Introduction: Increased arterial stiffness is currently recognized as an independent risk factor for atrial fibrillation, but the pathophysiological mechanisms of this arrhythmia remain poorly understood.Objectives: This study aims to investigate the association of arterial stiffness with the presence of nonsustained atrial tachycardia (NSAT) in hypertensive patients, possibly a premonitory phase of atrial fibrillation.Methods: Cross-sectional, exploratory, proof-of-concept study.Arterial stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV) and by the Augmentation Index corrected for a heart rate of 75 bpm (AIx@75).Speckle-tracking echocardiography was used to assess left atrial (LA) function, including its reservoir, conduit and contraction properties.Patients with NSAT of 10 or more beats on 24h-ECG were categorized in the NSAT group and controls without this arrhythmia were selected for the non-NSAT group.Results: Seventy participants from a single centre without evident cardiovascular disease after undergoing a standard cardiovascular clinical examination were included.The NSAT group, when compared to the control group, had a higher mean age (70.09 ± 7.29 vs. 63.68 ± 7.11, p-value 0.001), a higher BNP levels (28.1% vs. 0.0%, p-value <0.001), lower HDL cholesterol levels (51.03 ± 12.16 vs. 58.81±16.50, p-value 0.027), higher left ventricular (LV) mass index (90.00±19.95 vs. 76.05 ±15.60, p-value 0.002) and higher density of premature atrial beats in 24h (531.00 [173.00;5890.00]vs 17.00 [9.00;35.00],p-value <0.001).The cfPWV was correlated with highest premature atrial beats density in 24h Holter monitoring, independently of the LV mass index, and the increase in cfPWV correlated with the decrease in LA strain values (reservoir and conduit). Conclusion:In this study with 70 hypertensive patients, it was possible to demonstrate a positive correlation between cfPWV and the presence of higher density of atrial arrhythmias on 24-hour Holter Monitoring.In addition, higher cfPWV was associated with lower left atrial strain values for reservoir and conduit functions, thus representing a possible pathophysiological mechanism in the development of atrial arrhythmias other than atrial fibrillation.