Circadian variation in blood pressure: dipper or nondipper

Abstract

Awareness of an increased incidence of cardiovascular events shortly after awakening has heightened interest in the chronopathology of cardiovascular diseases. Blood pressure varies according to cycles characterized by a reduction during sleep and an increase on awakening. The surge in blood pressure coincides with the circadian nature of various endocrine and hematologic parameters that also have a putative role in triggering the onset of cardiovascular events. The nighttime decrease is absent or blunted in some hypertensive patients (termed nondippers), an effect associated with increased morbidity. Drugs can influence the effect of these circadian patterns. Research efforts are focused on clarifying an underlying pathophysiologic process that could be modified by pharmacologic or other means. Long-acting angiotensin II receptor blockers have an effect on blood pressure over 24 hours due to their long half-life, but could also limit the morning surge in blood pressure through an effect on the renin-angiotensin-aldosterone and noradrenergic systems.

Figure 1

Twenty‐four‐hour blood pressure profile of dipper and nondipper hypertensive patients. 6, 7, 8, 9, 10, 11

Figure 2

Reduction in vascular resistance by nitroprusside (A) and the α‐adrenoceptor antagonist phentolamine (B). Drugs were infused into the forearm of volunteers. ¹⁷ Reprinted with permission from Panza JA, et al. N Engl J Med. 1991;325:986–990. Copyright ©1991 Massachusetts Medical Society. All rights reserved.

Figure 3

Circadian incidence of sudden cardiac death, adjusted for time of awakening. ² Reprinted from Willich SN, et al. Increased onset of sudden cardiac death in the first three hours after awakening. Am J Cardiol. 1992;70:65–68. © 1992, with permission from Excerpta Medica Inc.

Figure 4

Comparison of the risk of mortality in extreme dippers (ED), dippers (D), nondippers (ND), and inverted dippers (IND) after an average follow‐up of 5.1 years. RH=relative hazard; *p=0.02; **p=0.004 vs. D Reprinted with permission of Elsevier Science from Am J Hypertens. 1997;10:1201–1207. ⁴⁰