Morning Surges in Blood Pressure

Hypertension is an undisputed risk factor for cerebrovascular accidents, in addition to cardiovascular events. A recent meta‐analysis on the circadian timing of stroke onset ¹ reported that strokes (transient ischemic attack, ischemic, and hemorrhagic), like heart attacks, occur more frequently in the first hours after waking—between 6 a.m. and 12 p.m.—compared with the rest of the day. Blood pressure (BP), which fluctuates over 24 hours, is usually higher in the morning and declines as the day progresses. In some people, particularly those who are older, the magnitude of the BP increase in the early morning hours can be considerable.

A relationship between this pronounced increase in systolic BP as one transitions from sleep to wakefulness is known as the “morning surge.” It's usually calculated by subtracting the mean systolic BP during hours of lowest sleep BPs from the mean systolic BP during the 2 hours after waking. When the systolic increase is >55 mm Hg (e.g., sleep systolic BP, 100 mm Hg; systolic BP at 11 a.m., 160 mm Hg), it appears to be associated with both silent (as found by MRI scanning, for example) as well as clinically manifest cerebrovascular disease. This has recently been reported by Kario et al. ² in older Japanese patients. In their experience, increases in systolic pressure on arising of ≥55 mm Hg were associated with more than a doubling of the risk of stroke independent of other risk factors such as ambulatory BP levels, nocturnal dip in pressure, and target organ damage. It should be remembered, however, that in Japan coronary artery disease is less frequent when compared with the United States, and stroke as a target organ event is seen more commonly than in the United States.

What drives this increase in systolic pressure in certain patients is partially understood. Excessive sympathetic activation is currently the most likely mechanism, with the resulting hemodynamic effect of an increased shear stress on atherosclerotic cerebral vessels contributing to the stroke outcome. ³ The unfavorable circadian variations in hemostatic and fibrinolytic factors that result in morning hypercoagulability and hypofibrinolysis ⁴ also likely play a role in the promotion of intraluminal thrombi, perhaps more so in patients who show the morning surge.

A logical question then arises: “What do I do with this information?” We suggest three things. First, awareness of the morning surge in BP and increased risk of stroke may be a help in managing older patients (who are at greatest risk). Second, it may behoove some patients to make the modest investment in a home BP monitor and take periodic BP readings within the few hours of awakening. Sleeping BP values may not be available, but it may be possible to determine that the current BP medication regimen is not controlling the early morning BP changes. Lastly, in people whose typical systolic pressures are high in the morning, shifting medications to a p.m. dosing or adding a p.m. medication may cover the early morning period. What medication to shift or add is still empiric; we favor an α‐adrenergic type of antihypertensive drug based on the sympathetic nervous system's role, but we await further evidence.