Delayed Enhancement Magnetic Resonance Imaging Research Articles

Serum YKL-40 as a Marker of Left Atrial Fibrosis Assessed by Delayed Enhancement MRI in Lone Atrial Fibrillation.

Assessment of the left atrial (LA) fibrosis by using delayed-enhanced magnetic resonance imaging (DE-MRI) in atrial fibrillation (AF) patients is a pioneering noninvasive method. Serum YKL-40 is a novel marker for inflammation and known to play a role in ongoing tissue fibrosis. However, its role in LA fibrosis is unclear. We aimed to investigate the association of serum YKL-40 with the presence and extent of LA fibrosis. A total of 50 patients with lone paroxysmal AF (62% male; age: 47.2 ± 7.0 years) underwent cardiac DE-MRI according to study protocol. Cardiac DE-MRI at 1.5 Tesla scanner was used to quantify LA fibrosis. Serum YKL-40 levels and clinical and echocardiographic data were recorded in all participants. DE-MRI revealed any degree of LA fibrosis in 31 (62%) patients. Median serum YKL-40 was significantly higher (P = 0.008) and left venticular ejection fraction was lower (P = 0.047) in patients with LA fibrosis as compared to patients without LA fibrosis. Extent of LA fibrosis was significantly correlated with age, duration of AF history, serum C-reactive protein, and serum YKL-40 levels. Only log (YKL-40) level was found as independent predictor for the presence of LA fibrosis (odds ratio: 1.626, P = 0.022). Multivariate linear regression analysis pointed out that duration of AF history (β = 0.330, P = 0.003) and serum log (YKL-40) levels (β = 0.546, P < 0.001) were significantly and independently associated with the extent of LA fibrosis. Higher levels of serum YKL-40 are associated with the presence and more extensive LA fibrosis in patients with lone AF. As a marker of inflammation, serum YKL-40 may also be used as an indicator for the degree of LA fibrosis.

Assessment of the acute effects of glucocorticoid treatment on coronary microembolization using cine, first-pass perfusion, and delayed enhancement MRI.

To assess the acute effects of methylprednisone treatment (MPT) on coronary microembolization (CME) by cardiac cine, first-pass perfusion, and delayed gadolinium enhancement magnetic resonance imaging (DE-MRI) in an experimental swine model. Microembolization was established by intracoronary infusion of microspheres into the left anterior artery. Swine received placebo (n = 12) or methylprednisolone (n = 10, 30 mg/kg) intravenously 30 minutes before microembolization. Perfusion and DE-MRI was performed 6 hours after microembolization. Cine MR images of pre-/post-CME were obtained using 1.5T scanner. Cine MRI demonstrated relative amelioration of the post-CME myocardial contractile dysfunction in the glucocorticoid-treated group compared to the placebo group (P < 0.001). Post-CME target myocardial perfusion parameters decreased in both groups after microembolization. The extent of these decreases were the same for the embolized-to-control area ratio of maximum upslope (P = 0.245; 95% confidence interval of the difference [CID], -0.041/0.148) and time to peak ratio (P = 0.122; 95% CID, -0.201/0.026); however, the maximum signal intensity was higher in the glucocorticoid-treated group (P = 0.012; 95% CID, 0.023/0.156). DE-MRI revealed patchy hyperenhancement in all placebo pigs (n = 12/12) after microembolization, but no hyperenhanced regions in the glucocorticoid-pretreated pigs (n = 0/10). Standard, readily available, cardiac MRI techniques are useful in demonstrating post-CME myocardial dysfunction and the acute effects of glucocorticoid treatment on CME. Glucocorticoid pretreatment improves myocardial contractile dysfunction, prevents hyperenhancement, and partially ameliorates the decline of myocardial perfusion in the embolized area.

Ischemic Postconditioning After Routine Thrombus Aspiration During Primary Percutaneous Coronary Intervention: Rationale and Design of the POstconditioning Rotterdam Trial.

Whether ischemic postconditioning (IPOC) immediately after routine thrombus aspiration (TA) reduces infarct size (IS) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI) has not been established. The POstconditioning Rotterdam Trial (PORT) is a dual-center, prospective, open-label, randomized trial with blinded endpoint evaluation enrolling 72 subjects with first-time STEMI, and an occluded infarct-related artery (IRA) without collaterals undergoing PPCI. Subjects are randomized 1:1 to a strategy of IPOC immediately after TA followed by stenting of the IRA or to conventional percutaneous coronary intervention (PCI), including TA followed by stenting of the IRA (controls). Cardiac magnetic resonance imaging (MRI) is performed at 3-5 days after STEMI and at 3 months. The primary endpoint is IS at 3 months measured by delayed enhancement MRI. Other secondary endpoints include MRI-derived microvascular obstruction (MVO), left ventricular ejection fraction, myocardial salvage index, enzymatic IS, ST-segment resolution, myocardial blush grade, microcirculatory resistance, inflammation markers, and clinical events through 3-month follow-up. PORT is testing the hypothesis that adding IPOC (against lethal reperfusion injury) to TA (against distal embolization and MVO) is cardioprotective and reduces ultimate IS in STEMI patients undergoing PPCI (Dutch Trial Register identifier: NTR4040). © 2015 Wiley Periodicals, Inc.

Noninvasive electrocardiographic imaging of chronic myocardial infarct scar

BackgroundMyocardial infarction (MI) scar constitutes a substrate for ventricular tachycardia (VT), and an accurate delineation of infarct scar may help to identify reentrant circuits and thus facilitate catheter ablation. One of the recent advancements in characterization of a VT substrate is its volumetric delineation within the ventricular wall by noninvasive electrocardiographic imaging. This paper compares, in four specific cases, epicardial and volumetric inverse solutions, using magnetic resonance imaging (MRI) with late gadolinium enhancement as a gold standard. MethodsFor patients with chronic MI, who presented at Glasgow Western Infirmary, delayed-enhancement MRI and 120-lead body surface potential mapping (BSPM) data were acquired and 4 selected cases were later made available to a wider community as part of the 2007 PhysioNet/Computers in Cardiology Challenge. These data were used to perform patient-specific inverse solutions for epicardial electrograms and morphology-based criteria were applied to delineate infarct scar on the epicardial surface. Later, the Rochester group analyzed the same data by means of a novel inverse solution for reconstructing intramural transmembrane potentials, to delineate infarct scar in three dimensions. Comparison of the performance of three specific inverse-solution algorithms is presented here, using scores based on the 17-segment ventricular division scheme recommended by the American Heart Association. ResultsThe noninvasive methods delineating infarct scar as three-dimensional (3D) intramural distribution of transmembrane action potentials outperform estimates providing scar delineation on the epicardial surface in all scores used for comparison. In particular, the extent of infarct scar (its percentage mass relative to the total ventricular mass) is rendered more accurately by the 3D estimate. Moreover, the volumetric rendition of scar border provides better clues to potential targets for catheter ablation. ConclusionsElectrocardiographic inverse solution providing transmural distribution of ventricular action potentials is a promising tool for noninvasively delineating the extent and location of chronic MI scar. Further validation on a larger data set with detailed gold-standard data is needed to confirm observations reported in this study.

Relationship of T2-Weighted MRI Myocardial Hyperintensity and the Ischemic Area-At-Risk.

After acute myocardial infarction (MI), delineating the area-at-risk (AAR) is crucial for measuring how much, if any, ischemic myocardium has been salvaged. T2-weighted MRI is promoted as an excellent method to delineate the AAR. However, the evidence supporting the validity of this method to measure the AAR is indirect, and it has never been validated with direct anatomic measurements. To determine whether T2-weighted MRI delineates the AAR. Twenty-one canines and 24 patients with acute MI were studied. We compared bright-blood and black-blood T2-weighted MRI with images of the AAR and MI by histopathology in canines and with MI by in vivo delayed-enhancement MRI in canines and patients. Abnormal regions on MRI and pathology were compared by (a) quantitative measurement of the transmural-extent of the abnormality and (b) picture matching of contours. We found no relationship between the transmural-extent of T2-hyperintense regions and that of the AAR (bright-blood-T2: r=0.06, P=0.69; black-blood-T2: r=0.01, P=0.97). Instead, there was a strong correlation with that of infarction (bright-blood-T2: r=0.94, P<0.0001; black-blood-T2: r=0.95, P<0.0001). Additionally, contour analysis demonstrated a fingerprint match of T2-hyperintense regions with the intricate contour of infarcted regions by delayed-enhancement MRI. Similarly, in patients there was a close correspondence between contours of T2-hyperintense and infarcted regions, and the transmural-extent of these regions were highly correlated (bright-blood-T2: r=0.82, P<0.0001; black-blood-T2: r=0.83, P<0.0001). T2-weighted MRI does not depict the AAR. Accordingly, T2-weighted MRI should not be used to measure myocardial salvage, either to inform patient management decisions or to evaluate novel therapies for acute MI.

A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted Human Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging

Heart failure is increasing at an alarming rate, making it a worldwide epidemic. As the population ages and life expectancy increases, this trend is not likely to change. Myocardial infarction (MI)-induced adverse left ventricular (LV) remodeling is responsible for nearly 70% of heart failure cases. The adverse remodeling process involves an extension of the border zone (BZ) adjacent to an MI, which is normally perfused but shows myofiber contractile dysfunction. To improve patient-specific modeling of cardiac mechanics, we sought to create a finite element model of the human LV with BZ and MI morphologies integrated directly from delayed-enhancement magnetic resonance (DE-MR) images. Instead of separating the LV into discrete regions (e.g., the MI, BZ, and remote regions) with each having a homogeneous myocardial material property, we assumed a functional relation between the DE-MR image pixel intensity and myocardial stiffness and contractility--we considered a linear variation of material properties as a function of DE-MR image pixel intensity, which is known to improve the accuracy of the model's response. The finite element model was then calibrated using measurements obtained from the same patient--namely, 3D strain measurements-using complementary spatial modulation of magnetization magnetic resonance (CSPAMM-MR) images. This led to an average circumferential strain error of 8.9% across all American Heart Association (AHA) segments. We demonstrate the utility of our method for quantifying smooth regional variations in myocardial contractility using cardiac DE-MR and CSPAMM-MR images acquired from a 78-yr-old woman who experienced an MI approximately 1 yr prior. We found a remote myocardial diastolic stiffness of C(0) = 0.102 kPa, and a remote myocardial contractility of T(max) = 146.9 kPa, which are both in the range of previously published normal human values. Moreover, we found a normalized pixel intensity range of 30% for the BZ, which is consistent with the literature. Based on these regional myocardial material properties, we used our finite element model to compute patient-specific diastolic and systolic LV myofiber stress distributions, which cannot be measured directly. One of the main driving forces for adverse LV remodeling is assumed to be an abnormally high level of ventricular wall stress, and many existing and new treatments for heart failure fundamentally attempt to normalize LV wall stress. Thus, our noninvasive method for estimating smooth regional variations in myocardial contractility should be valuable for optimizing new surgical or medical strategies to limit the chronic evolution from infarction to heart failure.

Age, atrial fibrillation, and structural heart disease are the main determinants of left atrial fibrosis detected by delayed-enhanced magnetic resonance imaging in a general cardiology population.

We studied the extent and distribution of left atrial (LA) fibrosis on delayed-enhanced (DE) MRI in a general cardiology population. One hundred ninety consecutive patients referred for cardiac MRI underwent DE imaging using a free breathing method. The population comprised 60 AF patients and 130 patients without AF, including 75 with structural heart disease (SHD). DE was quantified using histogram thresholding, expressed in % of the wall. Regression analysis was performed to identify predictors of DE. Additionally, DE was registered on a template to study its distribution in subpopulations. In the total population, age, AF, and SHD were independently associated with DE. DE was increasingly observed from 11.1 ± 4.7% in patients with no SHD nor AF, 18.8 ± 7.8% in SHD and no AF history, 22.9 ± 7.8% in paroxysmal AF, to 27.8 ± 7.7% in persistent AF. Among non-AF patients, age and SHD were independently associated with DE. Among AF patients, female gender and AF persistence were independently associated with DE. DE was variably distributed but more frequently detected in the posterior wall. Age, history of AF, and SHD are the most powerful predictors of atrial fibrosis, as detected by MRI, in a general cardiology population. Atrial fibrosis predominates in the posterior LA wall.

Monitoring vascular permeability and remodeling after endothelial injury in a murine model using a magnetic resonance albumin-binding contrast agent.

Despite the beneficial effects of vascular interventions, these procedures may damage the endothelium leading to increased vascular permeability and remodeling. Re-endothelialization of the vessel wall, with functionally and structurally intact cells, is controlled by endothelial nitric oxide synthase (NOS3) and is crucial for attenuating adverse effects after injury. We investigated the applicability of the albumin-binding MR contrast agent, gadofosveset, to noninvasively monitor focal changes in vascular permeability and remodeling, after injury, in NOS3-knockout (NOS3(-/-)) and wild-type (WT) mice in vivo. WT and NOS3(-/-) mice were imaged at 7, 15, and 30 days after aortic denudation or sham-surgery. T1 mapping (R1=1/T1, s(-1)) and delayed-enhanced MRI were used as measurements of vascular permeability (R1) and remodeling (vessel wall enhancement, mm(2)) after gadofosveset injection, respectively. Denudation resulted in higher vascular permeability and vessel wall enhancement 7 days after injury in both strains compared with sham-operated animals. However, impaired re-endothelialization and increased neovascularization in NOS3(-/-) mice resulted in significantly higher R1 at 15 and 30 days post injury compared with WT mice that showed re-endothelialization and lack of neovascularization (R1 [s(-1)]=15 days: NOS3 (-/-)4.02 [interquartile range, IQR, 3.77-4.41] versus WT2.39 [IQR, 2.35-2.92]; 30 days: NOS3 (-/-)4.23 [IQR, 3.94-4.68] versus WT2.64 [IQR, 2.33-2.80]). Similarly, vessel wall enhancement was higher in NOS3(-/-) but recovered in WT mice (area [mm(2)]=15 days: NOS3 (-/-)5.20 [IQR, 4.68-6.80] versus WT2.13 [IQR, 0.97-3.31]; 30 days: NOS3 (-/-)7.35 [IQR, 5.66-8.61] versus WT1.60 [IQR, 1.40-3.18]). Ex vivo histological studies corroborated the MRI findings. We demonstrate that increased vascular permeability and remodeling, after injury, can be assessed noninvasively using an albumin-binding MR contrast agent and may be used as surrogate markers for evaluating the healing response of the vessel wall after injury.

The Association of Serum Galectin-3 Levels with Atrial Electrical and Structural Remodeling.

Left atrial (LA) interstitial fibrosis is known to have a role in the initiation and maintenance of atrial fibrillation (AF). The role of galectin-3 in the pathogenesis of cardiac fibrosis has been demonstrated in previous studies. We aimed to determine whether serum galectin-3 level is associated with markers of atrial remodeling, including the extent of LA fibrosis detected by delayed enhancement magnetic resonance imaging (DE-MRI) and atrial electromechanical delay (AEMD) in paroxysmal AF patients with preserved left ventricular (LV) functions. Thirty-three patients (58 [28-74] years, 51.5% male) with paroxysmal AF who underwent DE-MRI prior to cryoballoon-based AF ablation were included in the study. Serum galectin-3 levels were measured with ELISA. LA volume index (B ± SE: 0.424 ± 0.504, 95% CI: 0.560-2.627, P = 0.004) and serum galectin-3 levels (B ± SE: 0.549 ± 7.745, 95% CI: 16.874-47.550, P < 0.001) were found to be independently correlated with extent of LA fibrosis detected with DE-MRI in paroxysmal AF patients with preserved LV function. Correlation analysis between AEMD parameters and baseline characteristics showed that galectin-3 was significantly correlated with intra-left (ρ = 0.432, P = 0.012) and inter-AEMD (ρ = 0.395, P = 0.023). Duration of AF, LAD, and extent of LA fibrosis were also found to be significantly correlated with AEMD parameters. This is a hypothesis-generating study pointing out that serum galectin-3 level is significantly associated with atrial remodeling in paroxysmal AF patients with preserved LV function. Further studies are necessary to provide exact pathophysiological mechanisms.

Differential MR delayed enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.

ObjectivesBecause the distribution volume and mechanism of extracellular and intravascular MR contrast media differ considerably, the enhancement pattern of chronic myocardial infarction with extracellular or intravascular media might also be different. This study aims to investigate the differences in MR enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.Materials and MethodsTwenty pigs with myocardial infarction underwent cine MRI, first pass perfusion MRI and delayed enhancement MRI with extracellular or intravascular media at four weeks after coronary occlusion. Myocardial blood flow (MBF) was determined with microsphere measurement. The infarction histopathological changes were evaluated by hematoxylin and eosin staining and Masson's trichrome method.ResultsCine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium. Moreover, significant wall thinning in chronic infarction was observed in cine MRI. Peak first-pass signal intensity didn’t significantly differ between chronic infarction and normal myocardium no matter what kinds of contrast media. At the following delayed enhancement phase, extracellular media-enhanced signal intensity was significantly higher in chronic infarction than in normal myocardium. Conversely, intravascular media-enhanced signal intensity was almost equivalent among chronic infarction and normal myocardium. At four weeks after infarction, MBF in chronic infarction approached to that in normal myocardium. Large thick-walled vessels were detected at peri-infarction zones. The cardiomyocytes were replaced by scar tissue consisting of dilated blood vessels and discrete fibers of collagen.ConclusionsChronic infarction was characterized by the significantly reduced wall thickening and the definite wall thinning. First-pass myocardial perfusion defect was not detected in chronic infarction with two media due to the significantly recovered MBF and well-developed collateral vessels. Infarction remodeling enlarged the extracellular compartment, which was available for extracellular media but not accessible to intravascular media. Extracellular media identified chronic infarction as the hyper-enhancement; nonetheless, intravascular media didn’t provide delayed enhancement.

CT and MRI evaluation of cardiac complications in patients with hematologic diseases: a pictorial review

Cardiac complications with hematologic diseases are not uncommon but it is difficult to diagnose, due to non-specific clinical symptoms. Prompt recognition of these potentially fatal complications by cardiac computed tomography (CT) or cardiac magnetic resonance imaging (MRI) may help to direct clinicians to specific treatments according to causes. Thrombosis is often related to central venous catheter use and is usually located at the catheter tip near the atrial wall. Differentiation of thrombosis from normal structure is possible with CT and, distinction of a thrombus from a tumor is possible on a delayed enhancement MRI with a long inversion time (500-600ms). Granulocytic sarcoma of the heart is indicated by an infiltrative nature with involvement of whole layers of myocardium on CT and MRI. MRI with T2* mapping is useful in evaluating myocardial iron content in patients with hemochromatosis. Diffuse subendocardial enhancement is typically observed on delayed MRIs in patients with cardiac amyloidosis. T1 mapping is an emerging tool to diagnose amyloidosis. Myocardial abscess can occur due to an immunocompromised status. CT and MRI show loculated lesions with fluid density and concomitant rim-like contrast enhancement. Awareness of CT and MRI findings of cardiac complications of hematologic diseases can be helpful to physicians for clinical decision making and treatment.

Influence of time to treatment and other risk factors on infarct size and transmurality in the case of ST-elevated myocardial infarction managed by primary angioplasty and assessed by delayed enhancement magnetic resonance imaging

Objectives: To evaluate the association between time to treatment and to check the effect of various risk factors such as diabetes mellitus, hypertension (HTN), smoking, family history of coronary artery disease (CAD) and obesity on infarct size (IS), transmurality and ST-segment resolution (STR) with DE-MRI (delayed enhancement magnetic resonance imaging) on 3-month follow-up in patients treated for ST-elevated myocardial infarction (STEMI), with primary percutaneous coronary intervention (PPCI). Background: Early PPCI decreases IS and transmurality but increases STR. Materials and Methods: Fifty consecutive patients with STEMI treated with reperfusion therapy in the form of PPCI and underwent cardiac MRI at 3-month interval follow-up. The primary endpoint is final IS and transmurality as assessed by DE-MRI at 3-month follow-up. Results: IS and transmurality increase and STR decreases with increase in duration to percutaneous coronary intervention from the onset of symptoms. Similarly, the effect of various confounding factors such as diabetes mellitus, HTN, smoking, family history of CAD and obesity on IS, transmurality and STR was assessed which did not affect immediate prognosis during treatment. Conclusion: Primary angioplasty is the treatment modality of choice in the case of STEMI when available. Time to treatment directly influences STR, final IS and transmurality, that is, the earlier the intervention done, more will be STR and lesser will be final IS and transmurality. There is no significant effect of confounding variables such as cardiac risk factors except family history of CAD on immediate prognosis during treatment.

Fusion of Delayed-enhancement MR Imaging and Contrast-enhanced MR Angiography to Visualize Radiofrequency Ablation Scar on the Pulmonary Vein.

Delayed-enhancement magnetic resonance imaging (DE-MRI) is reported to detect the radiofrequency (RF) ablation scar of pulmonary vein isolation. However, the precise localization of RF scar is difficult to recognize due to the poor anatomical information of the 3-dimensionally reconstructed DE-MRI. We report 2 cases in which fusion of DE-MRI and contrast-enhanced MR angiography facilitated the identification of RF scar, and we detail our fusion method.

DECAAF: Emphasizing the importance of MRI in AF ablation.

Atrial fibrillation ablation is a complex and challenging procedure. Appropriate patient selection is the most critical step to ensure safe and successful atrial fibrillation ablation procedure. The DECAAF study (Delayed-Enhancement MRI Determinant of Successful Radiofrequency Catheter Ablation of Atrial Fibrillation) showed that atrial tissue fibrosis, as estimated by delayed enhancement magnetic resonance imaging, was independently associated with recurrent arrhythmia post atrial fibrillation ablation. Magnetic resonance imaging also detected left atrial volume and shape. Integrating the data provided by magnetic resonance imaging into the pre-procedural planning is crucial.

A prospective DE-MRI study evaluating the role of TGF-β1 in left atrial fibrosis and implications for outcomes of cryoballoon-based catheter ablation: new insights into primary fibrotic atriocardiomyopathy.

Transforming growth factor (TGF)-β1 mediated atrial fibrosis plays a major role in the development of vulnerable atrial substrate for atrial fibrillation (AF). Although cryoablation effectively eliminates the triggers for AF, the impact of atrial substrate on the success of cryoablation remains unclear. We aimed to investigate the association of plasma TGF-β1 level with extent of left atrium (LA) fibrosis using delayed-enhanced magnetic resonance imaging (DE-MRI) and also effects of LA fibrosis on the success of cryoablation. A total of 41 symptomatic lone paroxysmal AF patients (58.5% male; age: 49.2 ± 7.6 years) underwent initial cryoablation. Cardiac DE-MRI at 1.5-Tesla scanner to quantify atrial fibrosis, plasma TGF-β1, clinical and echocardiographic data were collected before cryoablation. Postablation blanking period was observed for 3 months. DE-MRI revealed LA fibrosis in 27 (65.9%) patients with a median enhancement of 5% of the LA surface area. A total of 179 pulmonary veins (PV) were successfully isolated without any major complication. At median 18 months follow-up, 32 patients (78.1%) remained free of AF recurrence. Only plasma TGF-β1 level (P = 0.001) was found to be the predictor of the extent of LA fibrosis. Multivariate Cox regression analysis pointed out that the extent of LA fibrosis (HR: 1.127, P = 0.007) and early AF recurrence (HR: 1.442, P = 0.011) were the independent predictors of AF recurrence in late follow-up. Higher levels of TGF-β1 are associated with more extensive LA fibrosis and extent of LA fibrosis predict recurrences in patients undergoing cryoablation for lone AF.

Visualization of the radiofrequency lesion after pulmonary vein isolation using delayed enhancement magnetic resonance imaging fused with magnetic resonance angiography

BackgroundThe radiofrequency (RF) lesions for atrial fibrillation (AF) ablation can be visualized by delayed enhancement magnetic resonance imaging (DE-MRI). However, the quality of anatomical information provided by DE-MRI is not adequate due to its spatial resolution. In contrast, magnetic resonance angiography (MRA) provides similar information regarding the left atrium (LA) and pulmonary veins (PVs) as computed tomography angiography. We hypothesized that DE-MRI fused with MRA will compensate for the inadequate image quality provided by DE-MRI. MethodsDE-MRI and MRA were performed in 18 patients who underwent AF ablation (age, 60±9 years; LA diameter, 42±6mm). Two observers independently assessed the DE-MRI and DE-MRI fused with MRA for visualization of the RF lesion (score 0–2; where 0: not visualized and 2: excellent in all 14 segments of the circular RF lesion). ResultsDE-MRI fused with MRA was successfully performed in all patients. The image quality score was significantly higher in DE-MRI fused with MRA compared to DE-MRI alone (observer 1: 22 (18, 25) vs 28 (28, 28), p<0.001; observer 2: 24 (23, 25) vs 28 (28, 28), p<0.001). ConclusionsDE-MRI fused with MRA was superior to DE-MRI for visualization of the RF lesion owing to the precise information on LA and PV anatomy provided by DE-MRI.

Postmyocarditis ventricular tachycardia in patients with epicardial-only scar: a specific entity requiring a specific approach.

Nonischemic cardiomyopathy is a heterogeneous condition providing a favorable substrate for ventricular tachycardia (VT). The purpose of this study is to further characterize the substrate in a subset of postmyocarditis patients with epicardial-only scar. Twelve postmyocarditis patients (11 male, 49 ± 14 years, left ventricular ejection fraction 49 ± 12%) with VT and epicardial-only scar were included for analysis comparing automatic high-amplitude normal activity (HANA) maps to manually adjusted maps of based on local abnormal ventricular activity (LAVA) electrograms when present. A combined endocardial (endo) and epicardial (epi) approach was used in 11/12 with usual bipolar/unipolar voltage thresholds and analyzed using image integration. A delayed enhancement MRI scar area of 52 cm(2) (38, 59) and multidetector CT wall thinning area of 18 cm(2) (14, 35) was found. Bipolar voltage substrate mapping (160 points [101, 239] endo, 553 points [232, 713] epi and LAVA were found only epicardially [443 LAVA points] in all) illustrated a low-voltage area of HANA: 1 cm(2) (0, 10) endo, 25 cm(2) (22, 39) epi and LAVA: 1 cm(2) (0, 10) endo, 39 cm(2) (28, 51) epi. Manual maps performed better than automatic maps for delineating low-voltage area with a higher overlap with scar area on delayed enhancement magnetic resonance imaging (DE-MRI; 76% [66, 94] vs. 45% [35, 62]; P = 0.04). In addition, manual voltage maps also showed a higher overlap with location of LAVA (LAVA in normal voltage area: 3% [0, 9] vs. 35% [32, 41]; P < 0.05). In postmyocarditis patients with epicardial-only scar, automatic voltage mapping may miss or minimize the electrical VT substrate. DE-MRI and manual LAVA-based voltage mapping are necessary to optimize scar delineation. Epicardial access is critical for mapping and ablation in this condition.

GW25-e1624 Delayed-enhancement MRI using low-dose contrast for the assessment of myocardial infarction

A recent multicenter study shows delayed-enhanced magnetic resonance imaging (DE-MRI) using contrast doses of ≥0.2 mmol/kg is effective in the assessment of myocardial infarction (MI), and 0.1 mmol/kg is not enough; intermediate doses between 0.1 and 0.2 mmol/kg have not been tested. The aim of

Magnetic resonance imaging of the left atrial appendage post pulmonary vein isolation: Implications for percutaneous left atrial appendage occlusion

BackgroundThere is increasing interest in performing left atrial appendage (LAA) occlusion at the time of atrial fibrillation (AF) ablation procedures. However, to date there has been no description of the acute changes to the LAA immediately following pulmonary vein (PV) isolation and additional left atrium (LA) substrate modification. This study assessed changes in the size and tissue characteristics of the LAA ostium in patients undergoing PV isolation. MethodsThis series included 8 patients who underwent cardiovascular magnetic resonance evaluation of the LA with delayed enhancement magnetic resonance imaging and contrast enhanced 3-D magnetic resonance angiography pre-, within 48h of, and 3 months post ablation. Two independent cardiac radiologists evaluated the ostial LAA diameters and area at each time point in addition to the presence of gadolinium enhancement. ResultsCompared to pre-ablation values, the respective median differences in oblique diameters and LAA area were +1.8mm, +1.7mm, and +0.6cm2 immediately post ablation (all NS) and −2.7mm, −2.3mm, and −0.5cm2 at 3 months (all NS). No delayed enhancement was detected in the LAA post ablation. ConclusionNo significant change to LAA diameter, area, or tissue characteristics was noted after PV isolation. While these findings suggest the safety and feasibility of concomitant PV isolation and LAA device occlusion, the variability in the degree and direction of change of the LAA measurements highlights the need for further study.

M2-muscarinic acetylcholine receptor autoantibody levels predict left atrial fibrosis severity in paroxysmal lone atrial fibrillation patients undergoing cryoablation.

Atrial fibrosis has been found to be associated with recurrent atrial fibrillation (AF) following catheter ablation. Autoantibodies against M2-muscarinic receptors (anti-M2-R) may play a role in the development of AF by inducing left atrial (LA) fibrosis. In this study, we aim to compare anti-M2-R levels between paroxysmal lone AF patients and healthy control subjects and to investigate the relationship between pre-ablation anti-M2-R level, LA fibrosis quantified by delayed enhancement magnetic resonance imaging (DE-MRI), and AF recurrence following cryoablation. Thirty-one patients with paroxysmal lone AF (53.4 ± 8.0 years, 61% male), who underwent cryoballoon-based ablation, along with 31 healthy control subjects were included. Enzyme-linked immunosorbent assay tests to measure serum anti-M2-R levels were performed in both groups and DE-MRI was done to quantify LA fibrosis prior to the ablation in the patients. Anti-M2-R levels were higher in the study population when compared with control subjects [212.4 (103.2-655.5) vs. 73.0 (39.5-299.1) ng/mL, P < 0.001]. Anti-M2-R level predicted moderate-extensive LA fibrosis independent of other measures [odds ratio: 1.26 (95% confidence interval (CI): 1.04-1.53), P = 0.017]. At a mean follow-up of 35.2 ± 3.5 months, nine patients (29.0%) had AF recurrence. In the Cox regression model including pre-ablation anti-M2-R level, LA diameter, LA volume index, and moderate-extensive LA fibrosis, only moderate-extensive LA fibrosis predicted late AF recurrence independent of other measures [hazard ratio: 29.41 (95% CI: 3.52-250.00), P = 0.002]. Serum anti-M2-R levels may be associated with the severity of LA fibrosis and may be implicated in the pathophysiology of AF recurrence following cryoablation. Detection of anti-M2-R levels may help select appropriate patients for the procedure.