Left ventricular noncompaction (LVNC), formally classified as a distinct cardiomyopathy by the American Heart Association in 2006, is characterized by prominent trabeculae, intertrabecular recesses, and a bilayered myocardium [[1], [2], [3]]. The clinical manifestations of LVNC are highly heterogeneous, ranging from asymptomatic cases to severe events such as ventricular arrhythmias, heart failure, thromboembolism, and sudden cardiac death [4]. Previous studies have shown that left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) imaging are the two most important prognostic factors in patients with LVNC [[5], [6], [7]]. Electrocardiography (ECG) is an essential diagnostic tool in clinical practice, providing important information for a variety of cardiovascular conditions. While studies have reported common ECG abnormalities in LVNC, including intraventricular conduction delays, repolarization abnormalities, and left ventricular (LV) hypertrophy, no specific ECG pattern has been conclusively linked to LVNC [[8], [9], [10]]. Population-based studies have demonstrated that abnormal P wave terminal force in lead V1 (PTFV1), which is a simplified ECG marker for left atrial (LA) abnormalities such as enlargement and elevated filling pressure, can independently predict an increased risk of atrial fibrillation, cerebrovascular events, heart failure hospitalizations, and cardiac death across a range of cardiovascular diseases, regardless of clinical risk factors [[11], [12], [13]]. However, the potential role of PTFV1 in patients with LVNC has not been reported. Therefore, this study aims to investigate the prevalence of PTFV1 in patients with LVNC and explore its possible association with abnormalities in both LA and LV.