 It has also been suggested that nocturnal HTN and non-dipping of BP during sleep are distinct entities that often occur together and are regarded as important harbingers of poor cardiovascular prognosis. Recently, Pierdomenico et al., showed that non-dipper sustained hypertensives have a two-fold greater risk of developing AF than dipper ones. This may be due to the fact that nighttime HTN may be a powerful determinant of long-standing left ventricular diastolic dysfunction, which subsequently increases atrial stretch. Furthermore, it has been observed that nighttime hemodynamics, are associated with higher sympathetic and reduced vagal activity, which may trigger AF. Additionally, sympathetic activation is associated with the stimulation of the renin-angiotensin-aldosterone axis RAAA, which leads to increased left ventricular diastolic preload, both atrial and ventricular fibrosis, exerting thus direct cellular electrophysiological effects. Besides, scientists suggested that nighttime HTN is better associated with cardiovascular target organ damage TOD as compared with the non-dipping pattern. 