Laboratory-based blood pressure recovery is a predictor of ambulatory blood pressure.

Exaggerated cardiovascular response during exposure to acute laboratory stressors has been postulated to be a risk factor for the development of hypertension (Manuck et al., 1990; Pickering & Gerin, 1990). Historically, research has focused on cardiovascular reactivity, defined as the magnitude of cardiovascular arousal occurring during acute stress exposure (Linden et al., 1997). Repeated elevations in blood pressures (BP) are believed to favor pathogenic adaptations, such as left ventricular remodeling and reduction in endothelial integrity (Lovallo & Gerin, 2003; Manuck et al., 1990; Obrist, 1981; Schwartz, 2003). However, recent commentaries have criticized reactivity research as being conceptually and methodologically narrow, with limited predictive ability (Carroll et al., 2001; Kamarck & Lovallo, 2003; Linden, et al., 2003; Schwartz et al., 2003; Treiber et al., 2003). An aspect of the stress response that is receiving increasing attention is the stress recovery phase (Christenfeld et al., 2000; Haynes et al., 1991; Stewart & France, 2001; Stewart, et al., 2006). BP recovery may be defined as the extent to which elevations in BP persist following the cessation of a stressor (Linden et al., 1997). In other words, recovery emphasizes the persistence of the stress response rather than its acute magnitude. The measurement of recovery BP centers on the notion that persistently elevated BP can lead to sustained cardiovascular burden, which has been linked with end-organ damage (Devereux & Pickering, 1991). The available evidence regarding BP recovery supports its potential pathophysiological significance. Hypertensive individuals have been characterized by abnormally persistent BP responses following acute stressors (Borghi et al, 1986; Falkner & Kushner, 1989; Frederikson & Engel, 1985; Light et al., 1987; Schuler & O’Brien, 1997; Seibt et al., 1998). Prospective studies in normotensive populations have demonstrated poorer systolic BP recovery following laboratory stressors (Stewart & France, 2001; Stewart et al., 2006). Risk factors for hypertension, including African American ethnicity, male gender, and family history of hypertension also have been related to poor BP recovery (Gerin & Pickering, 1995; Gillin et al., 1996; Jackson et al., 1999). However, the utility of evaluating BP recovery has been questioned due to its potential redundancy after considering reactivity (Linden et al., 1997). Although recovery and reactivity are unlikely to be independent characteristics, their relative importance has received little systematic scrutiny to date. Recent investigations point towards the independent utility, and perhaps superiority, of recovery compared to reactivity in predicting future BP (Rutledge et al., 2000; Stewart & France, 2001; Stewart et al., 2006). A key criticism of the laboratory-based reactivity/recovery literature is its questionable generalizability to psychophysiological responses to real-world stressors, such as job stress or marital discord (Ming et al., 2004; Verdecchia at al., 1990). This criticism has been addressed methodologically by using laboratory BP to predict ambulatory measures of BP (ABP), typically taken over a 24 hour period outside of the laboratory. Twenty-four hour ABP measures are considered superior to laboratory measures in predicting preclinical and clinical disease states as it allows for aggregating across multiple real-world stimuli (Mancia et al., 1997; Perloff et al., 1983; Staessen et al., 1999). Earlier studies examining the predictive power of laboratory based stress reactivity have demonstrated mixed results. Morales-Ballejo (1988) reported strong correlations between systolic and diastolic BP reactivity with systolic and diastolic ABP at work, when the stressor response was aggregated. Cornish, Blanchard & Jaccard (1994) found laboratory BP to be consistent predictors of ABP, although resting BP was superior to BP measured during the stress response. In contrast, Ironson et al. (1989) found that although work ABP was correlated with laboratory-based resting BP, reactivity BP did not correlate significantly with work ABP. Similarly, Langewitz et al. (1989) did not find correlations between laboratory reactivity BP and ABP, nor did they find variability in the laboratory BP comparable to the variability in ABP. In their study of 56 hypertensive participants, Floras et al. (1987) concluded that variability of laboratory-based reactivity BP was a poor predictor of ABP variability. Results from these studies are difficult to interpret as they often did not control for covariates or were based on correlational data. Knox, Hausforff, & Markovitz (2002) found that the reactivity response to two stressors (cold pressor and star racing) significantly predicted ABP 3 years following laboratory measurement in African American, normotensives participants but not in White participants. These mixed findings may reflect the methodological challenges inherent in the measurement of reactivity BP. Indeed, various authors have argued that reactivity measures may be neither reliable predictors of 24-h ABP nor reliable predictors of diurnal variation in BP (Kamarck & Lovallo, 2003; Manuck, Kasprowicz & Muldoon, 1990; Parati et al., 1991). To date, studies examining the relationship between recovery BP and ABP are limited. In a sample of 22 normotensives and 30 hypertensives, Guasti et al. (1998) found that DBP and SBP recovery were correlated to ABP, although their predictive power was not examined. Conversely, Seibt et al. (1998) found that laboratory recovery measures did not significantly improve predictive models of ABP despite finding that hypertensives demonstrated impaired recovery compared with normotensives. Recent prospective studies suggest that SBP and DBP recovery provide incremental validity in daily ABP measurements 3 years following baseline measurements, after controlling for baseline BP and reactivity (Moseley & Linden, 2006; Rutledge et al., 2000). In their sample of young, healthy college students, Rutledge et al. (2000) found that while reactivity, recovery, and resting BP were predictive of ABP, only resting and recovery BP remained significant in models which simultaneously assessed all three measures. Moseley & Linden (2006) also found recovery to be a significant predictor of ABP at 3-year follow-up. Whereas both studies provide evidence regarding the value of recovery BP, their generalizability is limited as both samples consisted of normotensives participants and were primarily Caucasian. The purpose of the current investigation was two-fold: first, to determine the generalizability of laboratory measures of BP in predicting ambulatory daytime and nighttime BP, and second, to further evaluate the unique contribution of BP recovery to the prediction of ABP in a biracial sample of men and women with BP extending from normal through Stage II hypertension. We hypothesized that recovery BP measured in the laboratory would predict daytime and nighttime ABP after accounting for resting BP and BP reactivity.