One of the most obvious observations among early studies that employed ambulatory measures of blood pressure recording was the fact that blood pressure tended to decrease (or dip) during nighttime hours or the hours during which the patient was sleeping. In brief, blood pressure typically exhibits a circadian rhythm, with lowest values occurring at night among persons on a normal sleep-wake cycle.
This was certainly no surprise, as comparable reductions in nighttime blood pressure were observed in hospitalized patients when intra-arterial recordings of blood pressure were being assessed. What became of interest to these investigators, however, was the considerable variability of the observed reduction in blood pressure that occurred during nighttime or periods of sleep. While many participants in these studies exhibited reductions in nocturnal blood pressure of 10percent or more (dippers), about one third of them showed very little reduction at all (non-dippers; Verdecchia, Schillaci, and Porcellati, 1991).
In contrast to dippers, research has shown that non-dippers exhibit higher left ventricular mass (Verdecchia et al., 1990), increased secretion of albumen (Bianchi et al., 1994), and increased incidence of stroke (Phillips et al., 2000) as well as cardiovascular disease (Ohkubo et al., 1997; Verdecchia et al., 1994). However, target organ pathology or risk for cardiovascular disease do not always differ in comparisons between dippers and non-dippers (Cuspidi et al., 1999; Roman et al., 1997), indicating that the association between dipper status and risk for cardiovascular disease may not be that robust. Furthermore, there is some evidence suggesting that extreme dipping (defined as a reduction in blood pressure during night greater than 20 percent) might also be associated with increased risk for cerebrovascular damage (Kario et al., 1996).
Therefore, the association between the degree of dipping during nighttime and risk for cardiovascular or cerebrovascular disease may be curvilinear in nature. Certainly, additional prospective trials are needed to clarify the inconsistent findings in this body of literature.
Part of the reason for these conflicting findings has been thought to be related to the unreliability associated with measurement of dipping status. Simply put, a significant number of individuals who exhibit a given dipping status during an ambulatory blood pressure monitoring period fail to show that same status during a second monitoring period (Dimsdale and Herren, 1998; Manning et al., 2000).
It is also possible that non-dipping is associated with increased disease risk only among a subgroup of individuals. For example, rates of non-dipping have been found to be greater among persons of African American ethnicity (Sherwood et al., 2001; Wilson, Sica, and Miller, 1999) or among persons who are sodium sensitive (Sica, 1999; Wilson et al., 1999), indicating that perhaps the increased risk associated with non-dipping may be uniquely linked to other constitutional differences of non-dippers.