Noemí Ramos-López, Nerea Mora-Ayestarán, Juan Pablo Ochoa, Eduard Claver, Cristina Gómez González, Edwin Poel, Mónica García Monsalvo, Guillem Casas, Carmen Muñoz-Esparza, María Teresa Basurte-Elorz, José M Larrañaga-Moreira, Jose M García-Pinilla, María Victoria Mogollón Jiménez, Gonzalo Cabezón Villalba, Victoria Espejo Bares, María Ruiz-Cueto, Bernardo López-Abel, Ana García-Álvarez, Vicente Climent-Payá, Coloma Tirón, Eva Cabrera-Borrego, María Luisa Peña-Peña, Tomas Ripoll-Vera, Esther Zorio, Javier Sanaú, Elena Rodríguez González, Connie R Bezzina, María Gallego Delgado, José F Rodríguez-Palomares, Andrea di Marco, María Ángeles Espinosa Castro, Ahmad S Amin, Pablo Garcia-Pavia, Jesús G Mirelis
LGE corridors and HRGs provide additive value for arrhythmic risk stratification in patients with nonischemic dilated cardiomyopathy. These findings support MVA multiparametric prediction over the traditional left ventricular ejection fraction ≤35% threshold.
BACKGROUND: Fibrosis assessed through late gadolinium enhancement (LGE) in cardiac magnetic resonance imaging and genetics have emerged as risk markers of ventricular arrhythmias in nonischemic dilated cardiomyopathy. Conduction corridors detected within LGE (ie, LGE corridors) have been associated with ventricular arrhythmias in ischemic cardiomyopathy. This study sought to evaluate major ventricular arrhythmic events (MVAs) according to the presence of LGE corridors combined with high-risk genotypes (HRGs) in nonischemic dilated cardiomyopathy.
METHODS: We studied consecutive patients with nonischemic dilated cardiomyopathy from 22 European centers who had undergone genetic testing and cardiac magnetic resonance imaging.
RESULTS: Among 925 patients (mean age, 54.5 years [interquartile range, 43.7-63.9 years]; 64% men; mean left ventricular ejection fraction, 37.6% [26.9%-44.8%]; LGE in 24.3%), LGE corridors were present in 160 patients (17.3%), and HRG in 119 (12.9%). After a median follow-up of 5.4 years (interquartile range, 3.3-7.7), 95 patients (10.3%) experienced an MVA. In multivariable competing-risk analysis adjusted for left ventricular ejection fraction and extent of LGE, the number of LGE corridors and HRGs were independently associated with MVA (subdistribution hazard ratio, 1.25 [95% CI, 1.11-1.42]; P<0.001; and subdistribution hazard ratio, 2.28 [95% CI, 1.32-3.96]; P=0.003, respectively). An optimal cutoff of ≥4 LGE corridors predicted MVA. A stepwise risk stratification algorithm to predict MVA integrating LGE, the presence of ≥4 LGE corridors, and HRG outperformed left ventricular ejection fraction ≤35%-based classification proposed in guidelines (5-year time-dependent area under the curve, 0.72 [95% CI, 0.65-0.78] versus 0.57 [95% CI, 0.51-0.64]; P=0.001), showing a progressive increase in arrhythmic risk across categories (Gray test P<0.001), and allowing clinically meaningful arrhythmic risk classification.
CONCLUSIONS: LGE corridors and HRGs provide additive value for arrhythmic risk stratification in patients with nonischemic dilated cardiomyopathy. These findings support MVA multiparametric prediction over the traditional left ventricular ejection fraction ≤35% threshold.