Author + information
- Kevin D. Monahan, PhD⁎ ( and )
- Chester A. Ray, PhD
- ↵⁎Penn State Heart and Vascular Institute, The Milton S. Hershey Medical Center, Campus Box H047, 500 University Drive, Hershey, Pennsylvania 17033-2390
Recently in the Journal, Radaelli et al. (1) reported that 4 months of dietary polyunsaturated fatty acid (PUFA) supplementation enhanced baroreflex control of the circulation in heart failure patients. Augmented cardiac-vagal baroreflex control was suggested from increased bradycardiac responses to neck suction as well as enhanced cardiac period fluctuations during spontaneous blood pressure oscillations after PUFA supplementation. These effects of PUFAs on the cardiac-vagal arm of the baroreflex in heart failure patients were impressive and may be of clinical importance.
Based on the detrimental role sympathoexcitation is believed to exert in heart failure, a separate but equally important question is the effect that PUFAs exert on both basal and reflexive measures of sympathetic outflow. To address this question, Radaelli et al. (1) used several indirect indices. First, increased low frequency heart rate variability after PUFA supplementation was used as evidence of reduced sympathetic activity at rest (1). Second, a greater depressor response to neck suction, which likely is mediated via both cardiac (vagal and sympathetic) and peripheral (sympathetic) effects, after PUFA supplementation, was suggested to indicate enhanced sympathoinhibitory baroreflex function (1). As pointed out, these effects of PUFAs in heart failure patients may need to be confirmed using more robust measures of sympathetic outflow, which should also include responses to sympathoexcitatory stimuli (2).
To date, only a single study performed in humans has determined the effect that PUFA supplementation exerts on a directmeasure of sympathetic outflow (muscle sympathetic nerve activity [MSNA]) (3). In that study we demonstrated that PUFA supplementation had no effect on MSNA at rest(against our hypothesis that it would reduce it). Furthermore, we observed augmented (not depressed as we hypothesized) increases in MSNA during several distinct sympathoexcitatory stressors (exercise and cold stress) in young healthy adults (3). Because sympathetic outflow at rest is increased and reflex responses to baroreflex activation/deactivation may be impaired in heart failure patients, it is unclear whether similar effects of PUFAs on MSNA would be observed in heart failure patients. Accordingly, it appears that studies employing more robust methodologies are needed to more definitively determine the effect that PUFAs exert on basal and reflexive (both sympathoinhibitory and sympathoexcitatory during baroreflex and nonbaroreflex stimuli) regulation of sympathetic outflow in heart failure patients.
- American College of Cardiology Foundation
- Radaelli A.,
- Cazzaniga M.,
- Viola A.,
- et al.
- Floras J.,
- Bagai A.