remature ventricular contractions (PVCs) are a common arrhythmia, even in people without structural heart disease, and has been reported at an incidence rate of approximately 1% on standard 12-lead ECGs and 40-75% on routine 24-h Holter ECG. 1,2 PVCs in a structurally normal heart are almost idiopathic, but multiform PVCs, high PVC burden, or the presence of non-sustained ventricular tachycardia (VT) are associated with inverse clinical outcomes such as death, heart failure and cardiovascular hospitalization. 3-5 Many previous reports show that PVCs can develop into cardiomyopathy and that risk factors include PVC frequency, PVC origin, short PVC coupling interval (CI), and VT. 6-9 Some patients have symptoms that were seemingly associated with PVCs and require treatment such as antiarrhythmic drugs 10-12 or catheter ablation, 13-15 which have been reported as effective. PVC-related symptoms include pulse deficit, palpitations, shortness of breath, malaise and syncope. Yet no explicit relationship between the presence of symptoms and the frequency of PVCs has been observed. 16 The mechanism of symptomatic PVCs is still unknown, although the PVC CI is associated with symptoms. 17 There have been few reports on the relationship between PVCs and these symptoms, and the cause of symptomatic PVCs remains unclear. Therefore, we investigated the hemodynamic features that could cause symptomatic PVCs. Methods Patients We enrolled 189 consecutive patients with frequent monomorphic PVCs on standard 12-lead or 24-h Holter ECG who visited Hyogo College of Medicine for examination of PVCs between November, 2016 and January, 2018. We defined frequent PVC when â„2 beats of PVC were recorded on 12-lead ECG during a 10-s period more than twice. Of the patients, 27 who had structural heart disease (11 cases of ischemic heart disease, 2 of hypertrophic cardiomyopathy, 4 of hypertensive heart disease, 1 case each of dilated cardiomyopathy and severe aortic valve regurgitation, 5 other cases) or rhythm abnormality (3 cases of atrial fibrillation, 2 cases of pacemaker rhythm) were excluded. Among the remaining 162 patients, 1 case of bigeminy of PVCs, one of unstable interval of preceding R wave and PVC, and 7 cases of an unclear relationship between PVCs and symptoms were also excluded. Patients with polymorphic PVCs on standard 12-lead or 24-h Holter ECG were not included. Another 44 cases of patients who did not have PVCs recorded during echocardiography were also excluded, and the remaining 109 patients were studied. All patients underwent standard 12-lead ECG, 24-h Holter ECG and echocardiography. Blood samples for atrial natriuretic peptide (ANP) and B-type natriuretic pep