RESUMO
OBJECTIVE: Investigate the capacity of MRI to evaluate efficacy of radiofrequency (RF) ablations delivered to MRI-defined arrhythmogenic substrates. METHODS: Baseline MRI was performed at 3T including 3D LGE in a swine model of chronic myocardial infarct (N=8). MRI-derived maps of scar and heterogeneous tissue channels (HTCs) were generated using ADAS 3D. Animals underwent electroanatomic mapping and ablation of the left ventricle in CARTO3, guided by MRI-derived scar maps. Post-ablation MRI (in vivo at 3T in 5/8 animals; ex vivo at 1.5T in 3/8) included 3D native T1-weighted IR-SPGR (TI=700-800ms) to visualize RF lesions. T1-derived RF lesions were compared against excised tissue. The locations of T1-derived RF lesions were compared against CARTO ablation tags, and segment-wise sensitivity and specificity of lesion detection were calculated within the AHA 17-segment model. RESULTS: RF lesions were clearly visualized in HTCs, scar, and myocardium. Ablation patterns delivered in CARTO matched T1-derived RF lesion patterns with high sensitivity (88.9%) and specificity (94.7%), and were closely matched in registered MR-EP data sets, with a displacement of 5.4 ±3.8mm (N=152 ablation tags). CONCLUSION: Integrating MRI into ablative procedures for RF lesion assessment is feasible. Patterns of RF lesions created using a standard 3D EAM system are accurately reflected by MRI visualization in healthy myocardium, scar, and HTCs comprising the MRI-defined arrhythmia substrate. SIGNIFICANCE: MRI visualization of RF lesions can provide near-immediate (<24h) assessment of ablation, potentially indicating whether critical MRI-defined ventricular tachycardia substrates have been adequately ablated.
RESUMO
Stress imaging identifies ischemic myocardium by comparing hemodynamics during rest and hyperemic stress. Hyperemia affects multiple hemodynamic parameters in myocardium, including myocardial blood flow (MBF), myocardial blood volume (MBV), and venous blood oxygen levels (PvO2 ). Cardiac T2 is sensitive to these changes and therefore is a promising non-contrast option for stress imaging; however, the impact of individual hemodynamic factors on T2 is poorly understood, making the connection from altered T2 to changes within the tissue difficult. To better understand this interplay, we performed T2 mapping and measured various hemodynamic factors independently in healthy pigs at multiple levels of hyperemic stress, induced by different doses of adenosine (0.14-0.56 mg/kg/min). T1 mapping quantified changes in MBV. MBF was assessed with microspheres, and oxygen consumption was determined by the rate pressure product (RPP). Simulations were also run to better characterize individual contributions to T2. Myocardial T2, MBF, oxygen consumption, and MBV all changed to varying extents between each level of adenosine stress (T2 = 37.6-41.8 ms; MBF = 0.48-1.32 mL/min/g; RPP = 6507-4001 bmp*mmHg; maximum percent change in MBV = 1.31%). Multivariable analyses revealed MBF as the dominant influence on T2 during hyperemia (significant ß-values >7). Myocardial oxygen consumption had almost no effect on T2 (ß-values <0.002); since PvO2 is influenced by both oxygen consumption and MBF, PvO2 changes detected by T2 during adenosine stress can be attributed to MBF. Simulations varying PvO2 and MBV confirmed that PvO2 had the strongest influence on T2, but MBV became important at high PvO2 . Together, these data suggest a model where, during adenosine stress, myocardial T2 responds predominantly to changes in MBF, but at high hyperemia MBV is also influential. Thus, changes in adenosine stress T2 can now be interpreted in terms of the physiological changes that led to it, enabling T2 mapping to become a viable non-contrast option to detect ischemic myocardial tissue.
