Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Matthias Koopmann, MD, Nazem Akoum, MD, MS, Nassir Marrouche, MD



A 75-year-old woman with paroxysmal atrial fibrillation (AF) presented to our clinic for evaluation. The patient had been having AF for a few years. During AF episodes, she has palpitations and an irregular heart beat. Recently, the frequency of her episodes increased, and antiarrhythmic drug therapy with sotalol and flecainide failed to satisfactorily improve her symptoms, so she presents to discuss further treatment options. No significant comorbidities were apparent. A CHADS2 score of 1 (age) and a transthoracic echocardiogram showed normal left ventricular systolic function. Late gadolinium enhancement magnetic resonance imaging (LGE-MRI) demonstrated 12% LA tissue fibrosis, consistent with Utah stage II (Figure 40-1). After careful consideration and because of severe symptoms associated with AF, the patient elected to undergo an AF ablation. Given an early disease stage, the ablation procedure was limited to pulmonary vein antrum isolation (PVAI) only. Repeat LGE-MRI 10 months postablation demonstrated 12.5% LA scar formation (see Figure 40-1). After follow-up of 15 months, the patient remains free of AF.


FIGURE 40-1 Three-dimensional LA reconstruction showing LASRM (A) and chronic LA Scar (B) after PVAI. (A) LASRM estimated at 12% (stage II). (B) LGE-MRI was obtained 10 months post-AF ablation, exhibiting 12.5% LA scar. Blue, healthy myocardium; green, LASRM; red, scarred tissue. Dark green/red indicates transmurality; white indicates nontransmurality. Wall contours are smoothened.


A 68-year-old man presents who was first diagnosed with paroxysmal AF at the age of 52. Initially, episodes lasted 2 to 3 days and were associated with palpitations. Over the following 15 years, the frequency, duration, and severity of symptoms of AF episodes increased, some lasting for weeks. While initially he only felt palpitations, with time he increasingly had shortness of breath, with a sensation of not getting enough oxygen, and lightheadedness. He always, however, converted spontaneously to sinus rhythm. During those episodes his quality of life was significantly impacted. Antiarrhythmic drug therapy with flecainide failed after a short period of success in suppressing AF. Four years ago he experienced a stroke, which occurred 1 day after a liposuction procedure. Fortunately he does not exhibit any residual effects. No other significant cardiovascular risk factors were apparent, thus having a CHADS2score of 2. Due to increased symptoms, he elected to undergo AF ablation. Cardiac LGE-MRI was performed, and postimage acquisition processing revealed 22% atrial tissue fibrosis (Figure 40-2), fitting with stage III disease as depicted in Figure 40-3, which illustrates the Utah classification. Based on this individual’s extent of fibrosis, he was deemed eligible for ablation with an approach tailored to pulmonary vein antrum isolation (PVAI) and fibrotic area debulking. Immediate postablation, MRI demonstrated acute tissue lesions with regions of “no-reflow” at the posterior and septal wall (Figure 40-4), a predictor of appropriate scarring or lesion formation on MRI. Three months later MRI was repeated to assess chronic atrial scarring, which showed a scar burden of 19% of the LA volume (see Figure 40-2). Figure 40-5 illustrates 3 consecutive MRIs at preablation, immediate postablation, and 3 months postablation. At follow-up of 12 months the patient remains free of AF.


FIGURE 40-2 Three-dimensional LA reconstruction showing LASRM (A) and chronic LA scar (B) after PVAI and PWD. (A) LASRM estimated at 22% (stage III). (B) LGE-MRI 3 months post-AF ablation, exhibiting 19.1% LA scar.


FIGURE 40-3 Utah classification of LASRM, a quantitative LGE-MRI based clinical staging system reflecting disease progression of atrial fibrillation. Utah stage I (minimal) as <10% LASRM, stage II (mild) as ≥10% and <20%, stage III (moderate) as ≥20% and <30%, and stage IV (extensive) as ≥30%.


FIGURE 40-4 Three-dimensional LA reconstruction showing areas of no-reflow (yellow) indicating regions of catheter-induced tissue injury, immediately after AF ablation. Regions of no-reflow later enhance on 3 months postablation LGE-MRI, predicting permanent scar formation. Yellow, regions of no-reflow; blue, normal myocardium.


FIGURE 40-5 LGE-MRIs prior to ablation with LASRM, immediate postablation with dark regions of no-reflow at the posterior and septal wall (yellow arrows), and their transformation into areas that enhance on LGE-MRI, indicating permanent atrial scarring (red arrows) 3 months postablation.


A 29-year-old man was referred to our electrophysiology clinic for paroxysmal AF. He reported having episodes of fast heart rates for several years, occurring at a frequency of 1 to 3 times per months, each lasting about 2 to 3 days. He had a remarkable family history with many family members with sudden cardiac death (SCD), cardiomyopathy, and early onset AF. A thorough workup including cardiac MRI was performed given his significant family history of SCD. MRI showed normal left ventricular function, no signs of ventricular delayed enhancement, myocardial infarction, or scar. Postimage acquisition processing revealed 24% left atrial fibrosis (Utah stage III; Figure 40-6). Hence the patient was eligible for catheter ablation for AF with a tailored approach of pulmonary vein antrum isolation (PVAI) and posterior wall debulking. Acute postablation MRIs were performed within 24 hours and uncovered extensive posterior wall and esophageal enhancement. A day following ablation the patient complained of symptoms of heartburn and some pain with swallowing. Endoscopy was performed showing esophageal injury at the level of the left atrium (maximum diameter 11 mm) with no bleeding 30 to 31 cm from the incisors (Figure 40-7). LGE-MRI was repeated at 48 and 96 hours following AF ablation. Three-dimensional segmentations of the preablation MRI in this patient demonstrated the close topographic anatomical relationship between the left atrium and the posteriorly located esophagus (Figure 40-8). Figure 40-9 shows the temporal evolvement of the esophageal lesions. Proton pump inhibitors were initially given intravenously, sucralfate suspension (1 gram per mouth 4 times a day for 5 weeks), and mechanically soft diet was instituted for 5 weeks. Repeat endoscopies over the next days showed progressive healing of the esophageal ulcerations. After a clinical follow-up of more than 12 months, the patient remains free of AF, without any gastrointestinal symptoms.


FIGURE 40-6 Three-dimensional LA reconstruction showing preablation LASRM of 24% fibrosis (stage III). Note the extensive fibrosis in this young patient (aged 29 years) with a CHADS2 score of 0.


FIGURE 40-7 Repeat upper gastrointestinal endoscopies at (A) 24 hours, (B) 48 hours, (C) 96 hours, and (D) 16 days post-AF ablation. Spatial and temporal development of two distinct esophageal lesions (lesion 1, yellow arrows; lesion 2, blue arrows).


FIGURE 40-8 Three-dimensional reconstruction of the LA and esophagus in right-lateral (left), PA (middle), and left-lateral (right) views. Note the close spatial anatomical proximity between the anterior-located LA to the posterior-located esophagus. The distance between these structures varies among individuals and is about 3 to 13 mm away from the LA endocardium (frequently around 5 mm).


FIGURE 40-9 Consecutive 2-D LGE-MRI slices in axial (top) and sagital (bottom) views. Catheter ablation caused significant LA posterior wall and esophageal wall (yellow arrows) enhancement, indicating remarkable thermal tissue injury. Note the spatial extention and temporal behavior of the thermal eosphageal injuries.


Late gadolinium enhancement magnetic resonance imaging has emerged as a key noninvasive modality in the armory of heart imaging in modern cardiology. The well established ability to assess precisely myocardial viability and accurately depict anatomy and function has lead to its widespread clinical use. Left atrial and pulmonary vein anatomy (including anatomic variability) and major thoracic structures such as the esophagus have been thoroughly investigated using MRI.1,2 Recently, the utility of LGE-MRI has been significantly expanded with the demonstration of its ability to assess atrial tissue changes that contribute to the arrhythmic substrate, as well as acute and chronic postablation tissue lesions. In this chapter, we illustrate these MRI-based approaches and emphasize how the clinical application of these modalities are instrumental in tailoring treatment by selecting appropriate ablation candidates and the adequate ablation strategy, and predicting individual ablation outcome.


Atrial fibrillation is associated with atrial electrical, contractile, and structural remodeling. As AF perpetuates, apoptosis of atrial myocytes and fibrotic replacement occurs. Conversely, an increase in fibrosis within atrial tissue contributes to the arrhythmic substrate for AF. While for a long time the evaluation of tissue relied on invasive means either through surgical or postmortem histological specimens, MRI is now the noninvasive gold standard for tissue characterization, especially for the ventricular myocardium. Imaging of the atrial myocardium is more challenging, particularly due to the much thinner and nonuniform atrial wall, ranging from 1 to 7 mm. LGE-MRI relies on the differences in washout kinetics of gadolinium, an extracellular contrast agent, to differentiate between healthy myocardium and diseased tissue. Unlike in normal tissue where intracellular myocyte space forms the vast volume, in chronic diseased tissue the extracellular space is increased due to fibrous tissue replacement. This eventually leads to increase of gadolinium concentration and therefore delayed washout and subsequent enhancement. Figure 40-10illustrates workflows which are used to generate different LA images. The detection and quantification of fibrous tissue in the LA wall using LGE-MRI was first introduced by our group at the University of Utah. We demonstrated that low-voltage areas derived by electroanatomical mapping during AF ablation correlated well with areas showing enhancement on LGE. Further, AF recurrence following ablation was best predicted by the degree of fibrosis3(Figure 40-11). Using this approach assessment of distribution, amount, and transmurality of diseased fibrotic tissue was feasible. LA fibrosis seems to have no significant association with clinical congestive heart failure, coronary artery disease, arterial hypertension, or diabetes mellitus. However, an association was found with left ventricular hypertrophy4 and left ventricular dysfunction5 in AF patients. Paroxysmal AF is more prevalent in Utah I while persistent AF is more in Utah IV. Nevertheless, all 4 Utah stages include a heterogeneous mix of both AF phenotypes.


FIGURE 40-10 Workflows from LGE-MRI image acquisition to quantification/detection of LASRM (top), acute atrial lesions after ablation of AF with regions of no-reflow (middle), and chronic atrial scarring postablation (bottom). Figures A, D, and G show 2-D image slices; B, E, and H show endo- and epicardial LA wall contours; and C, F, and I show 3-D reconstructions.


FIGURE 40-11 Kaplan-Meier curve demonstrating freedom of arrhythmia recurrence in days following a single AF ablation procedure based on the Utah classification (mean follow-up 746 ± 428 days). Note the strong correlation between recurrence arrhythmias to higher LASRM (unpublished data).

Subsequent work of our group investigated the value of guiding treatment of AF patients based on their individual degree and distribution of LASRM.6 Patients with more advanced AF tend to have more LA tissue involved with fibrosis, and our data support extending the ablation strategy from pulmonary vein antrum isolation (PVAI) to posterior and septal wall debulking to improve ablation outcome.7,8 Patients in Utah stages I and II receive PVAI alone, while Utah IV patients are counseled to receive medical therapy rather than ablation. An inverse relationship of complex fractionated atrial electrograms (CFAEs) to atrial fibrosis has also been defined using LGE-MRI. Almost 90% of CFAE sites were found to occur at nonfibrotic and patchy fibrosis locations in the LA.9 Further, as sinus node dysfunction (SND) is a frequent phenomenon in AF patients, significant atrial fibrosis assessed by LGE-MRI is associated with clinically significant SND requiring pacemaker implantation, while fibrosis affects the left atrium more than the right.10

Ischemic stroke is an imminent threat in AF patients. Current schemes to predict stroke risk, such as the widely used CHADS2 score, do not include any assessment of individual LA structural remodeling. We showed that AF patients who experienced an ischemic stroke exhibit significantly higher levels of LA fibrosis as quantified by LGE-MRI.11 LGE-MRI has also uncovered an association of higher levels of fibrosis in the left atrial appendage, a common site of thrombus formation in AF, to echocardiographic findings of LAA thrombi and spontaneous echocardiographic contrast (SEC).12 Knowledge of individual LA fibrosis degrees in conjunction with the CHADS2 score may help clinicians improve stroke risk stratification and weigh risk and benefits for anticoagulation regimens.


Significant heterogeneity is seen in the LA wall on acute LGE-MRI following AF ablation, and those changes occur and dissolve quickly within the first 24 hours. Delivery of radiofrequency energy to the myocardial tissue creates remarkable edema with hyperenhancement, as well as nonenhancing regions showing characteristics similar to the no-reflow phenomenon. Unlike chronic myocardial remodeling, the mechanism of gadolinium enhancement in the setting of acute LGE-MRI is based on cell membrane rupture, allowing Gadolinium to diffuse into what was previously intracellular space, causing an increase in gadolinium concentration and therefore LGE. The proposed mechanism for the no-reflow phenomenon is based on intracapillary red blood cell stasis in the central necrotic region caused by capillary plugging. Those vascular changes induced either by an infarction or via catheter induced tissue injury result in tissue hypoperfusion, thus regions or no-reflow will appear dark on LGE-MRI. Nonenhancing or regions of no-reflow are more likely to transform into permanent scar on repeat LGE-MRI than hyperenhancing regions representing edema.13 Interestingly, edema is not only seen in regions directly subjected to RF energy but also in distant nonablated regions, such as parts of the anterior LA wall. It is worth noting that those regions do not predict final scar formation, even though they correlate with low-voltage areas during the procedure. The optimal timing of imaging postablation is crucial to visualize no-reflow phenomena. Those observations shed important light on the importance of early scar detection following ablation. However, with the expansion of knowledge regarding early lesion formation, the ultimate goal remains to titrate and monitor lesion formation in real time during the procedure.


Time periods ranging from weeks to months after ablation have been thoroughly investigated using LGE-MRI to assess chronic atrial ablation induced scarring. Tissue edema and regions of no-reflow observed acutely result in a heterogeneous mix of recovered and permanently scarred tissue in different subjects. Early studies demonstrated that subjects undergoing AF ablation exhibit LGE in the LA and around the PV ostia 1 to 3 months postablation.14Subsequently, this finding was confirmed using a novel imaging approach and processing methods,15 also showing that catheter-induced scarring on MRI predicted procedural outcome. Later studies proposed a time period of approximately 3 months postablation to permanently reflect chronic atrial scar formation.13 The amount of LA scar and the number of scarred pulmonary vein antra is associated with better ablation outcome; however, attaining complete PV encirclement as defined by LGE-MRI is difficult to achieve.15,16 Specifically higher procedure success was seen in those individuals exhibiting >23% LA scar, with lower success rates in those with <23% LA scar. The mechanism is likely multifactorial, but is at least in part due to the fact that certain tissue changes seen acutely (especially edema) will resolve over time, thus not being detectable on repeat MRI at 3 months. Catheter ablation of AF has also been associated with a decrease of LA size and systolic function, with a correlation to the total LA scar volume.17 LGE-MRI enables further to accurately define atrial scarring after AF ablation, and to identify gaps in PV lesion sets, which can be specifically targeted during a repeat ablation procedure.18 Of note, achieving complete circumferential isolation of all four PVs is a difficult task to achieve, and is likely less frequently achieved than previously assumed. It is important to mention that patients who remained in sinus rhythm exhibited incomplete PV scarring. This observation suggests the involvement of other mechanisms influencing AF recurrence after ablation. Since AF ablation procedures are guided by electroanatomic mapping systems, another study compared intended radiofrequency ablation sites using CARTO with postablation LA scar location detected by LGE-MRI and reported good qualitative and quantitative agreement between CARTO representations of ablation sites and LA scar by LGE-MRI.19 Both early and chronic atrial scar imaging is of significant clinical interest. While the presence of no-reflow phenomena likely predicts permanent scarring, lesion breaks on chronic scar imaging helps to individually plan redo procedures in patients who failed previous ablation.


MRI is an extremely valuable tool in planning, performing, and follow-up of catheter-based ablation procedures in EP. Consequently, there is a growing interest in cardiac MRI in EP, and the past 7 years have witnessed major strides in this field. Specifically, imaging of remodeled atrial tissue, acute and chronic ablation-induced tissue lesions, and scarring have seen improved accuracy, reliability, and reproducibility. The proposed modalities, however, allow clinicians to better select appropriate ablation candidates, plan the ablation strategy prior to the procedure, individually predict stroke risk and ablation outcome, and plan redo procedures as necessary. Moreover, MRI precisely elaborates left atrial, pulmonary vein anatomy, and the anatomical relationship to critical adjacent mediastinal structures, which is of particular interest for planning an invasive procedure. Further, LGE-MRI is instrumental for the detection and management of ablation-related complications, such as in our case of thermal esophageal injury.

To further improve arrhythmia management, future work will focus on intraprocedural real-time visualization of tissue lesions, giving the operator immediate feedback during energy delivery. Real-time MRI would further allow monitoring of critical adjacent anatomical structures, such as the esophagus, pericardial space, and PVs, thereby improving both efficacy and safety of ablation procedures. Safely navigating catheters in the heart, pacing maneuvers, recording intracardiac ECGs, transseptal punctures, and exploring all four cardiac chambers under real-time MRI is feasible. While major steps have already been accomplished, hurdles remain, including MRI-compatible EP catheters and equipment. Accomplishments of those steps will serve to expand further the utility of MRI in modern cardiac electrophysiology, increase curative rates for AF and other arrhythmias, while simultaneously decreasing procedural-associated complications.


  1. Hauser TH, Peters DC, Wylie JV, Manning WJ. Evaluating the left atrium by magnetic resonance imaging. Europace. 2008;10(Suppl 3):iii22-27.

  2. Mansour M, Holmvang G, Sosnovik D, et al. Assessment of pulmonary vein anatomic variability by magnetic resonance imaging: implications for catheter ablation techniques for atrial fibrillation. J Cardiovasc Electrophysiol. 2004;15(4):387-393.

  3. Oakes RS, Badger TJ, Kholmovski EG, et al. Detection and quantification of left atrial structural remodeling with delayed-enhancement magnetic resonance imaging in patients with atrial fibrillation.Circulation. 2009;119(113):1758-1767.

  4. Akkaya M, Higuchi K, Koopmann M, et al. Relationship between left atrial tissue structural remodelling detected using late gadolinium enhancement MRI and left ventricular hypertrophy in patients with atrial fibrillation. Europace. 2013;15(12):1725-1732.

  5. Akkaya M, Higuchi K, Koopmann M, et al. Higher degree of left atrial structural remodeling in patients with atrial fibrillation and left ventricular systolic dysfunction. J Cardiovasc Electrophysiol. 2013;24(5):485-491.

  6. Akoum N, Daccarett M, McGann C, et al. Atrial fibrosis helps select the appropriate patient and strategy in catheter ablation of atrial fibrillation: a DE-MRI guided approach. J Cardiovasc Electrophysiol. 2011;22(1):16-22.

  7. Segerson NM, Daccarett M, Badger TJ, et al. Magnetic resonance imaging-confirmed ablative debulking of the left atrial posterior wall and septum for treatment of persistent atrial fibrillation: rationale and initial experience. J Cardiovasc Electrophysiol. 2010;21(2):126-132.

  8. Daccarett M, McGann CJ, Akoum NW, MacLeod RS, Marrouche NF. MRI of the left atrium: predicting clinical outcomes in patients with atrial fibrillation. Expert Rev Cardiovasc Ther. 2011;9(1):105-111.

  9. Jadidi AS, Cochet H, Shah AJ, et al. Inverse relationship between fractionated electrograms and atrial fibrosis in persistent atrial fibrillation: combined magnetic resonance imaging and high-density mapping. J Am Coll Cardiol. 2013;62(9):802-812.

 10. Akoum N, McGann C, Vergara G, et al. Atrial fibrosis quantified using late gadolinium enhancement MRI is associated with sinus node dysfunction requiring pacemaker implant. J Cardiovasc Electrophysiol. 2012;23(1):44-50.

 11. Daccarett M, Badger TJ, Akoum N, et al. Association of left atrial fibrosis detected by delayed-enhancement magnetic resonance imaging and the risk of stroke in patients with atrial fibrillation. J Am Coll Cardiol. 2011;57(7):831-838.

 12. Akoum N, Fernandez G, Wilson B, McGann C, Kholmovski E, Marrouche N. Association of atrial fibrosis quantified using LGE-MRI with atrial appendage thrombus and spontaneous contrast on transesophageal echocardiography in patients with atrial fibrillation. [Epub ahead of print]. J Cardiovasc Electrophysiol. 2013. doi:10(10) 1104-1109.1111/jce.12199.

 13. McGann C, Kholmovski E, Blauer J, et al. Dark regions of no-reflow on late gadolinium enhancement magnetic resonance imaging result in scar formation after atrial fibrillation ablation. J Am Coll Cardiol. 2011;58(2):177-185.

 14. Peters DC, Wylie JV, Hauser TH, et al. Detection of pulmonary vein and left atrial scar after catheter ablation with three-dimensional navigator-gated delayed enhancement mr imaging: initial experience.Radiology. 2007;243(3):690-695.

 15. McGann CJ, Kholmovski EG, Oakes RS, et al. New magnetic resonance imaging-based method for defining the extent of left atrial wall injury after the ablation of atrial fibrillation. J Am Coll Cardiol. 2008;52(15):1263-1271.

 16. Peters DC, Wylie JV, Hauser TH, et al. Recurrence of atrial fibrillation correlates with the extent of postprocedural late gadolinium enhancement: a pilot study. JACC Cardiovasc Imaging. 2009;2(3):308-316.

 17. Wylie JV Jr, Peters DC, Essebag V, Manning WJ, Josephson ME, Hauser TH. Left atrial function and scar after catheter ablation of atrial fibrillation. Heart Rhythm. 2008;5(5):656-662.

 18. Badger TJ, Daccarett M, Akoum NW, et al. Evaluation of left atrial lesions after initial and repeat atrial fibrillation ablation: lessons learned from delayed-enhancement MRI in repeat ablation procedures.Circ Arrhythm Electrophysiol. 2010;3(3):249-259.

 19. Taclas JE, Nezafat R, Wylie JV, et al. Relationship between intended sites of RF ablation and post-procedural scar in AF patients, using late gadolinium enhancement cardiovascular magnetic resonance.Heart Rhythm. 2010;7(4):489-496.