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Significance: Despite 20 years of research and new treatment methods, diabetic foot ulcer (DFU) remains a common problem with frequent recurrences and complications. Recent Advances: There are reports that nerve decompression (ND) surgery has been observed to produce significantly fewer DFU recurrences than standard of care (SOC). The explanation of this apparent superiority has not been understood. Critical Issues: Microcirculation is understood to be involved in diabetic peripheral neuropathy (DPN) and DFU. There is an underappreciation of the participation in DPN of entrapment neuropathy (EN) due to nerve swelling and impingement in fibro-osseous tunnels. Reducing c-fiber compression in EN by ND generates recovery of subepidermal capillary flow. ND studies have found improved neuromuscular function and epidermal microcirculation phenomena, including chronic capillary ischemia (CCI) and pressure-induced vasodilatation (PIV). There is no current therapy recommended for impaired microcirculation. Clinical and animal evidence has demonstrated that release of locally compressed peripheral nerves improves the epidermal microcirculation which is under sympathetic control. Future Directions: Using epineurolysis to relieve nerve compressions is a physiology-based therapeutic intervention and provides the scientific foundation clarifying how ND reduces DFU recurrence risk. Incorporating ND with current SOC treatments could improve DFU recurrence risk, hard-to-heal ulcers, neuroischemic wounds, amputation risk, and the resulting costs to society. More studies using ND for DFU, especially evidence-based medicine Level I studies, are needed to confirm these preliminary outcomes.

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PURPOSE OF REVIEW: Risks for developing cardiovascular disease and cognitive decline increase with age. In women, these risks may be influenced by pregnancy history. This review provides an integrated evaluation of associations of pregnancy history with hypertension, brain atrophy, and cognitive decline in postmenopausal women. RECENT FINDINGS: Atrophy in the occipital lobes of the brain was evident in women who had current hypertension and a history of preeclampsia. Deficits in visual memory in women with a history of preeclampsia are consistent with these brain structural changes. The blood velocity response to chemical and sympathoexcitatory stimuli were altered in women with a history of preeclampsia linking impairments in cerebrovascular regulation to the structural and functional changes in the brain. Having a history of preeclampsia should require close monitoring of blood pressure and initiation of anti-hypertensive treatment in perimenopausal women. Mechanisms by which preeclampsia affects cerebrovascular structure and function require additional study.

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AIMS: Autonomic dysfunction determines the advance of dilated cardiomyopathy (DCM) and is related to poor outcomes. However, this autonomic imbalance is unknown in patients with restrictive cardiomyopathy (RCM) even though they have similar symptoms and poor quality of life as DCM patients have. The aim of this study was to evaluate if autonomic and neurovascular controls were altered in RCM patients. METHODS AND RESULTS: Fifteen RCM patients, 10 DCM patients, and 10 healthy subjects were evaluated. Heart rate and blood pressure (BP) were recorded. Peripheral sympathetic activity [muscle sympathetic nerve activity (MSNA)] by microneurography and cardiac sympathetic activity by power spectrum analysis of heart rate variability. Spontaneous baroreflex sensitivity (BRS) was evaluated by the sequence method and forearm blood flow by venous occlusion plethysmography. Both cardiomyopathy groups had higher MSNA frequency (P < 0.001) and MSNA incidence (P < 0.001), higher cardiac sympathovagal balance (P < 0.02), reduced BRS for increase (P = 0.002) and for decrease in BP (P = 0.002), and lower forearm blood flow (P < 0.001) compared with healthy subjects. We found an inverse correlation between BRS for increase and decrease in BP and peripheral sympathetic activity (r = -0.609, P = 0.001 and r = -0.648, P < 0.001, respectively) and between BRS for increase and decrease in BP and cardiac sympathetic activity (r = -0.503, P = 0.03 and r = -0.487, P = 0.04, respectively). CONCLUSIONS: The RCM patients had cardiac and peripheral autonomic dysfunctions associated with peripheral vasoconstriction. Nonetheless, the presence of normal ejection fraction underestimates the evolution of the disease and makes clinical treatment difficult. These alterations could lead to a similar cardiovascular risk as that observed in DCM patients.

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Heart failure (HF) is characterized by decreased exercise capacity, attributable to neurocirculatory and skeletal muscle factors. Cardiac resynchronization therapy (CRT) and exercise training have each been shown to decrease muscle sympathetic nerve activity (MSNA) and increase exercise capacity in patients with HF. We hypothesized that exercise training in the setting of CRT would further reduce MSNA and vasoconstriction and would increase Ca2+-handling gene expression in skeletal muscle in patients with chronic systolic HF. Thirty patients with HF, ejection fraction <35% and CRT for 1 mo, were randomized into two groups: exercise-trained (ET, n = 14) and untrained (NoET, n = 16) groups. The following parameters were compared at baseline and after 4 mo in each group: V̇o2 peak, MSNA (microneurography), forearm blood flow, and Ca2+-handling gene expression in vastus lateralis muscle. After 4 mo, exercise duration and V̇o2 peak were significantly increased in the ET group (P = 0.04 and P = 0.01, respectively), but not in the NoET group. MSNA was significantly reduced in the ET (P = 0.001), but not in NoET, group. Similarly, forearm vascular conductance significantly increased in the ET (P = 0.0004), but not in the NoET, group. The expression of the Na+/Ca2+ exchanger (P = 0.01) was increased, and ryanodine receptor expression was preserved in ET compared with NoET. In conclusion, the exercise training in the setting of CRT improves exercise tolerance and neurovascular control and alters Ca2+-handling gene expression in the skeletal muscle of patients with systolic HF. These findings highlight the importance of including exercise training in the treatment of patients with HF even following CRT.

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