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Integration of Delayed-Enhanced MRI in ICD Patients to Guide Ventricular Tachycardia Ablation

Background

Ventricular tachycardia (VT) ablation is the next frontier in clinical electrophysiology. The indications for life-saving defibrillator therapy have been extended to an increasing number of patients in multiple clinical trials. A large number of patients with a structurally abnormal heart benefit from ICD placement without previous arrhythmia in addition to those with previous cardiac death. Frequent and appropriate defibrillator shocks for ventricular arrhythmias can occur in a large number of those patients. VT storm (≥3 shocks per 24 hours) has been observed in up to 5% and 40% of patients who received an ICD for primary or secondary prevention. 

While pharmacological therapy is the first-line therapy in many of these patients, its efficacy and side effects limit the usage and make VT ablation an attractive and appropriate next step. Additionally, two randomized studies demonstrate a decrease of future ICD shocks with a “prophylactic” VT ablation at the time of ICD implantation in patients with ischemic heart disease.

However, procedure times still surpass five hours on average with a recurrence rate of 50+% at long-term follow-up.

Therefore, a clinical need exists to make VT ablations faster, safer and more efficient to meet the growing clinical need.

Although detailed mapping of the VT pathways during VT often results in acute elimination of the arrhythmia, 60–90% of VTs are either non-sustained or hemodynamically unstable and require a substrate-guided approach. In this case, the amplitude of bipolar voltage recordings is used to classify a location point as healthy myocardium, scar or border zone (“voltage mapping”). Up to several hundred of those mapping points are combined to build a voltage map of the heart with a clinical mapping system. The system provides information about the anatomic location and extent of the scar and border zone. An ablation catheter is used to pace within the scar and along its border zone trying to match the 12-lead morphology of the VT (“pace mapping”). An identical morphology of the pace map and VT suggest a location close to the VT exit site from the scar; ablation lesions at that site have a good chance of eliminating the VT.

Unfortunately, voltage mapping has several important limitations. Voltage mapping can take >1–2 hours and prolong the procedure times. This also limits the average spatial resolution of voltage maps, and small areas of scar between two mapping points may be overlooked. Low voltage recordings can represent true myocardial scar, but also be the result of poor catheter contact with the cardiac muscle. Importantly, a single endocardial voltage recording is a poor surrogate of a complex intramural scar with variable degrees of scar transmurality or patchy myocardial fibrosis. Therefore, a detailed assessment of myocardial scar using a different approach than voltage mapping alone has the potential of providing helpful information and improving VT ablations.

Cardiac imaging has the ability to non-invasively differentiate normal from abnormal myocardium. Of special interest is late gadolinium-enhanced (LGE) magnetic resonance imaging (MRI). MRI has the ability to accurately delineate myocardial scar, but ICDs, which are present in the majority of VT patients, are still considered a contraindication and impact imaging quality. A recent study by Dickfeld et al examined the potential of 3D MRI imaging to facilitate VT ablations.1 In this novel approach, the authors evaluated safety/diagnostic yield of cardiac MRI in the largest reported ICD patient cohort to date, and are the first to assess the feasibility of registered 3D MRI scar reconstructions to facilitate VT ablations in ICD patients.1

Methods and Results

Twenty-two patients with non-ischemic or ischemic cardiomyopathy that were scheduled to undergo a clinically indicated VT ablation at the University of Maryland were enrolled in the study. Patients were on average 58 years old and had advanced heart failure with an ejection fraction of 34%. ICD interrogation was performed immediately before and after the 1.5 T MRI with a SAR limitation of 2.0W/kg, as well as during follow-up clinic visits. No significant changes in ICD parameters or programming changes were found in this study, which used all three major device manufacturers and single, dual and BiV devices. While most patients requiring VT ablations have ICDs, defibrillators are still considered a contraindication for MRI in most circumstances, which is reflected by a recent FDA summary statement.2 Several recent phantom, animal and patient series have suggested that MRI might be able to be performed safely with appropriate ICD and patient selection. To our knowledge, this is the largest study performed with dedicated cardiac MR imaging.2–5

Anatomic-dynamic and first-pass perfusion MR sequences demonstrated limited artifacts and allowed detailed assessment of the septal, inferior, lateral and anterior wall regarding anatomic-dynamic (100%/100%/100%/82%) and perfusion (100%/100%/100%/91%) characteristics.1 The anatomic-dynamic and perfusion imaging sequences were less susceptible to ICD artifacts and allowed the supplemental characterization of the anterior wall scar substrate based on anatomic (e.g. wall thinning), dynamic (e.g. hypocontractility), and first-pass perfusion (hypoenhancement) characteristics.

In delayed enhancement MRI sequences for scar visualization, ICD artifacts were more pronounced and appeared as a central signal void (ICD generator) with a surrounding rim of increased signal intensity. Artifacts affected the anterior wall in all cases with partial artifacts also noted in the septal and lateral wall. The authors used the 17-segment AHA classification to assess LGE in segments without any artifact (9±4 segments) and partially artifact (12±3 segments). In the ischemic patients, 82±7% of scar had endocardial components with mid-myocardial or epicardial components being predominantly seen as <1 cm scar extensions in the border zone. Of the seven patients with non-ischemic cardiomyopathy, two (29%) had exclusively epicardial or mid-myocardial scar. Two non-ischemic patients (29%) had no identifiable scar. 

The investigators used 3D reconstruction software to extract myocardial scar based on contrast-enhanced cardiovascular magnetic resonance (CE-CMR) and integrated scar into a mapping system (CartoMerge, Biosense Webster Inc.) prior to VT ablation in 14 patients. 

The investigators performed “early registration” of the MRI dataset in the first nine patients using only 13±3 RV points and 54±4 LV points with a registration accuracy of 5.7±3.9 mm. In the last five patients, MRI-derived LV/scar maps were registered to Biosense Webster CartoSound-reconstructed shells with a registration error of 4.6±3.1 mm. The “early registration” or “CartoSound registration” strategy allowed the visualization of MRI-derived scar during 71% and 100% of the LV mapping. This is the first time that early registration approaches have been used to display the intramural scar location and transmurality to guide most of the LV substrate mapping. “Final registration” accuracy of the completed voltage map was 3.9±1.8 mm.

The authors of the original research identified a good correlation between myocardial scar defined by CMR and voltage defined scar. Endocardial voltage points of <0.1mV, <0.5mV and mapping points of <1.5mV demonstrated MRI-defined scar 100%, 87% and 75%, respectively. Increasing transmurality of MRI-derived scar correlated with decreasing endocardial bipolar voltage (r = 0.72; p<0.05). ROC curves demonstrated the best correlation between endocardial MRI-defined scar and bipolar/unipolar voltage to be 1.49mV and 4.46mV, respectively.

Display of the MRI scar guided the further mapping/ablation in several ways. First, voltage maps were compared with MRI image to investigate the potential mismatch. In the situation with immediate identification of low voltage recordings (<1.5mV) in areas without associated MRI-derived scar, imperfect catheter contact was suggested. Repeat mapping using echocardiographic contact confirmation demonstrated that 78±12% of those points (average voltage: 0.83±0.52mV) were shown to have voltages >1.5mV. This represented 4.1±1.9% of the total original <1.5mV mapping points. Locations of incorrectly labeled <1.5mV mapping points were mid-anterior (41%), septal (37%), infero-basal (13%) and lateral (9%). The study demonstrated that integration of MRI can prevent the labeling of falsely-low voltage recordings and thereby may minimize unnecessary ablation lesions.

Second, targeted mapping of Voltage/DP/FP was performed. The integration of 3D MRI-defined scar provided an anatomic characterization of the 3D scar/border zone geometry displaying varying transmurality and epi-, mid- and endocardial scar components that could not be appreciated from voltage mapping alone. Visualization of transition zones of scar transmurality within scar or scar border zones allowed anatomically targeted mapping for FPs/DPs or preserved voltages.

Third, targeted pacemapping/entrainment/ablation was conducted. Empiric pacemap sites were selected along the displayed MRI border zone guided by the 12-lead VT morphology prior to completing LV voltage mapping. In this study, for over 60% of the patients, the early display of the MRI border zone combined with the 12-lead VT morphology allowed the identification of ≥11/12 pacemap sites prior to detailed voltage mapping (normally required to determine the border zone and pacemap sites). Importantly, MRI was able to detect surviving papillary muscle within a large area of infarcted myocardium or display mid-myocardial scar, which both represented the VT exit site and was not readily identifiable by voltage mapping alone. Interestingly, a >2 mm rim of alive endocardium observed in 14% of patients appeared sufficient to prevent the detection of intramyocardial scar of up to ~60% transmurality.

Twenty-two VTs were targeted for ablation. All successful ablation sites demonstrated MRI scar and demonstrated an average scar transmurality of 68±26%. Eighty-one percent of ablation sites had ≥50% transmural scar components and were located within 10 mm of transition zones to 0–25% transmural scar in 71%. Successful ablation sites were more commonly located in the scar periphery (76%).

Hemodynamically tolerated VT was induced in 14% of patients. Registration of MRI-defined scar to the CartoSound shell enabled entrainment mapping within the scar substrate without prior voltage mapping and facilitated the identification of the successful ablation site. In three of the five patients using the CartoSound registration strategy, real-time visualization of RF lesions within the MRI-defined abnormal substrate could be confirmed by increasing local ultrasound signal intensity.

No procedure-related complications were observed. At 15±12 months of follow-up, 54% of patients had evidence of non-sustained or sustained VT documented by ICD interrogation (time to first occurrence 5±4 months post ablation). Appropriate ICD shocks were seen in 4 of the 14 patients. Of those, ICD shocks occurred in two patients during a heart failure exacerbation, which resulted ultimately in the patients’ deaths 1 week and 20 months after ablation. One patient underwent a second ablation and one patient was treated medically.

Conclusions

In this study, 3D MRI scar maps could be created in ICD patients and were successfully extracted/registered. This allowed an increased understanding of the 3D scar geometry and allowed an early approach for mapping and ablation of VT exit sites. The identification of the scar substrate, evaluation of ablation lesion under real-time ultrasound within the scar substrate, and a better understanding of critical VT circuit sites may allow, in the future, a comprehensive and imaging-guided approach for VT ablations.

References

  1. Dickfeld T, Tian J, Ahmad G, et al. MRI-Guided Ventricular Tachycardia Ablation: Integration of Late Gadolinium Enhanced 3D Scar in Patients with ICD. Circ Arrhythm Electrophysiol 2011;4:172–184. Epub 2011 Jan 26.
  2. Faris OP, Shein M. Food and Drug Administration perspective: Magnetic resonance imaging of pacemaker and implantable cardioverter-defibrillator patients. Circulation 2006;114:1232–1233.
  3. Gimbel JR, Kanal E, Schwartz KM, Wilkoff BL. Outcome of magnetic resonance imaging (MRI) in selected patients with implantable cardioverter defibrillators (ICDs). Pacing Clin Electrophysiol 2005;28:270–273.
  4. Naehle CP, Strach K, Thomas D, et al. Magnetic resonance imaging at 1.5-T in patients with implantable cardioverter-defibrillators. J Am Coll Cardiol 2009;54:549–555.
  5. Nazarian S, Roguin A, Zviman MM, et al. Clinical utility and safety of a protocol for noncardiac and cardiac magnetic resonance imaging of patients with permanent pacemakers and implantable-cardioverter defibrillators at 1.5 tesla. Circulation 2006;114:1277–1284.

Editor’s Note: This article underwent peer review by one or more members of EP Lab Digest’s editorial board.


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