Many studies in the past decade have demonstrated diurnal variation in the onset of acute cardiovascular disorders in hypertensive patients, such as acute coronary syndrome like heart attack, angina etc and ischemic and hemorrhagic stroke occurring in the morning (6:00AM to noon) after a nadir in these events during the night.

Blood pressure falls during the night because of the reduction of sympathetic activity that is brought about by sleep and then increases steeply when in the morning the subject awakes and resumes his or her daily activities. This increase occurs together with a peak incidence of cerebral and cardiac events in the morning hours. Moreover, a recent prospective study suggests that higher morning BP surge (MBPS) might be an independent risk factor of atherosclerotic events beyond ambulatory BP and nocturnal BP falls. the molecular mechanism associating MBPS peak and vulnerable atherosclerotic plaque are not clear, although inflammation which plays a central role in the cascade of events that result in plaque erosion and fissuring also were related to MBPS. Because study suggests that both ischemic and hemorrhagic strokes showed a greater tendency to cluster in the morning period, it is reasonable to suppose that an excessive MBPS increase might trigger strokes through some hemodynamic mechanism, such as increased shear stress, that in turn may activate the molecular pathwayfavoring plaque instability, such as increased oxidative stress.