(607.1) Autonomic Responses to Acute Hyperoxia are Impaired in Patients with Peripheral Artery Disease

Poster Board Number: E526

Jian Cui (Pennsylvania State University College of Medicine), Urs Leuenberger (Pennsylvania State University College of Medicine), Faisal Aziz (Pennsylvania State University College of Medicine), Jonathan Luck (Pennsylvania State University College of Medicine), Jonathan Stavres (Pennsylvania State University College of Medicine), Danielle Kim (Pennsylvania State University College of Medicine), Zhaohui Gao (Pennsylvania State University College of Medicine), Cheryl Blaha (Pennsylvania State University College of Medicine), Aimee Cauffman (Pennsylvania State University College of Medicine), Lawrence Sinoway (Pennsylvania State University College of Medicine)

Prior reports suggest that oxidative stress plays an important role in the development of atherosclerotic diseases such as peripheral artery disease (PAD). The effects of acute hyperoxia, an important acute oxidative stressor, on autonomic function have not been well studied in PAD. We hypothesized that the autonomic responses to acute hyperoxia would be impaired in PAD. We studied 17 patients with PAD (12M, 5F, 67 ± 2 yrs) and 15 healthy controls (10M, 5F, 65 ± 2 yrs). The ankle-brachial indexes in the patients were 0.57 ± 0.03 in the most affected leg and 0.77 ± 0.04 in the less affected leg, respectively. Beat-by-beat heart rate (HR, from ECG) and blood pressure (BP, with Finometer) were recorded for 10 min under normoxic resting conditions and during 5-min hyperoxia (100% oxygen) as an acute oxidative stress test. HR variability (HRV) was calculated and cardiac baroreflex sensitivity (BRS) was estimated with the sequence technique. Under resting conditions, mean HR and mean arterial pressure (MAP) were not significantly different between the groups.  Resting values of the root mean square of successive differences between normal heartbeats (RMSSD, a HRV index for parasympathetic activity; 14.1 ± 1.0 vs. 19.8 ± 2.2 ms, P = 0.032) and cardiac BRS (6.43 ± 0.78 vs. 14.86 ± 2.56 ms/mmHg, P = 0.001) were significantly lower in PAD than in healthy controls. Hyperoxia lowered HR in both groups and raised MAP only in patients with PAD. During hyperoxia both HR and MAP were significantly higher in PAD than in controls.  Hyperoxia induced an increase in RMSSD and the high frequency (HF) component of HRV (another index for parasympathetic activity) in healthy subjects. However, during hyperoxia no increase in parasympathetic activity was observed in PAD. Both RMSSD and the HF component of the whole trial (i.e. baseline and hyperoxia) in PAD were lower than those in healthy control subjects. Hyperoxia did not induce changes in cardiac BRS in either group, while cardiac BRS of the whole trial in PAD was lower than that in healthy controls. These data suggest that resting parasympathetic activity and cardiac baroreflex function are impaired in PAD. Moreover, the autonomic response to acute oxidative stress (i.e. an increase in parasympathetic activity) is also impaired in PAD. Further studies are needed to examine if antioxidant agents can improve autonomic function in PAD.

Supported by National Institutes of Health Grants P01 HL134609, MPI R01 HL141198 and UL1 TR002014.