- Top of page
- Acknowledgments and disclosures:
J Clin Hypertens (Greenwich). 2011;13:557–562. ©2011 Wiley Periodicals, Inc.
Failure of blood pressure (BP) to decline appropriately overnight (nondipping) is associated with increased risk. This may be due to inappropriately raised supine central BP and this study’s first aim was to examine this hypothesis. Secondly, aortic stiffness, central hemodynamics, and left ventricular (LV) mass were measured as other possible mechanisms of higher risk. Brachial and central BP (supine and seated), aortic stiffness, central hemodynamics, and LV dimensions were measured in 95 patients with hypertension (mean age 62±8 standard deviation). Central hemodynamics were recorded by combined radial tonometry and 3-dimensional echocardiography. Seated brachial and central systolic BP (SBP) were similar between dippers (n=52) and nondippers (n=43). However, nondippers had higher supine brachial (132±14 mm Hg vs 126±11 mm Hg; P=.029) and central (121±15 mm Hg vs 115±11 mm Hg; P=.024) SBP. Aortic stiffness was not different between groups (P=.76), but LV mass index (33.0±6.2 vs 29.4±7.2 g/m2.7; P=.019), stroke volume index (30.2±6.2 mL/m2 vs 27.4±6.0 mL/m2; P=.040), and LV stroke work (3246±815 mm Hg/mL/m2 vs 2778±615 mm Hg/mL/m2; P=.005) were all higher in nondippers. Dipper status independently predicted LV mass index (β=3.61; P=.001). Nondippers have higher supine brachial and central SBP, significantly different central hemodynamics, and elevated LV mass index compared with dippers. These cardiovascular anomalies possibly contribute to increased mortality risk.
In normotensive and hypertensive individuals, the failure of nighttime blood pressure (BP) to decline >10% compared with daytime BP (nondipping) is associated with increased target organ damage1 and risk of cardiovascular and all-cause mortality.2–4 Nondipping is a relatively common condition that occurs in 25% of patients with hypertension, but with greater prevalence in certain patient populations such as those with diabetes.5 The mechanisms underlying the increased risk associated with nondipping are incompletely understood. Some data indicate that nondippers may have higher supine stroke volume6 and increased large artery stiffness.7,8 This hemodynamic milieu, involving delivery of increased stroke volume into a noncompliant proximal aorta, may reasonably expect to result in an increase in supine brachial BP (the hallmark of nondipping) and central BP. The first aim of this study was to determine the postural (supine and seated) differences in brachial and central BP between patients with a dipping and nondipping BP profile. We hypothesized that nondippers would have higher supine brachial and central BP. Secondly, in addition to BP, we sought to determine other factors that potentially contribute to increased risk in nondippers. This was assessed from arterial stiffness, ventricular-vascular interaction, and target organ damage defined by left ventricular (LV) mass.
- Top of page
- Acknowledgments and disclosures:
There are several novel findings of this study. Firstly, despite similar seated office BP and no difference in aortic stiffness, nondippers had significantly higher supine brachial SBP compared with dippers. Secondly, the supine brachial SBP abnormality was accompanied by significantly higher central SBP in the supine, but not seated, position. This is an observation that, together with raised LV mass index, may help to explain (at least in part) the increased cardiovascular risk associated with nondipping. Finally, stroke volume and cardiac stroke work were higher in nondippers, with the latter being highly correlated with supine SBP, thus providing a possible hemodynamic explanation for the raised supine BP level in these patients.
Mechanisms of Abnormal Supine BP
The characteristic feature of nondipping is a significantly elevated nighttime (supine) BP relative to daytime BP. This abnormally raised supine brachial BP was also evident in the office after a few minutes of supine rest. Acute cardiovascular responses to postural change (within seconds) involve complex neural and vascular interactions. However, after <3 minutes of stabilization in the supine position, under normal circumstances, mean arterial pressure should be lower than in the seated position as a result of peripheral vascular vasodilation and reduced heart rate. Further to this, pulse pressure should increase because DBP falls while SBP remains relatively unchanged.19 These hemodynamic alterations are initiated by posture-induced stimulation of cardiopulmonary low-pressure and arterial (carotid and aortic) high-pressure sensors.20
In this current study, patients who were dippers followed a normal hemodynamic response to postural change as described above. Conversely, when the nondippers moved into the supine position, brachial and central SBP increased, while mean arterial pressure failed to change, despite a drop in heart rate. Our data potentially explain these anomalies by an increase in stroke volume and LV stroke work, which, in the absence of differences in other functional parameters related to brachial or central BP (ie, aortic stiffness, EA, peripheral vascular resistance, heart rate) would generate a greater rise in both brachial and central SBP. This chronic elevation of central BP in the supine state would reasonably be expected to contribute toward increases in LV mass21,22 (as was observed in nondippers) and additional risk related to cardiovascular mortality.14,23
Our findings lend support to those of Takakuwa and colleagues,6 who reported that nocturnal cardiac output and stroke volume were significantly higher in nondippers. On the other hand, in general disagreement with two other studies,7,8 we found that neither central (EA and aortic), peripheral (brachial), nor systemic (augmentation index) arterial stiffness measures were abnormally elevated in nondippers. An important difference of our study was that dippers and nondippers had similar BP at the time arterial stiffness measures were acquired. Thus, our data are unlikely to be confounded by between-group BP variations.24 Different measuring techniques for arterial stiffness, as well as classifications of nocturnal BP and racial variation between studies could also account for discrepancies. The mechanisms underlying abnormal hemodynamics related to nondipping may be multifactorial, including disordered supine natriuresis,25 volume expansion,6 or neurohormonal irregularity with raised norepinephrine,26 to name a few, and further studies are required to tease out direct causes of nondipping.
This was a selected population of patients receiving treatment for hypertension. Thus, it is unknown whether these findings are broadly applicable and more research with greater numbers of patients is required. Although 24-hour ABP is regarded as the “gold standard” method for determining BP control, some studies have reported weak reproducibility of the method.27 Therefore, since we did not perform multiple 24-hour ABP recordings, it may be possible that patients in the current study were incorrectly assigned to either the dipper or nondipper groups. Furthermore, our protocol of 60-minute intervals between nighttime BP readings was made for the benefit of patient comfort, so as to lessen the possibility of sleep disturbance that may raise nighttime BP values. Nonetheless, this protocol may have also contributed to incorrect assignment of dipper status.
This study found that nondippers had significantly raised brachial and central SBP while in the supine position, but not while seated. Central hemodynamics related to ventricular-vascular interaction were also altered and LV mass index was significantly raised compared with dippers. Irregular supine hemodynamics were related to LV stroke work and, in the long-term, higher central BP may contribute to adverse cardiac remodeling. Together, these unfavorable changes may help to explain the extra cardiovascular risk associated with nondipping.