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.