Introduction
Ventricular arrhythmias (VAs) are commonly recorded electrocardiographic abnormalities, including premature ventricular complexes (PVCs), non-sustained ventricular tachycardia (NSVT), accelerated idioventricular rhythm, sustained ventricular tachycardia (SVT), and ventricular fibrillation (VF).1 These arrhythmias, especially PVCs, can be observed in individuals without structural heart diseases.2-7 In these conditions, they are usually believed to be benign.3,6,8 However, frequent and polymorphic VAs, as well as malignant ventricular arrhythmias, could contribute to worse prognoses, such as cardiomyopathies, high heart failure risks, and even sudden cardiac death (SCD).3, 4, 6, 9-11
Myocardial fibrosis/scars provide potential substrates for the initiation and perpetuation of ventricular arrhythmias,11-13 which propagate around localized scar regions and along slow conduction zones.12Previous studies have reported that myocardial fibrosis plays an important role in risk stratifications of nonischemic cardiomyopathy.12-14 Cardiac magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE) is a noninvasive tool that can accurately identify and quantify ventricular myocardial fibrosis.12,15 Conversely, the presence of VAs can result in myocardial fibrosis. A previous study reported that multiple PVC morphologies could increase the prevalence of left ventricular fibrosis in patients undergoing ablation.11 It is unclear whether VAs in apparently normal hearts could induce fibrosis. To date, few studies have explored the association between VAs occurrence and morphologies and left-ventricular late gadolinium enhancement (LV-LGE) characteristics in apparently normal hearts.
Therefore, the purpose of our study was to investigate the relationship between VA occurrence and morphologies and LV-LGE characteristics in patients without known structural heart diseases.