Why the study?
Does NIDDM with or without diabetic nephropathy affect nocturnal blood pressure decline and autonomic function compared to nondiabetic controls?
Does NIDDM with or without diabetic nephropathy affect nocturnal blood pressure decline and autonomic function compared to nondiabetic controls?
NIDDM patients, particularly those with diabetic nephropathy, exhibit a blunted nocturnal decline in blood pressure and a high prevalence of autonomic neuropathy, which may contribute to their increased cardiovascular risk.
Answers are grounded in this paper and cite their sources.
Impaired nocturnal BP dipping in NIDDM may signal autonomic neuropathy and CV risk; leaves open whether targeted interventions improve outcomes.
Nondiabetic hypertensive patients lacking the normal nocturnal decline in arterial blood pressure have enhanced cardiovascular complications. Since cardiovascular morbidity and mortality are increased in non-insulindependent diabetes mellitus (NIDDM), we performed a prospective cross-sectional case-controlled study comparing the diurnal variation in arterial blood pressure, prevalence of dippers, cardiac autonomic nervous function (beat-to-beat variation during deep breathing), and extracellular fluid volume (51Cr-labeled EDTA) in 55 NIDDM patients with diabetic nephropathy (group 1), 55 NIDDM patients with normoalbuminuria (group 2), and 22 nondiabetic control subjects (group 3). All antihypertensive treatments were withdrawn at least 2 weeks before the study. The nocturnal blood pressure reduction (daytime-to-nighttime)/daytime (mean ± SE) was impaired in group 1 (6.6 ± 1.5%) and group 2 (11.1 ± 1.4%) as compared with group 3 (17.6 ± 1.7%), and it was impaired in group 1 as compared with group 2 (JP <0.05 for each comparison). The prevalence of dippers (95% confidence interval) was lower in group 1 (42% [29–56]) as compared with group 2 (58% [44–71]; P = 0.08) and group 3 (86% [65+97]; P < 0.001) and in group 2 as compared with group 3 (P < 0.01). Abolished beat-to-beat variation was more prevalent in group 1 (63% [50–76]) as compared with group 2 (15% [7–27]) and with group 3 (5% [0–23]) (P < 0.001). Nocturnal blood pressure reduction was associated with beat-to-beat variation during deep breathing (r = 0.22, P < 0.01). Extracellular fluid volume (mean ± SE) was higher in group 1 (15.9 ± 0.5 1/m2) as compared with group 3 (14.1 ± 0.8 1/m2) (P < 0.05) with group 2 between the two (15.1 ± 0.4 1/m2). Extracellular fluid volume was not associated with the degree of nocturnal blood pressure reduction. In conclusion, NIDDM patients with and without diabetic nephropathy have blunted nocturnal decline in arterial blood pressure, a condition that might enhance the strain on the microvascular and cardiovascular system. The high prevalence of autonomic neuropathy may also contribute to the increased cardiovascular morbidity and mortality characteristically found in these patients.
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Nielsen et al. (1995) studied this question.
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