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BACKGROUND: Cardiac magnetic resonance (CMR) characteristics of ventricular radiofrequency ablation (RFA) lesions have only been incompletely defined. AIM: To determine the detectability and imaging characteristics of ventricular RFA lesions in an unselected patient cohort undergoing ventricular arrhythmia ablation. METHODS AND RESULTS: A retrospective chart review (n = 249) identified 36 patients with either pre-/postablation CMR (n = 14) or only postablation CMR (n = 22). Ablation lesions could be identified in 50% (n = 18) of patients. Nonvisualized lesions had more preexisting transmural late gadolinium enhancement (LGE) >75% at the ablation sites (21% vs 0.0%, P = .042), more prevalent ICD artifact (50% vs 0%, P = .001), and lower ejection fraction (35.8 ± 14.2% vs 45.3 ± 13.4%, P = .048). Early CMR imaging demonstrated a central "black" signal void (microvascular obstruction [MVO], n = 12, 67%) up to 32 days post-RFA, whereas late imaging showed a homogenously "white" gadolinium enhancement pattern (n = 6, 33%). MVO was only observed in nonfibrotic myocardium without preexisting LGE (n = 12) but was not observed in the scar with preexisting LGE (n = 3, P = .002) suggesting different wash-in/wash-out kinetics in scar/nonscar myocardium. Signal intensity (1909 vs 2534, P = .009) and contrast-to-noise ratio (-7.8 vs 16.3, P = .009) were significantly different between MVO and LGE lesions, respectively. CONCLUSION: Ventricular ablation lesions visualization is negatively affected by preexisting transmural scar, ICD artifact, and low ejection fraction. The transition of "black" MVO appearance to "white" LGE appearance on CMR occurs around 1 month following ablation, suggesting a change in histological characteristics of ablation lesions. This may affect the utility of CMR in the evaluation of the ventricular lesions, when undergoing real-time or repeat VT ablations.
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Ablação por Cateter , Imagem Cinética por Ressonância Magnética/métodos , Taquicardia Ventricular/diagnóstico por imagem , Taquicardia Ventricular/cirurgia , Complexos Ventriculares Prematuros/diagnóstico por imagem , Complexos Ventriculares Prematuros/cirurgia , Meios de Contraste , Técnicas Eletrofisiológicas Cardíacas , Feminino , Humanos , Masculino , Meglumina/análogos & derivados , Pessoa de Meia-Idade , Compostos Organometálicos , Estudos Retrospectivos , Taquicardia Ventricular/fisiopatologia , Complexos Ventriculares Prematuros/fisiopatologiaRESUMO
BACKGROUND: A significant number of ventricular tachycardia circuits are located close to the epicardial surface and are amendable to epicardial ablation. Epicardial fat often interferes with substrate mapping and ablation, though little is known regarding the distribution of fat and its fluctuation with the cardiac cycle. METHODS: We studied 40 patients who underwent a 64-slice multidetector computed tomography in order to describe patterns of epicardial fat distribution, variation during cardiac cycle, and clinical predictors of epicardial fat. Multiplanar reconstructions were analyzed during systole and diastole in six cross-sections. Epicardial fat thickness was measured across multiple wall segments in each view. RESULTS: Epicardial fat was found to be thicker in areas overlying coronary vasculature (7.8 ± 2.6 mm vs 3.5 ± 0.9 mm, P = 0.001), along with the right ventricular wall (3.9 ± 0.8 mm vs 2.6 ± 0.6 mm, P = 0.001) and the ventricular base (6.1 ± 1.7 mm vs 4.6 ± 1.6 mm, P < 0.01). Epicardial fat thickness increased 27% during systole as compared to diastole (4.9 ± 2.7 mm vs 6.2 ± 3.0 mm, P = 0.04). Variation with cardiac cycle was most evident along the right ventricular wall (3.9 ± 0.8 mm vs 5.0 ± 1.3 mm, P = 0.001) and nonvascular areas (P = 0.001), especially at the ventricular base (3.7 ± 1.1 mm vs 5.3 ± 1.5 mm, P = 0.001). In multivariate logistic regression, we found that age >50 years (P = 0.031) and coronary artery disease (P = 0.023) were statistically correlated with epicardial fat >5-mm thickness and body mass index > 33 (P = 0.052) nearly so. CONCLUSIONS: Baseline epicardial fat thickness >5 mm is common in areas typically targeted during epicardial ablation and further increases during the cardiac cycle. Simple clinical characteristics can identify patients with >5 mm epicardial fat in which preprocedural computed tomography imaging and three-dimensional fat map reconstruction may facilitate epicardial ablation.
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Tecido Adiposo/diagnóstico por imagem , Ablação por Cateter/métodos , Mapeamento Epicárdico/métodos , Tomografia Computadorizada Multidetectores , Pericárdio/diagnóstico por imagem , Cirurgia Assistida por Computador , Taquicardia Ventricular/cirurgia , Procedimentos Cirúrgicos Cardíacos/métodos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos RetrospectivosRESUMO
INTRODUCTION: Visualization of left atrial (LA) anatomy using image integration modules has been associated with decreased radiation exposure and improved procedural outcome when used for guidance of pulmonary vein isolation (PVI) in atrial fibrillation (AF) ablation. We evaluated the CARTOSEG™ CT Segmentation Module (Biosense Webster, Inc.) that offers a new CT-specific semiautomatic reconstruction of the atrial endocardium. METHODS: The CARTOSEG™ CT Segmentation Module software was assessed prospectively in 80 patients undergoing AF ablation. Using preprocedural contrast-enhanced computed tomography (CE-CT), cardiac chambers, coronary sinus (CS), and esophagus were semiautomatically segmented. Segmentation quality was assessed from 1 (poor) to 4 (excellent). The reconstructed structures were registered with the electroanatomic map (EAM). PVI was performed using the registered 3D images. RESULTS: Semiautomatic reconstruction of the heart chambers was successfully performed in all 80 patients with AF. CE-CT DICOM file import, semiautomatic segmentation of cardiac chambers, esophagus, and CS was performed in 185 ± 105, 18 ± 5, 119 ± 47, and 69 ± 19 seconds, respectively. Average segmentation quality was 3.9 ± 0.2, 3.8 ± 0.3, and 3.8 ± 0.2 for LA, esophagus, and CS, respectively. Registration accuracy between the EAM and CE-CT-derived segmentation was 4.2 ± 0.9 mm. Complications consisted of one perforation (1%) which required pericardiocentesis, one increased pericardial effusion treated conservatively (1%), and one early termination of ablation due to thrombus formation on the ablation sheath without TIA/stroke (1%). All targeted PVs (n = 309) were successfully isolated. CONCLUSIONS: The novel CT- CARTOSEG™ CT Segmentation Module enables a rapid and reliable semiautomatic 3D reconstruction of cardiac chambers and adjacent anatomy, which facilitates successful and safe PVI.
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Fibrilação Atrial/diagnóstico por imagem , Fibrilação Atrial/cirurgia , Ablação por Cateter , Veias Pulmonares/cirurgia , Validação de Programas de Computador , Tomografia Computadorizada por Raios X , Meios de Contraste , Ecocardiografia Transesofagiana , Técnicas Eletrofisiológicas Cardíacas , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Pericardiocentese , Estudos Prospectivos , Ondas de Rádio , Interpretação de Imagem Radiográfica Assistida por ComputadorRESUMO
Edema resulting from the initiation of insulin therapy or intensification of glycemic control is a rare and under-recognized complication. In this report, we present a case of a 46-year-old patient with insulin-dependent diabetes mellitus (IDDM) who avoided insulin treatment due to associated peripheral edema. Though rare, this phenomenon is typically seen in patients with elevated glucose levels who are initiated on insulin treatment, resulting in rapid correction and tight control of glucose levels. The diagnosis of insulin-induced edema is made after other causes of acute edema are ruled out. Furthermore, in this case report, we will also discuss the postulated mechanisms for the edema-causing property of insulin.
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The functional and molecular imaging characteristics of ischemic ventricular tachycardia (VT) substrate are incompletely understood. Our objective was to compare regional 18F-FDG PET tracer uptake with detailed electroanatomic maps (EAMs) in a more extensive series of postinfarction VT patients to define the metabolic properties of VT substrate and successful ablation sites. Methods: Three-dimensional (3D) metabolic left ventricular reconstructions were created from perfusion-normalized 18F-FDG PET images in consecutive patients undergoing VT ablation. PET defects were classified as severe (defined as <50% uptake) or moderate (defined as 50%-70% uptake), as referenced to the maximal 17-segment uptake. Color-coded PET scar reconstructions were coregistered with corresponding high-resolution 3D EAMs, which were classified as indicating dense scarring (defined as voltage < 0.5 mV), normal myocardium (defined as voltage > 1.5 mV), or border zones (defined as voltage of 0.5-1.5 mV). Results: All 56 patients had ischemic cardiomyopathy (ejection fraction, 29% ± 12%). Severe PET defects were larger than dense scarring, at 63.0 ± 48.4 cm2 versus 13.8 ± 33.1 cm2 (P < 0.001). Similarly, moderate/severe PET defects (≤70%) were larger than areas with abnormal voltage (≤1.5 mV) measuring 105.1 ± 67.2 cm2 versus 56.2 ± 62.6 cm2 (P < 0.001). Analysis of bipolar voltage (23,389 mapping points) showed decreased voltage among severe PET defects (n = 10,364; 0.5 ± 0.3 mV) and moderate PET defects (n = 5,243; 1.5 ± 0.9 mV, P < 0.01), with normal voltage among normal PET areas (>70% uptake) (n = 7,782, 3.2 ± 1.3 mV, P < 0.001). Eighty-eight percent of VT channel or exit sites (n = 44) were metabolically abnormal (severe PET defect, 78%; moderate PET defect, 10%), whereas 12% (n = 6) were in PET-normal areas. Metabolic channels (n = 26) existed in 45% (n = 25) of patients, with an average length and width of 17.6 ± 12.5 mm and 10.3 ± 4.2 mm, respectively. Metabolic channels were oriented predominantly in the apex or base (86%), harboring VT channel or exit sites in 31%. Metabolic rapid-transition areas (>50% change in 18F-FDG tracer uptake/15 mm) were detected in 59% of cases (n = 33), colocalizing to VT channels or exit sites (15%) or near these sites (85%, 12.8 ± 8.5 mm). Metabolism-voltage mismatches in which there was a severe PET defect but voltage indicating normal myocardium were seen in 21% of patients (n = 12), 41% of whom were harboring VT channel or exit sites. Conclusion: Abnormal 18F-FDG uptake categories could be detected using incremental 3D step-up reconstructions. They predicted decreasing bipolar voltages and VT channel or exit sites in about 90% of cases. Additionally, functional imaging allowed detection of novel molecular tissue characteristics within the ischemic VT substrate such as metabolic channels, rapid-transition areas, and metabolism-voltage mismatches demonstrating intrasubstrate heterogeneity and providing possible targets for imaging-guided ablation.
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Fluordesoxiglucose F18 , Isquemia Miocárdica , Idoso , Cicatriz , Humanos , Pessoa de Meia-Idade , Taquicardia VentricularRESUMO
Postischemic adaptation results in characteristic myocardial structural and functional changes in the ventricular tachycardia (VT) substrate. The aim of this study was to compare myocardial structural and functional adaptations (late gadolinium enhancement/abnormal innervation) with detailed VT mapping data to identify regional heterogeneities in postischemic changes. Methods: Fifteen patients with ischemic cardiomyopathy and drug-refractory VT underwent late gadolinium enhancement cardiac MRI (CMR), 123I-metaiodobenzylguanidine SPECT, and high-resolution bipolar voltage mapping to assess fibrosis (>3 SDs), abnormal innervation (<50% tracer uptake), and low-voltage area (<1.5 mV), respectively. Three-dimensional reconstructed CMR/123I-metaiodobenzylguanidine models were coregistered for further comparison. Results: Postischemic structural and functional adaptations in all 3 categories were similar in size (reported as median [quartile 1-quartile 3]: CMR scar, 46.1 cm2 [33.1-86.9 cm2]; abnormal innervation, 47.8 cm2 [40.5-68.1 cm2]; and low-voltage area, 29.5 cm2 [24.5-102.6 cm2]; P > 0.05). However, any single modality underestimated the total VT substrate area defined as abnormal in at least 1 of the 3 modalities (76.0 cm2 [57.9-143.2 cm2]; P < 0.001). Within the total VT substrate area, regions abnormal in all 3 modalities were most common (25.2%). However, significant parts of the VT substrate had undergone heterogeneous adaptation (abnormal in <3 modalities); the most common categories were "abnormal innervation only" (18.2%), "CMR scar plus abnormal innervation only" (14.9%), and "CMR scar only" (14.6%). All 14 VT channel/exit sites (0.88 ± 0.74 mV) were localized to myocardium demonstrating CMR scar and abnormal innervation. This specific tissue category accounted for 68.3% of the CMR scar and 31.2% of the total abnormal postischemic VT substrate area. Conclusion: Structural and functional imaging demonstrated regional heterogeneities in the postischemic VT substrate not appreciated by any single modality alone. The coexistence of abnormal innervation and CMR scar may identify a particularly "proarrhythmic" adaptation and may represent a potential novel target for VT ablation.