Assessing heterogeneity on cardiovascular magnetic resonance imaging: a novel approach to diagnosis and risk stratification in cardiac diseases.

Cardiac disease affects the heart non-uniformly. Examples include focal septal or apical hypertrophy with reduced strain in hypertrophic cardiomyopathy, replacement fibrosis with akinesia in an infarct-related coronary artery territory, and a pattern of scarring in dilated cardiomyopathy. The detail and versatility of cardiovascular magnetic resonance (CMR) imaging mean it contains a wealth of information imperceptible to the naked eye and not captured by standard global measures. CMR-derived heterogeneity biomarkers could facilitate early diagnosis, better risk stratification, and a more comprehensive prediction of treatment response. Small cohort and case-control studies demonstrate the feasibility of proof-of-concept structural and functional heterogeneity measures. Detailed radiomic analyses of different CMR sequences using open-source software delineate unique voxel patterns as hallmarks of histopathological changes. Meanwhile, measures of dispersion applied to emerging CMR strain sequences describe variable longitudinal, circumferential, and radial function across the myocardium. Two of the most promising heterogeneity measures are the mean absolute deviation of regional standard deviations on native T1 and T2 and the standard deviation of time to maximum regional radial wall motion, termed the tissue synchronization index in a 16-segment left ventricle model. Real-world limitations include the non-standardization of CMR imaging protocols across different centres and the testing of large numbers of radiomic features in small, inadequately powered patient samples. We, therefore, propose a three-step roadmap to benchmark novel heterogeneity biomarkers, including defining normal reference ranges, statistical modelling against diagnosis and outcomes in large epidemiological studies, and finally, comprehensive internal and external validations.

Ischemic ventricular tachycardia: Multimodality imaging in precision ablation guidance.

Radiofrequency ablation is commonly performed in the management of incessant ventricular tachycardias. Pre-procedural planning using different imaging modalities including cardiac computed tomography and cardiac magnetic resonance plays an integral role in understanding the anatomy and potential origin of the arrhythmias to guide successful targeted ablation.

Impact of Intramural Scar on Mapping and Ablation of Premature Ventricular Complexes.

OBJECTIVES: This study sought to determine intramural scar characteristics associated with successful premature ventricular complex (PVC) ablations. BACKGROUND: Ablating ventricular arrhythmias (VAs) originating from intramural scarring can be challenging. Imaging of intramural scar location may help to determine whether the scar is within reach of the ablation catheter. METHODS: Mapping and ablation of premature ventricular complexes (PVCs) was performed in a consecutive series of patients with intramural scarring and frequent PVCs. Data from delayed enhanced cardiac magnetic resonance were assessed and the proximity of the endocardium containing the breakout site to the intramural scar was correlated with outcomes. RESULTS: Fifty-six patients were included, and intramural VAs were successfully targeted in 42 patients (75%) and ablation failed in 14 patients (25%). Scarring was more superficial to the endocardium in patients with successful ablations compared with patients with failed procedures (0.35 mm [interquartile range (IQR): 0.22 to 1.20 mm] vs. 2.45 mm [IQR: 1.60 to 3.13 mm]; p < 0.001). In 18 (32%) patients, ablation at the breakout site resulted in a significant change of the PVC-QRS morphology that could successfully be ablated in 9 of 12 patients from another anatomical aspect of the wall harboring the intramural scar. The scar was larger in size (1.79 cm3 [IQR: 1.25 to 2.85 cm3] vs. 1.00 cm3 [IQR: 0.59 to 1.68 cm3]; p < 0.005) compared with patients who did not have a change in the PVC-QRS morphology with ablation. CONCLUSIONS: VAs in patients with intramural scaring can be successfully ablated especially if the intramural scar is within close proximity to the anatomic area containing the breakout site. Changes in the QRS-PVC morphology often precede successful ablation at another breakout site and indicate larger intramural scars.

Magnetic Resonance Mapping of Catheter Ablation Lesions After Post-Infarction Ventricular Tachycardia Ablation.

OBJECTIVES: This study sought to describe cardiac magnetic resonance (CMR) characteristics of ablation lesions within post-infarction scar. BACKGROUND: Chronic ablation lesions created during radiofrequency ablation of ventricular tachycardia (VT) in the setting of prior myocardial infarction have not been described in humans. METHODS: Seventeen patients (15 men, ejection fraction 25 ± 8%, 66 ± 6 years of age) with CMR imaging prior to repeat ablation procedures for VT were studied. Electroanatomic maps from first-time procedures and subsequent CMR images were merged and retrospectively compared with electroanatomic maps from repeat procedures. RESULTS: The delay between the index ablation procedure and the CMR study was 30 ± 29 months. Late gadolinium-enhanced CMR revealed a confluent nonenhancing subendocardial dark core within the infarct-related scar tissue in all patients. Intracardiac thrombi were ruled out by transthoracic and intracardiac echocardiography. These core lesions matched the distribution of prior ablation lesions, and corresponded to unexcitable areas at repeat procedures. CONCLUSIONS: Ablation lesions can be detected by CMR after VT ablation in post-infarction patients and have a different appearance than scar tissue. These lesions can be observed many months after an initial ablation.

Value of mapping and ablation of ventricular tachycardia targets within the coronary venous system in patients with nonischemic cardiomyopathy.

BACKGROUND: Patients with nonischemic cardiomyopathy (NICM) often require epicardial ventricular tachycardia (VT) ablation procedures via subxiphoid access. The coronary venous system (CVS) provides limited access to the epicardial space. OBJECTIVE: The purpose of this study was to determine the value of an approach targeting the CVS in these patients. METHODS: In a series of 41 consecutive patients (mean age 59.7 ± 11.5 years; 36 men [88%]; ejection fraction 34.5% ± 13.1%; 269 inducible VTs [6.6 ± 5.0 VTs per patient]) with NICM and VT, mapping and ablation were performed sequentially at the endocardium, then within the CVS, and finally within the pericardial space if required. RESULTS: VT target sites were identified within the CVS in 15 patients and by subxiphoid access to the pericardial space in 8 patients. Ablation within the CVS eliminated VT inducibility in 9 patients without the need for epicardial ablation. Cardiac magnetic resonance imaging demonstrated that the CVS was closer to a scarred area in patients with CVS-related VT target sites than in other patients (mean 3.5 ± 3.9 mm vs 14.3 ± 8.3 mm; P < .001). A cutoff distance of ≤9 mm from the scar (area under the curve 0.91; 95% confidence interval 0.82-0.99; sensitivity 0.78; specificity 0.93) identified patients with vs patients without VT target sites within the CVS. CONCLUSION: A stepwise approach with mapping/ablation in the endocardium followed by ablation within the CVS can reduce the need for subxiphoid epicardial access in some patients with NICM. Proximity of the scar to the CVS detected by cardiac magnetic resonance imaging can identify the patients most likely to benefit from this approach.

Predictors and Therapy of Cardiomyopathy Caused by Frequent Ventricular Ectopy.

PURPOSE OF REVIEW: The aim of this review is to describe predictors and therapeutic principles for PVC-induced cardiomyopathy. RECENT FINDINGS: PVC-induced cardiomyopathy is a treatable condition resulting in a reversible form of cardiomyopathy. PVC-induced cardiomyopathy has only recently been recognized as an entity that causes a reversible form of cardiomyopathy. The mechanism of development of PVC-induced cardiomyopathy has not yet been elucidated, although dyssynchrony appears to play a major role. Multiple factors have been described that are independently associated with PVC-induced cardiomyopathy. Predictors of PVC-induced cardiomyopathy include PVC prevalence, epicardial origin, male gender, longer symptom duration and asymptomatic status, presence of interpolated PVCs, lack of circadian variability, and a broader PVC-QRS width. In the presence of cardiomyopathy, work-up for structural heart disease and its etiology should be performed, followed by aggressive attempts at PVC reduction. There is evidence that ablation therapy is superior to medical therapy for frequent PVCs, but treatment decisions need to be individualized depending on the patients symptoms, PVC prevalence, PVC origin, patients comorbidities, and patient preference. The potential of sudden cardiac death associated with the presence of structural heart disease needs to be recognized, and appropriate risk stratification is mandatory.