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Randomized Controlled Trial
. 2008 Nov;3(6):1660-8.
doi: 10.2215/CJN.02920608. Epub 2008 Oct 15.

Physical activity and hemodynamic reactivity in chronic kidney disease

Affiliations
Randomized Controlled Trial

Physical activity and hemodynamic reactivity in chronic kidney disease

Rajiv Agarwal et al. Clin J Am Soc Nephrol. 2008 Nov.

Abstract

Background and objectives: Patients with chronic kidney disease (CKD) have an elevated cardiovascular risk. This study was designed to understand better the presence and strength of the relationship between physical activity and BP and to explore determinants of hemodynamic reactivity.

Design, setting, participants, & measurements: Twenty-four patients with CKD (mean age 69.5 yr; 3.1 antihypertensive drugs; estimated GFR 47 ml/min per 1.73 m(2), albumin/creatinine ratio 403 mg/g) were studied on three occasions during a 6-wk period with 24-h ambulatory BP monitoring and simultaneous activity monitoring with wrist actigraphy.

Results: Nondippers were found have a greater level of sleep activity compared with dippers, although the awake activity level was similar (7.06 versus 6.73) between groups (P = 0.042 for interaction). In 3587 BP activity pairs, hemodynamic reactivity was variable between individuals (systolic BP reactivity 1.06 [SD 10.50]; diastolic BP reactivity 0.89 [SD 7.80] heart rate reactivity 1.18 [SD 11.00]); those who were more sedentary had a greater increment in systolic BP compared with those who were less sedentary. Antihypertensive drugs blunted hemodynamic reactivity. Hemodynamic reactivity was greatest between 12 a.m. and 8 a.m., making this a vulnerable period for cardiovascular events.

Conclusions: Greater hemodynamic reactivity in sedentary people with CKD offers a possible and thus far unrecognized mechanism of cardiovascular damage. Besides reducing BP, antihypertensive drugs reduce hemodynamic reactivity, which offers another plausible mechanism of cardiovascular protection with their use.

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Figures

Figure 1.
Figure 1.
Relationship between circadian activity and dipping status of systolic BP (SBP). Awake activity was similar between dippers and nondippers, but dippers had a greater decline in sleep activity compared with nondippers (P = 0.042 for interaction effect; see Table 2 for details).
Figure 2.
Figure 2.
Relationship of activity and hemodynamic changes collected during a 24-h period from a single patient. A direct relationship between square root of the actigraph-recorded physical activity and hemodynamic parameters such as heart rate, SBP, and diastolic BP (DBP) is seen. The slope of the line reflects the hemodynamic reactivity.
Figure 3.
Figure 3.
Rank order of hemodynamic reactivity or the changes in heart rate, SBP, and DBP per square root of activity measured during a 15-s epoch. The error bars represent 1 SD. The numbers above the error bars represent the patient number.
Figure 4.
Figure 4.
Relationship of hemodynamic reactivity with activity as a function of mean level of activity. The solid line presents the hemodynamic change with activity in those who had median level of activity and were taking on average three antihypertension drugs. The short dashed line represents sedentary individuals, and the long dashed line represents active individuals. The hemodynamic reactivity slopes are blunted in those who were active and heightened in those who were sedentary (P < 0.01; see Table 4 for coefficients of slopes).
Figure 5.
Figure 5.
Hemodynamic reactivity varies with the time of the day. Error bars represent the SEM. The greatest reactivity is seen during the hours of sleep and the least between 8 a.m. and 12 p.m.

References

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