Applications of Cardiac Magnetic Resonance in Electrophysiology

Abstract

Contemporary methods for evaluation and treatment of arrhythmia are increasingly dependent upon characterization of the underlying myocardial substrate. Cardiovascular magnetic resonance offers unsurpassed soft tissue resolution capable of visualizing detailed cardiac anatomic features and intra-myocardial barriers to conduction. Non-invasive visualization of such anatomic detail has the potential to improve methods to diagnose, risk stratify, and treat patients with arrhythmia. This review describes a brief overview of the current knowledge on the applications of cardiac magnetic resonance for evaluation and treatment of patients with arrhythmia.

Due to its wide availability, echocardiography is the most frequently utilized diagnostic modality for diagnosis of the underlying substrate for cardiac arrhythmia. However, echocardiography is unable to visualize intra-myocardial substrates for reentrant arrhythmia such as fat or scar fibrosis. Replacement of myocytes with non-viable tissue results in hypertrophy of the remaining viable cells and yields altered ion channel and gap junction expression. These changes affect myocardial mechanical function as well as promoting arrhythmia.¹ Due to its soft tissue resolution and multi-planar imaging capabilities, cardiac magnetic resonance (CMR) offers significant advantages compared to echocardiography. Specialized CMR techniques are uniquely suited for diagnosis of various structural changes,² and can be applied to identify arrhythmic substrates.

Ischemic cardiomyopathy is left ventricular dysfunction resulting from coronary artery disease and myocardial infarction and is a common substrate of ventricular arrhythmia. Techniques to visualize infarcted myocardium in the acute^3–7 and chronic^8–11 settings have been well described and rely primarily upon steady state free precession (SSFP) cine CMR for evaluation of function, and late gadolinium enhancement (LGE) imaging to assess scar burden and distribution. The SSFP cine technique relies on short repetition times and electrocardiographic gating to provide dynamic visualization of the heart during the full cardiac cycle. The LGE technique utilizes an inversion recovery gradient echo sequence with an optimal inversion time set to null the signal of normal myocardium. In the setting of ischemic cardiomyopathy, images are acquired 10–15 minutes after intravenous administration of 0.2 mmol/kg gadolinium chelate. Gadolinium chelates are hydrophilic and have low molecular weights thereby concentrating into the extracellular fluid space. The extent of LGE is primarily determined by expansion of the extracellular space in fibrotic tissue which slows washout of the gadolinium chelates.¹² This “delayed” time period from contrast administration to scan acquisition allows clearance of the contrast medium from the normal myocardium, while non-viable myocardium shows LGE due to enhanced relaxivity of excited protons adjacent to retained gadolinium which increases the signal on T1 weighted images.

Hypertrophic cardiomyopathy is characterized by left and/or right ventricular hypertrophy resulting from an inherited defect in the protein components of the cardiac sarcomere. In cases where hypertrophy occurs at the basal septum, obstruction of the left ventricular outflow tract and mitral regurgitation due to systolic anterior motion of the anterior leaflet of the mitral valve can be present. Echocardiography is the standard technique for evaluation of hypertrophic cardiomyopathy.¹³ CMR is an appropriate alternative to confirm the diagnosis or identify atypical cases,^{14, 15} and is most useful when the echocardiography acoustic window is limited.¹⁶ LGE can detect midwall and patchy scar in regions with hypertrophy (Figure 1A).¹⁷ Necropsy studies have revealed good correlation between the LGE pattern of enhancement and the distribution of scar.^{16, 18}

Figure 1.

The figure illustrates LGE images in cardiomyopathies and delayed enhancement patterns (arrows). A) Hypertrophic cardiomyopathy, B) idiopathic cardiomyopathy, C) sarcoidosis, D) ARVD.

Non-Ischemic cardiomyopathy is characterized by left ventricular or biventricular dilatation and impaired contraction in the absence of flow limiting coronary disease. While some cases are due to viral, genetic, toxic, or immune causes, many are of unknown etiology. The anatomic and functional abnormalities of non-ischemic cardiomyopathy are readily assessed by cine CMR.¹⁹ As demonstrated in Figure 1B, LGE can be used in the evaluation of patients with non-ischemic cardiomyopathy. Although absence of hyper-enhancement is the most common finding in non-ischemic cardiomyopathy, midwall striae or patches of enhancement can be identified in approximately one third of cases.^20–22 Compared to ischemic cardiomyopathy, the pattern and location of LGE in non-ischemic cardiomyopathy is often atypical, making it difficult to distinguish artifact from true scar. The presence of scar should therefore be verified by use of multiple image planes and optimized inversion times.

Sarcoidosis with cardiac involvement is relatively uncommon (less than 5% of patients with pulmonary sarcoidosis). Currently used techniques, including echocardiography,²³ scintigraphy,²⁴ and myocardial biopsy²⁵ are often inadequate for early diagnosis. In patients with systemic sarcoidosis suspected of cardiac involvement, CMR may provide a diagnostic alternative and a method by which disease activity can be followed. Several authors have reported the occurrence of CMR abnormalities in patients with ongoing systemic sarcoidosis.^26–29 Due to increased T2 relaxation time, inflammatory sarcoid granules present as high signal intensity regions on T2 weighted images. Focal areas of hyper-enhancement likely representing fibrosis, can also be noted on LGE images (Figure 1C), most commonly in the basal segments of the left ventricle.³⁰

Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by enlargement, dysfunction, and fibro-fatty infiltration of the right ventricle. Clinical manifestations include ventricular tachycardia and symptoms of right heart failure. There are many methods to assess the right ventricle, but techniques like CMR that facilitate comprehensive coverage of the right ventricle are essential.³¹ Combined with its ability to characterize fibro-fatty infiltration of the right ventricle, CMR has rapidly evolved into the diagnostic standard for identifying ARVD.^32–34 CMR abnormalities in ARVD can be divided into functional and morphologic abnormalities.³⁵ Functional abnormalities include regional wall motion abnormalities, focal aneurysms, right ventricular dilation and/or systolic and diastolic dysfunction, and are best evaluated via SSFP cine imaging of the entire right ventricle in axial or long-axis stacks. Furthermore, substantial normal right ventricular variations, including reduced wall motion near the moderator band, variable trabeculation, and fat deposits surrounding the coronary vessels and epicardium can limit interpretation for the non-experienced observer.^36–38 Morphologic abnormalities include intramyocardial fatty infiltration, focal wall thinning, wall hypertrophy, trabencular hypertrophy and disarray, moderator band hypertrophy, and right ventricular outflow tract enlargement. LGE can show areas of delayed enhancement in both the right and left ventricles (Figure 1D). These findings are best identified on a series of long axis images of the right ventricle. Importantly, LGE for assessment of scar in the right ventricle must be performed with optimization of the inversion time for myocardial signal suppression for the right ventricle which is often substantially different than that optimized for the left ventricle.³⁹ Intramyocardial fatty infiltration can be observed as an area of high signal intensity on T1 weighted images. However, the normal presence of fat in the atrioventricular groove and anteroapical right ventricular epicardium, and artifacts due to motion, arrhythmia, and surface coil proximity can substantially reduce the specificity of high T1 signal intensity for the presence of intramyocardial fat INCLUDE REFERENCE: Macedo R, Prakasa K, Tichnell C, Marcus F, Calkins H, Lima JA, Bluemke DA. Marked lipomatous infiltration of the right ventricle: MRI findings in relation to arrhythmogenic right ventricular dysplasia. AJR Am J Roentgenol. 2007 May;188(5):W423–7. PMID: 17449737. It is also important to emphasize that identification of right ventricular fat signal by imaging is not unique to ARVD, or a recognized criterion for its diagnosis. The contribution of CMR to ARVD diagnostic criteria are primarily through functional assessments such as regional right ventricular wall motion abnormalities, dilatation, and aneurysms, and are summarized in the first row of Table 1.⁴⁰

Table 1.

The table provides a summary of current diagnostic criteria for ARVD. The diagnosis of ARVD would be fulfilled by the presence of two major, or one major plus two minor criteria or four minor criteria from different groups.⁴⁰

I. Global and/or Regional Dysfunction and Structural Alterations on echocardiography, angiography, CMR, or radionuclide scintigraphy.
Major	Severe dilatation and reduction of right ventricular ejection fraction with no (or only mild) left ventricular impairment Localized right ventricular aneurysms (akinetic or dyskinetic areas with diastolic bulging) Severe segmental dilatation of the right ventricle
Minor	Mild global right ventricular dilatation and/or ejection fraction reduction with normal left ventricle Mild segmental dilatation of the right ventricle Regional right ventricular hypokinesia
II. Tissue Characterization of Wall
Major	Fibrofatty replacement of myocardium on endomyocardial biopsy
III. Repolarisation Abnormalities
Minor	Inverted T waves in right precordial leads (V2 and V3) in people aged >12 years, in absence of right bundle branch block
IV. Depolarization/Conduction Abnormalities
Major	Epsilon waves or localized prolongation (>110 ms) of the QRS complex in right precordial leads (V1 - V3)
Minor	Late potentials (signal-averaged ECG)
V. Arrhythmias
Minor	Left bundle branch block type ventricular tachycardia (sustained and non-sustained) by ECG, Holter or exercise testing Frequent ventricular extra-systoles (>1000/24 hours) by Holter
VI. Family History
Major	Familial disease confirmed at necropsy or surgery
Minor	Family history of premature sudden death (<35 years) due to suspected right ventricular dysplasia Familial history (clinical diagnosis based on present criteria)

Acute inflammatory myocarditis can accompany systemic immune dysfunction or result from exposure to pathogens and toxins. Endomyocardial biopsy, the gold-standard for diagnosing myocarditis, is limited by inadequate sensitivity and specificity.⁴¹ LGE with early imaging (1–2 minutes) can show relative myocardial enhancement compared with skeletal muscle and is likely due to the loss of cellular membrane integrity which allows accumulation of gadolinium chelates.⁴² Abnormal myocardial signal may also be present with T2-weighted spin-echo CMR images, and is a result of interstitial edema which increases the T2 relaxation time. Normalization of signal intensity occurs with healing, unless cell death has occurred, in which case LGE may show patchy enhancement. LGE 2–4 weeks after the onset of symptoms can predict functional and clinical long-term outcomes.^42–44 Enhanced contrast is often observed in the epicardium of the lateral free wall, a finding that is consistent with postmortem studies.⁴⁵

Chagas disease is an inflammatory disease caused by the parasitic protozoan Trypanosome cruzi. Although most patients survive the acute phase of the disease and remain asymptomatic for many years, 20% eventually present with heart failure. CMR can accurately assess morphological and functional aspects of cardiac involvement in Chagas disease.⁴⁶

Surgical scar can serve as an anatomic barrier for arrhythmic reentry. CMR is capable of delineating cardiac structure and function post cardiac surgery, a setting where echocardiography is often hindered due to chest wall changes that diminish the acoustic window. LGE has been shown to identify fibrous tissue in the post surgical myocardium.⁴⁷

Atrial scar may occur in the setting of any of the above myopathies or in isolation.⁴⁸ While LGE imaging has been well established for detection of fibrosis in ventricular myocardium, imaging of scar in the atrium has proved challenging due to reduced wall thickness and the resulting requirement for higher spatial resolution. Recent studies have suggested a potential role for detection of atrial scar utilizing LGE after pulmonary vein isolation procedures for atrial fibrillation (Figure 2, from Peters et al).^{49, 50}

Figure 2.

Transverse inversion recovery gradient echo images of the left atrium obtained by Peters et al,⁵⁰ showing no LGE pre-ablation (left panel), in comparison to post ablation images (right panel) with LGE noted in the pulmonary vein ostial region where radiofrequency energy was delivered.

Applications of CMR for Arrhythmic Risk Assessment

Traditional techniques for arrhythmic risk assessment primarily rely upon the clinical history, electrocardiographic features, morphologic evaluation of ejection fraction or wall thickness by echocardiography, and electrophysiology study results. The mechanism of arrhythmia is often reentry or the propagation of activation around a barrier to conduction. This reentrant circuit is often complicated, involving parts or combinations of viable tissue channels delineated by scar islands (Figure 3). Since CMR is capable of imaging non-viable tissue, it stands to reason that it would be capable of identifying potential substrates for reentry. Several recent studies have highlighted a potential role for CMR to complement traditional approaches for risk stratification of ventricular arrhythmia. These studies have been summarized below and also in Table 2.

Figure 3.

The figure is a 3 dimensional processed LGE image of a patient with ischemic cardiomyopathy. Scar has been highlighted in red. The yellow curved arrows show potential pathways for reentry.

Table 2.

Summary of studies of the relation of LGE with arrhythmia

	Source	Number of Patients, study design	Finding
Ischemic Cardiomyopathy	Bello et al 54	48, prospective cohort	Infarct size and surface area was greater in patients with monomorphic ventricular tachycardia inducible at electrophysiology study.
	Yan et al 55	144, retrospective cohort	Mortality was higher in patients with greater peri-infarct zone extent to infarct extent ratio.
	Schmidt et al 56	47, prospective cohort	Higher LGE defined tissue heterogeneity at the infarct periphery was predictive of induciblity at electrophysiology study.
Hypertrophic Cardiomyopathy	Teraoka et al 60	59, prospective cohort	Presence and extent of LGE were directly correlated with the presence of non sustained ventricular tachycardia on Holter monitoring.
	Dimitro et al99	47, prospective cohort	Patients with non-sustained ventricular tachycardia on Holter monitoring were more likely to exhibit LGE. The extent of scar was not significantly different between the two groups.
	Adabag et al 61	177, prospective cohort	Non sustained ventricular tachycardia was more common in patients with LGE, and patients with LGE had greater numbers of non sustained ventricular tachycardia episodes. The extent of scar was not significantly different between the two groups.
Non-Ischemic Cardiomyopathy	Nazarian et al 64	26, prospective cohort	Predominance of scar distribution involving 26–75% of wall thickness predicted inducible ventricular tachycardia at electrophysiology study.
	Assomull et al65	101, prospective cohort	Midwall fibrosis was present in 35% of patients and predicted the combined endpoint of all cause death or hospitalization.
	Wu et al 66	65, prospective cohort	The presence of LGE predicted the composite endpoint of hospitalization for heart failure, appropriate ICD firing, and cardiac death.
ARVD	Tandri et al 38	30, prospective cohort	The presence of LGE predicted inducible ventricular tachycardia at electrophysiology study.
Chagas Disease	Rochitte et al80	51, retrospective cohort	LGE was present in 100% of patients with documented history of ventricular tachycardia.

Ischemic cardiomyopathy patients suffer from a significant risk of ventricular arrhythmia, and have been shown to derive survival benefit from implantable cardioverter defibrillators (ICD).^51–53 Bello et al showed that out of 48 patients referred for electrophysiology study, the 18 with monomorphic ventricular tachycardia had larger infarcts than the 21 patients with no inducible arrhythmia. Interestingly, the 9 patients with inducible polymorphic ventricular tachycardia or ventricular fibrillation had intermediate infarct mass. The authors also showed that in logistic regression models including both infarct mass and left ventricular ejection fraction, or both infarct surface area and left ventricular ejection fraction, infarct mass and surface area were the only significant predictors of inducible ventricular tachycardia.⁵⁴ Yan et al examined the extent of peri-infarct zone quantified by LGE as an independent predictor of mortality in patients with history of myocardial infarction. The authors found that out of 144 patients with coronary artery disease and LGE, those with above median peri-infarct zone extent to infarct extent ratios (defined by ratio of the extent of LGE region with intensity 2–3 standard deviations above null myocardium over extent of LGE region with intensity 3 standard deviations above null myocardium) had higher mortality. After adjusting for age and left ventricular ejection fraction, peri-infarct zone extent to infarct extent ratio remained predictive of all cause and cardiovascular mortality.⁵⁵ Schmidt et al also studied the utility of an LGE measure of peri-infarct tissue heterogeneity (defined as the myocardium with signal intensity > peak remote signal intensity but <50% of maximal signal intensity of the manually contoured high signal intensity myocardium) in 47 patients referred for prophylactic ICD implantation for ischemic cardiomyopathy. The authors found that higher tissue heterogeneity at the infarct periphery was predictive of induciblity at electrophysiology study and that it was the only significant predictor of induciblity in a stepwise logistic regression model containing infarct location and core extent, and left ventricular ejection fraction and end-diastolic volume.⁵⁶ These studies provide evidence that LGE may provide additional benefit for risk stratification of patients with ischemic cardiomyopathy. A prospective study to determine the benefits of ICD implantation in patients stratified by infarct morphology identified by LGE is currently underway.⁵⁷

Hypertrophic cardiomyopathy patients are at significant risk for sudden death, therefore accurate and early risk stratification is essential in this condition.¹³ Ventricular arrhythmia occurrence rates of 5% per year for primary events and double that for secondary events have been reported.⁵⁸ The degree of fibrosis in hypertrophic cardiomypathy appears to correlate with arrhythmia risk. Pathology studies in which hearts of patients with HCM were examined after death or transplantation have shown greater extent of fibrosis in patients with history of ventricular arrhythmia.⁵⁹ Therefore it is plausible that the extent of myocardial fibrosis in this disease may correlate with the occurance of ventricular arrhythmia. Teraoka et al performed CMR examinations in 59 patients with hypertrophic cardiomyopathy and noted that the presence and extent of LGE were directly correlated with the presence of nonsustained ventricular tachycardia on Holter monitoring.⁶⁰ Dimtrow et al also assessed LGE imaging in patients with hypertrophic cardiomyopathy and found lower likelihood of LGE in patients without non sustained ventricular tachycardia compared with those with non sustained ventricular tachycardia on Holter monitoring. However, the extent of scar was not significantly different between the two groups in Dimitrow et al’s study. Later, Adabag et al performed LGE imaging on 177 patients with hypertrophic cardiomyopathy and found that nonsustained ventricular tachycardia was more common in patients with LGE, and that patients with LGE had greater numbers of non sustained ventricular tachycardia episodes. Similar to the findings of Dimitrow et al, however, the extent of LGE was similar in patients with and without non sustained ventricular tachycardia.⁶¹ These findings suggest a potential utility of CMR for risk stratification of ventricular arrhythmia in patients with hypertrophic cardiomyopathy.

Non-ischemic cardiomyopathy commonly presents with atrial and ventricular arrhythmias. However, syncope and sudden death are rarely the initial manifestations of the disease.⁶² Current guidelines propose ICD implantation for prevention of sudden death in non-ischemic cardiomyopathy patients with left ventricular ejection fraction less than 35% and symptoms of congestive heart failure.⁶³ We performed LGE imaging prior to electrophysiology study in 26 patients with non-ischemic left ventricular dysfunction. We found that the predominance of scar distribution involving 26–75% of wall thickness was predictive of inducible ventricular tachycardia after adjusting for left ventricular ejection fraction.⁶⁴ Assomull and colleagues enrolled 101 patients with non-ischemic dilated cardiomyopathy and found that midwall fibrosis, which was present in 35% of patients, predicted the combined endpoint of all cause death or hospitalization. Midwall fibrosis was also predictive of the combined endpoint of sudden death and ventricular tachycardia after adjusting for left ventricular ejection fraction.⁶⁵ Similarly, Wu and colleagues found that the presence of LGE in the setting of non-ischemic left ventricular dysfunction predicts the composite endpoint of hospitalization for heart failure, appropriate ICD firing, and cardiac death.⁶⁶ Identification of scar fibrosis may assist non-ischemic cardiomyopathy patient selection for ICD implantation,⁶⁷ and help direct ventricular tachycardia ablation mapping efforts toward the site of scar related reentry.⁶⁸

Sarcoidosis involving the heart is uncommon, but sudden death due to arrhythmia may be its initial clinical presentation. Accurate diagnosis is essential as ICD implantation and early immunosuppressive therapy may improve prognosis.⁶⁹ The capability of LGE to identify cardiac sarcoidosis suggests utility for risk stratification in this condition.

Arrhythmogenic right ventricular cardiomyopathy may be responsible for 10–20% of sudden cardiac deaths among certain populations.⁷⁰ Tandri et al performed LGE imaging and electrophysiology testing in 30 patients being evaluated for ARVD. The authors found sustained ventricular tachycardia inducible in 6 of 8 patients with LGE, whereas none of the patients without LGE had inducible ventricular tachycardia at electrophysiology study.³⁸ While the long-term prognostic significance of this finding remains to be validated, it suggests that LGE has a potential role in risk stratification of patients with ARVD.

Acute inflammatory myocarditis can present with refractory ventricular tachycardia, torsade de pointes, or sudden cardiac death.^71–73 Refractory atrial fibrillation has also been associated with inflammatory infiltrates in the atrium.⁷⁴ The role of CMR for arrhythmia management has not been assessed in acute myocarditis.

Chagas disease is commonly associated with ventricular arrhythmia^75–77 often presenting during or after exercise.^{75, 78} Importantly, ventricular arrhythmia may develop before cardiomegaly and heart failure are detected.^{75, 79} Atrial arrhythmias, including atrial fibrillation have also been reported.⁷⁵ Rochitte et al performed LGE imaging in 51 patients with Chagas disease and found that 100% of those with previously documented ventricular tachycardia had fibrosis detectable by LGE.⁸⁰ This study suggests a potential role for use of CMR for prospective risk stratification in Chagas disease.

Surgical Scar can be associated with reentrant arrhythmias including atrial tachycardia status post atriotomy scars^81–83 and ventricular tachycardia after ventriculotomy or patch repair.^{84, 85} CMR can be used to characterize the anatomy and assess scar burden thus aiding risk stratification and pre-procedural planning, and is particularly useful in the case of complex post surgical congenital heart disease.

Atrial scar extent and distribution detected by LGE has been associated with atrial arrhythmias.⁴⁸ Recent studies have also suggested that post pulmonary vein isolation LGE may detect the extent of radiofrequency induced damage in the atria.⁵⁰ The extent of atrial scar appears to be inversely correlated with left atrial function⁸⁶ and appears to be directly correlated to the success of atrial fibrillation ablation. The role of CMR in detecting atrial scar remains experimental, and future studies to determine its potential utility toward management of atrial arrhythmia are warranted.

Applications of CMR for Catheter Ablation

Introduction of electro-anatomic mapping systems with the capability to merge pre-acquired images with procedural catheter positions and intra-cardiac voltage and activation sequence maps has led to rapid integration of CMR and computed tomography images into the clinical electrophysiology laboratory. Pre-acquired CMR images are commonly used to provide a “shell” of the endocardial/epicardial boundaries of cardiac chambers and other anatomic regions of interest such as the aortic root and coronary vessels. This technology has been particularly useful in atrial fibrillation ablation, where knowledge of the pulmonary vein anatomy can help avoid complications due to inadvertent ablation too far inside the vein or at the ostium of smaller variant branches.⁸⁷ Additionally, knowing the location of the left atrial appendage can help avoid perforation due to catheter advancement in this area. By providing an anatomic reference of the pre-procedural location of the esophagus, image integration may also help reduce the potential of collateral damage by ablating in close proximity to this structure.⁸⁸ However, this technique may be limited by potential movement of the esophagus compared to the time the pre-acquired image was obtained.⁸⁹ Software upgrades to enable integration of myocardial scar images into the electro-anatomic system are under development and will likely reduce procedural time devoted to voltage mapping in ventricular tachycardia. Importantly, such a capability may also allow the delivery of lesions targeted near midwall scar not otherwise identifiable via endocardial or epicardial voltage mapping.

Ultimately, pre-acquired image integration may be replaced by real-time CMR guidance of electrophysiology procedures. However, catheter guidance by real-time CMR may be limited by catheter heating,⁹⁰ current induction,⁹¹ image distortion,⁹² and electromagnetic signal interference.⁹³ We have recently reported the feasibility of performing electrophysiology studies with a custom electrophysiology system compatible with real-time CMR guidance.⁹⁴ In our study, heating, current induction and signal interference were mitigated by using non-ferromagnetic catheters, radiofrequency filters, and limiting the specific absorption rate of CMR sequences. Image distortion was minimized by shortening of the echo time, and the use of spin echo and fast spin echo CMR sequences. In the study we demonstrated successful anatomic targeting of catheters and comprehensive electrophysiology studies with recording of intracardiac electrograms and pacing in the CMR environment. The capabilities of real-time CMR guidance for superior resolution of anatomic soft tissues, identification of scar arrhythmia substrates, and monitoring of lesion formation within linear sets and with respect to surrounding structures may improve the safety and efficacy of complex electrophysiology procedures.

Safety Considerations

Patients with cardiac arrhythmia often have high acuity of disease associated with decreased renal function, or ferromagnetic implants as potential CMR contraindications. Recent studies have raised the possibility of gadolinium induced nephrotoxicity, and nephrogenic systemic fibrosis (progressive and severe fibrosis of the skin and other organs) in patients with advanced kidney disease and exposure to gadolinium chelates.⁹⁵ Current guidelines recommend avoidance of gadolinium chelates in patients with estimated glomerular filtration rate < 30 mL/min/1.73 m². Ferromagnetic materials in a magnetic field are subject to force and torque. The radio-frequency and pulsed gradient magnetic fields in the MRI environment may induce electrical currents in leads and other ferromagnetic wires within the field. Radio-frequency pulses may also lead to implant heating and tissue damage at the device-tissue interface. Additionally, sophisticated electronic implants, such as those in neuro-stimulators, pacemakers and implantable cardioverter defibrillators have the potential for receiving electromagnetic interference in the MRI environment, resulting in programming changes or loss of function. However, techniques for safe imaging with MRI in the setting of certain permanent pacemaker and implantable cardioverter defibrillator systems have been developed.^{96, 97} Familiarity with CMR contraindications and implantable device classes with potential for electro-magnetic interaction are essential for radiologists and cardiologists performing examinations in this population of patients. The reader is encouraged to consult web sites that provide more specific information regarding individual devices (e.g., www.mrisafety.com) for specific device testing details. Additionally, current guidelines recommend avoidance of CMR during the first three months of pregnancy due to potential tissue heating, acoustic fetal damage, and teratogenic effects of gadolinium.⁹⁸ The decision to perform CMR in patients with potential contraindications is frequently made by considering the potential benefit of CMR relative to the attendant risks. Given the potential risks, it is important to conduct a systematic review of the patient’s condition, implanted devices, and safety for CMR. At our institution all patients are asked to review and answer a safety questionnaire (Table 3).

Table 3.

Sample patient safety questionnaire.

This section is to be filled out by the PATIENT: The MRI room contains a very strong magnet. Before you go into the room, we must know if you have any metal in your body. Please complete the following:
Pacemaker/Wires	□ Yes    □ No	Recent Stent Placement	□ Yes    □ No
Aneurysm Clips	□ Yes    □ No	Shunt	□ Yes    □ No
Surgical Clips	□ Yes    □ No	Ear Implant	□ Yes    □ No
Eye Implant	□ Yes    □ No	IUD	□ Yes    □ No
Implantable Defibrillator	□ Yes    □ No	Blood Vessel Coil	□ Yes    □ No
Bullets, Pellets, BBs	□ Yes    □ No	Heart Valve	□ Yes    □ No
Stimulator/Wires	□ Yes    □ No	Artificial Limb	□ Yes    □ No
Infusion Pump	□ Yes    □ No	Cochlear Device	□ Yes    □ No
Penile Prosthesis	□ Yes    □ No	Tracheostomy	□ Yes    □ No
Do you have kidney disease? Have you ever been a machinist or metal worker? Have you ever had a facial injury from metal? Have you ever had metal removed from your eyes? Are you pregnant? Last menstrual period_____________________________ Do you have any allergies? If yes, please specify_________________________ Current medications______________________________________________ ______________________________________________________________ Weight________________________________________________________ Patient signature_____________________________ Date _______________			□ Yes    □ No □ Yes    □ No □ Yes    □ No □ Yes    □ No □ Yes    □ No □ Yes    □ No
This section is to be filled out by the RADIOLOGY STAFF:
Operations	□ Yes    □ No
Orbit Films	□ Yes    □ No
Anyone attending the patient in the MRI room has been cleared for MRI safety requirements.			□ Yes    □ No
Radiology staff signature/Title_______________________________________________ Date ___________________

Conclusion

CMR is increasingly recognized as an important imaging adjunct for the diagnosis of arrhythmogenic myocardial substrates. Advances in CMR, electroanatomic mapping technologies with image integration, and real-time CMR guidance of electrophysiology procedures will likely facilitate patient selection and catheter ablation.