DE-CMR) has emerged as the gold standard imaging technique for defining myocardial scar with high resolution. Gadolinium contrast washes out of the blood pool and accumulates in the extracellular space. Tissues with weak intracellular bonds and high amounts of non-cellular space, such as necrotic tissue or fibrous scar, will develop higher concentrations of this MRI contrast agent than will healthy tissues. Scar detected by DE-CMR has been shown to closely match histologically-proven myocardial infarction(1). Following an MI, cardiac myocytes become necrotic and cause an inflammatory response that initiates fibroblast replication, which replaces the necrotic tissue with non-cellular collage. This myocardial scar formation leads to cardiac dysfunction and ischemic cardiomyopathy. DE-CMR has demonstrated prognostic value post-MI for viability(1,2), functional recovery after MI(2), ventricular arrhythmia(3), and long-term mortality(4). Delayed-enhancement has been shown to correlate with areas of low voltage on electroanatomic mapping(5), and can define critical targets of VT circuits during ablation in patients with prior myocardial infarction(6). Presumably the presence of scar, and in particular the border zone between scar and normal myocardium, allows reentrant circuits to form.
Myocardial scar has also been detected by DE-CMR in patients with non-ischemic cardiomyopathy. The mechanism of scar formation in patients with non-ischemic cardiomyopathy is not clear, as neither obstructive coronary disease nor clinical ischemia is typically seen. Yet over half of these patients also show macroscopic evidence of cardiac tissue replacement with fibrous tissue. The regions of scarring may be different in these two disease processes; ischemia leads to a predominately endocardial scar that may be transmural whereas scar in non-ischemic cardiomyopathies tend to be isolated to the midwall or epicardium. In contrast to the studies establishing the utility of DE-CMR in ischemic cardiomyopathy, less data are available on the clinical utility of DE-CMR in the non-ischemic population. DE-CMR can differentiate ischemic from non-ischemic cardiomyopathies based on enhancement patterns(7). The presence of enhancement has been shown to be predictive of higher mortality as well as ventricular arrhythmia, even in the absence of coronary disease or infarction(8). In non-ischemic patients with monomorphic VT, basal scar has been associated with arrhythmia(9). However, prior studies have not clearly established that ventricular tachycardias are related to DE-CMR scar in patients without coronary disease, as has been shown in patients with healed infarction.
One challenge in catheter ablation of ventricular tachycardia, especially in the setting of non-ischemic cardiomyopathy, is that origin of VT is more often intramural or epicardial than it is in patients with coronary artery disease. Prior studies have examined the use of surface QRS configuration in an attempt to distinguish endocardial, mid-myocardial, and epicardial origins of ventricular tachycardia. Despite some encouraging preliminary results, algorithms in patients with non-ischemic cardiomyopathy that utilize surface ECG only have not proven to be highly accurate(10). An additional technique to direct the site of origin for VT ablation prior to performing catheter ablation would be useful. Also, monomorphic VT is often not reproducibly inducible in patients with non-ischemic dilated cardiomyopathy and thus a non-mapping technique that can distinguish the site of origin of VT remains attractive.
In this issue of the Journal, Bogun et al provide further compelling evidence that myocardial scarring, as identified by delayed-enhancement cardiac MRI (DE-CMR), is associated with ventricular arrhythmias and extends this observation to patients with non-ischemic cardiomyopathy(11). They also suggest that scar location can be a helpful guide to ablation. The study population consisted of 29 patients with non-ischemic cardiomyopathy who had been referred for catheter ablation due to either ventricular tachycardia (9 patients) or symptomatic PVCs (20 patients). Little information is provided about other comorbid diseases, but the average ejection fraction was 39%. Scar was classified as either endocardial, epicardial, intramural or transmural and scar volumes were quantified. Bogun et al showed that while 48% of the study population had scar by DE-CMR, all patients referred for sustained VT had some evidence of scar. In those patients where a critical site of VT was identified, it occurred within areas of scar in all cases(11). In patients with predominantly intramural delayed enhancement, catheter ablation was uniformly ineffective. Two patients had DE-CMR scar limited to the epicardial surface; neither of these patients had VTs that could be ablated from the endocardium. In contrast, in patients that had predominantly endocardial enhancement, 71% underwent successful catheter ablation of all VTs via an endocardial approach; the remaining 29% had a majority of VTs eliminated. In the entire cohort, there were 66 targeted arrhythmias of which 36 (55%) were successfully ablated.
The primary finding of this study is that DE-CMR enhancement can be used as a guide for VT and PVC ablation, even in patients considered to have non-ischemic cardiomyopathies. There are 2 potentially important implications. This finding could have important significance for planning invasive electrophysiologic interventions. In addition, the results of this study further reinforce the concept that scar burden by DE-CMR may be correlated with the incidence of ventricular tachyarrhythmia. Further studies are needed to define the role DE-CMR may have in non-invasive risk prediction of sudden cardiac death, both in the ischemic and non-ischemic cardiomyopathy populations.
Some limitations of the study should be noted. Only 29 patients were included in the study. Only 2 had scar confined to the epicardial surface. Thus, the observations made in this patient population are extremely preliminary. The number of patients with intramural scar was also limited. Given the inaccuracies of registering MRI images to electroanatomic maps (almost 5 mm in this study) and the resolution of DE-CMR images (1.4 mm in-plane, 8mm out-of-plane), it seems unlikely that the current technologies can be used to guide specific lesion delivery or identify the critical sites of ablation. Nonetheless, the results of the study by Bogun et al suggest that DE-CMR may be a useful technique in patients with ventricular tachycardia and non-ischemic cardiomyopathy.
Although not completely conclusive because of small patient number, the results of this study suggest that scar location, identified by DE-CMR prior to a catheter ablation procedure, may help localize sites for effective ablation. An endocardial approach, epicardial approach, or continued trials of medical therapy may be appropriate depending on scar location. The data in this manuscript seem strongest for the ability of DE-CMR to distinguish between endocardial and non-endocardial sites of VT origin. If these findings are confirmed in a larger patient population, scar localization could represent an important adjunct of catheter ablation in non-ischemic dilated cardiomyopathy. This study also gives hope that in the near future DE-CMR image integration in the EP lab will be a major component of VT ablation navigation.
Financial Support: Dr. Kadish has received grant support from St. Jude’s CRMD and Pre-DETERMINE 1 R01 HL091069
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