Utility of high-resolution electroanatomic mapping of the left ventricle using a multispline basket catheter in a swine model of chronic myocardial infarction.

BACKGROUND Standard electroanatomic mapping systems use a single catheter to perform left ventricular substrate mapping. A new mapping system uses a 64-electrode mini-basket catheter to perform rapid automated acquisition of chamber geometry, voltage, and activation. OBJECTIVE The aim of this study was to compare the accuracy of electroanatomic mapping using the basket catheter with that of mapping using a standard linear catheter in a swine model of chronic myocardial infarction. METHODS Ten swine underwent left anterior descending coronary artery occlusion to create an anteroseptal myocardial infarction. Animals underwent delayed-enhancement magnetic resonance imaging (MRI) and then detailed left ventricular voltage mapping with both the basket and the linear catheter. Map characteristics and scar area were compared between the basket catheter, linear catheter, and MRI. Induced ventricular tachycardia (VT) was mapped with the basket catheter. RESULTS More points were acquired with the basket catheter than with the standard catheter (8762 ± 3164 vs 1712 ± 551; P < .001). The fifth percentile of normal bipolar voltage distribution with the basket catheter was 1.54 mV. Using a bipolar voltage cutoff of 1.5 mV, the total infarct areas measured using the basket catheter, linear catheter, and MRI were similar (17.8 cm(2) vs 20.9 cm(2) vs 17.5 cm(2); P = .69); however, the correlation between MRI and catheter scar area measurement was best for the basket catheter (basket vs linear: r = .76 vs r = .71). In 3 animals, sustained poorly tolerated VT was initiated and the circuit mapped successfully with the basket catheter in <5 minutes. CONCLUSION Rapid substrate and activation mapping using a 64-electrode mini-basket catheter allows detailed voltage and activation mapping in postinfarction cardiomyopathy. This system may be useful for substrate and VT mapping in human postinfarction cardiomyopathy.