Premature ventricular contraction (PVC) is very commonly seen in healthy hearts, in clinical practice, in addition to the underlying heart diseases. The prevalence of PVC in the healthy population is around 6% [1]. Although the polymorphic PVC prevalence is known to be less than monomorphic PVC, the exact prevalence is unknown.

It causes symptoms such as palpitation, shortness of breath, and fatigue in many patients. It has been shown that PVC may cause tachycardiomyopathy and further decrease left ventricular ejection fraction (LVEF) in pre-existing cardiomyopathy [2]. PVC, in the case of underlying structural cardiac disease, may develop into malignant arrhythmias [3,4]. PVCs have been shown to affect the long-term outcome with a relatively low frequency in patients with a structurally healthy heart [5]. Left ventricular (LV) dysfunction caused by frequent PVC may improve by an effective drug or catheter ablation treatment [[6], [7], [8], [9]]. The pathophysiology associated with the development and recovery of PVC-related ventricular dysfunction is mostly unknown. It has been shown that PVC frequency should be >10% in 24 h to cause cardiomyopathy [8].

Catecholamines are hormones with arrhythmic effects through cardiac beta receptors [10]. Continuous stimulation of β-receptors by catecholamines in heart failure sets the ground for arrhythmias by triggered activity on the phase-4 portion of action potentials with molecular and structural changes, including hypertrophy, cardiac fibrosis, and electromechanical dysfunction [11,12]. There has been no previous study showing the relationship between catecholamine levels and PVC.

Our aim in this study is to investigate if excessive catecholamine synthesis without a condition that increases adrenergic activity such as heart failure or pheochromocytoma may lead to PVC due to chronic beta-receptor stimulation.