Is it Morning Blood Pressure Surge or Extreme Nocturnal Dipping That Accounts for the Increased Stroke Risk in the Morning Waking Hours?

Normal circadian rhythm of blood pressure (BP) shows a diurnal variation with the highest BP levels reached during the morning and then declining to a trough value around midnight. In the early morning, an abrupt and steep acceleration of BP occurs on arising from sleep.1 There is an increased risk of stroke, myocardial infarction, and sudden death in the first few hours after waking,2 but the reasons for this remain speculative. Although it has been postulated that the morning BP surge is directly related to the risk for cardiovascular (CV) events, it is unclear whether this increased risk is related to the morning BP itself, or to an extreme nocturnal decline (ie, exaggerated “dipping”) defined as more than a 20% difference between daytime and nighttime BP readings. A study by Kario and colleagues1 of silent cerebral infarcts and stroke assessed by brain magnetic resonance imaging in elderly hypertensive patients calculated the mean systolic BP (SBP) during the 2 hours after awakening minus the SBP during the lowest hour of sleep BP. After an average of 41 months, 44 stroke events occurred, with the highest likelihood in the 53 patients (top decile) whose morning SBP surge was greater than 55 mm Hg. This group had a higher baseline prevalence of multiple infarcts and a higher stroke incidence during the follow-up period than the group with less BP increase on arising. The relationship of morning BP surge to stroke events in the highest decile was independent of 24-hour BP, nocturnal dipping, and baseline prevalence of silent brain infarction. The study has limitations in that it was performed in an older Japanese population known to have a higher risk of stroke and may not be readily applicable to populations in the United States or Europe. A recent retrospective study from Brazil of 632 hypertensive adults confirmed these findings using a cutoff of 41 mm Hg for the morning surge in SBP.3 On the other hand, an Italian investigation of the association between morning surge in SBP and risk for stroke in 1191 elderly treated hypertensive patients divided according to tertiles of morning surge in SBP and dipping status showed no significant association with ischemic stroke during 9 years of follow-up.4 However, the stroke risk was different when nondippers and dippers were analyzed separately. They observed that the stroke risk was not associated with morning surge in nondippers, but, in dippers, stroke risk was significantly higher in the third tertile (>23 mm Hg) of morning surge in SBP. Stroke risk was similarly high in dippers with SBP morning surge greater than 23 mm Hg and in nondippers, arguing that higher morning surge values predicted stroke risk in dippers but not in nondippers because nondippers are at risk for stroke with or without a threshold value for morning surge. Finally, in another study from Italy, 2051 patients were followed up for 16 years logging the occurrence of CV events and all-cause deaths with the addition of echocardiography to assess for left ventricular hypertrophy 10 years after the baseline visit.5 In this population with a wide age spectrum (25–74 years), morning BP surge was not found to be an independent predictor of cardiovascular death, all-cause death, or the development of high cardiovascular risk (as documented by new-onset left ventricular hypertrophy). Our take on this is threefold. First, losing circadian variation in BP is not a good thing. Second, extreme dipping or an exaggerated morning surge in SBP may be two sides of the same coin. Lastly, when morning surge does exist it could represent a plausible intervention target for clinical trials, which are sorely needed to guide us in what to do. It may also be useful to tell patients with an early morning SBP surge to avoid intense physical exercise in the early morning. But what is the level of morning surge that is significant? We're going to sleep on that one, for now.