Aktuelle Neurologie 2005; 32 - P597
DOI: 10.1055/s-2005-919628

Impaired cardiovascular autonomic modulation in diabetic patients during lower body negative pressure

H Marthol 1, U Zikeli 1, C.M Brown 1, B Neundörfer 1, M.J Hilz 1
  • 1Erlangen; New York, USA

Introduction: Cardiac autonomic neuropathy (CAN) is among the common complications of diabetes mellitus and associated with an increased risk of mortality. Spectral analysis of heart rate and blood pressure variability during orthostatic challenge such as lower body negative pressure (LBNP) stimulation has been well established for the assessment of cardiovascular autonomic modulation, which might be compromised in diabetics.

Objective: To evaluate cardiovascular modulation during LBNP in diabetic patients.

Methods: 13 patients with diabetes mellitus type II (age 58±6 years, duration of diabetes 85±55 months) underwent a standardized battery of cardiovascular tests (heart rate variability (HRV) at rest, during 6/min. deep breathing, Valsalva maneuver and active standing). In addition, we continuously recorded heart rate (HR) as well as blood pressure (BP) at rest and during –20 and –40mmHg LBNP. Spectral powers of HR and BP were analyzed in the low (LF: 0.04–0.15Hz) and the high (HF: 0.15–0.5Hz) frequency ranges. As changes in LF- and HF-powers of HR may reflect changes in total power, we normalized both powers to total power. Results of patients were compared to results obtained from 15 age-matched controls (48±12 years).

Results: 9 of the 13 patients fulfilled the diagnostic criteria for CAN, i.e. more than two of the cardiovascular tests showed abnormal results. In 2 patients, the LBNP protocol had to be terminated due to symptoms of presyncope. In the remaining 11 patients (8 diagnosed with CAN) – as in the controls – LBNP significantly increased HR (78.0±21.7 vs. 88.6±25.5 bmp). LBNP decreased BP (123.0±18.4 vs. 113.8±21.0mmHg) in the patients, while BP remained stable in controls. LBNP did not change the LF- and HF-powers of HR and BP in the patients. Controls, however, had lower HF-power of HR (76.4±30.0 vs. 57.4±23.5%) and higher LF-power of BP (3.2±3.1 vs. 5.5±3.8mmHg2) during LBNP than at baseline.

Conclusion: The controls responded adequately to LBNP stimulation as they presented the typical decrease in the parasympathetically mediated HF-power of HR and the typical increase in the sympathetically mediated LF-power of BP, while both parameters did not change in the patients suggesting cardiac autonomic neuropathy. These results confirm the results of the HRV testing in our patients. Therefore, LBNP might be an alternative to the standardized HRV testing to identify patients with CAN, particularly independently from patient's cooperation.