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Patients with cardiovascular disease show autonomic dysfunction, including sympathetic activation and vagal withdrawal, which leads to fatal events. This review aims to place sympathovagal balance as an essential element to be considered in management for cardiovascular disease patients who benefit from a cardiac rehabilitation program. Many studies showed that exercise training, as non-pharmacologic treatment, plays an important role in enhancing sympathovagal balance and could normalize levels of markers of sympathetic flow measured by microneurography, heart rate variability or plasma catecholamine levels. This alteration positively affects prognosis with cardiovascular disease. In general, cardiac rehabilitation programs include moderate-intensity and continuous aerobic exercise. Other forms of activities such as high-intensity interval training, breathing exercises, relaxation and transcutaneous electrical stimulation can improve sympathovagal balance and should be implemented in cardiac rehabilitation programs. Currently, the exercise training programs in cardiac rehabilitation are individualized to optimize health outcomes. The sports science concept of the heart rate variability (HRV)-vagal index used to manage exercise sessions (for a goal of performance) could be implemented in cardiac rehabilitation to improve cardiovascular fitness and autonomic nervous system function.

We report for the first time that increased peripheral chemoreflex sensitivity directly decreases sympathetic baroreflex function in CHF patients. This interaction contributes to sympathetic overactivity and blunted sympathetic baroreflex function of CHF patients and may explain how chemoreceptors contribute to the bad prognosis of CHF patients.

We demonstrate that a single session of HIIE improves autonomic profile of CHF patients, leading to significant reductions of HR and arrhythmic events in a 24-h posttraining period. Cardioprotective effects of HIIE in CHF patients need to be confirmed in a larger study population and on a long-term basis.

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BackgroundThe exact pathophysiology of Tako-Tsubo cardiomyopathy (TTC) remains unknown but a role for sympathetic hyperactivity has been suggested. Up to now, no direct evidence of sympathetic nerve hyperactivity has been established nor involvement of sympathetic baroreflex identified. The aim of our study was to determine, by direct sympathetic nerve activity (SNS) recording if sympathetic nervous system activity is increased and spontaneous baroreflex control of sympathetic activity reduced in patients with TTC.MethodsWe included 13 patients who presented with TTC and compared their SNS activity and spontaneous baroreflex control of sympathetic activity with that of 13 control patients with acutely decompensated chronic heart failure. SNS activity was evaluated by microneurography, a technique assessing muscle sympathetic nerve activity (MSNA). Spontaneous baroreflex control of sympathetic activity was evaluated as the absolute value of the slope of the regression line representing the relationship between spontaneous diastolic blood pressure values and concomitant SNS activity. Control patients were matched for age, sex, left ventricular ejection fraction and creatinine clearance.ResultsThe mean age of the patients with TTC was 80 years, all patients were women. There were no significant differences between the two groups of patients for blood pressure, heart rate or oxygen saturation level. TTC patients presented a significant increase in sympathetic nerve activity (MSNA median 63.3 bursts/min [interquartile range 61.3 to 66.0] vs median 55.7 bursts/min [interquartile range 51.0 to 61.7]; p = 0.0089) and a decrease in spontaneous baroreflex control of sympathetic activity compared to matched control patients (spontaneous baroreflex control of sympathetic activity median 0.7%burst/mmHg [interquartile range 0.4 to 1.9] vs median 2.4%burst/mmHg [interquartile range 1.8 to 2.9]; p = 0.005).ConclusionsWe report for the first time, through direct measurement of sympathetic nerve activity, that patients with TTC exhibit elevated SNS activity associated with a decrease in spontaneous baroreflex control of sympathetic activity. These data may explain the pathophysiology and clinical presentation of patient with TTC.

BackgroundStroke patients have impaired postural balance that increases the risk of falls and impairs their mobility. Assessment of postural balance is commonly carried out by recording centre of pressure (CoP) displacements, but the lack of data concerning reliability of these measures compromises their interpretation. The purpose of this study was to investigate the between-day reliability of six CoP-based variables, in order to provide i) reliability data for monitoring postural sway and weight-bearing asymmetry of stroke patients in clinical practice and ii) consistent assessment method of measurement error for applications in physical medicine and rehabilitation.MethodsPostural balance of 20 stroke patients was assessed in quiet standing on a force platform, in two sessions, 7 days apart. Six CoP-based variables were collected in eyes open and eyes closed conditions: postural sway was assessed with mean and standart deviation of CoP-velocity, CoP-velocity along the mediolateral and anteroposterior axes, and confidence ellipse area (CEAREA); weight-bearing asymmetry was assessed with mean CoP position along the mediolateral axis (CoPML). The intraclass correlation coefficient (ICC) was used to determine the level of agreement between test-retest. Small real difference (SRD), corresponding to the smallest change that indicates a real improvement for a single individual, was used to determine the extent of measurement error.ResultsICCs were satisfactory (>0.9) for all CoP-based variables, except for CEAREA in eyes open condition and CoPML (<0.8). The SRDs (eyes open/closed conditions) were: 6.1/9.5 mm.s-1 for mean velocity; 12.3/12.2 mm.s-1 for standard deviation of CoP-velocity; 3.6/5.5 mm.s-1 and 4.9/7.3 mm.s-1 for CoP-velocity in mediolateral and anteroposterior axes, respectively; 17.4/21.4 mm for CoPML. Because CEAREA showed heteroscedasticity of measurement error distribution, SRD (eyes open/closed conditions) was expressed as a percentage (121/75%) and a ratio (3.68/2.16) obtained after log-antilog procedure.ConclusionsIn clinical practice, the CoP-based velocity variables should be prefer to CEAREA to assess and monitor postural sway over time in hemiplegic stroke patients. The poor reliability of CoPML compromises its use to assess weight-bearing asymmetry. The procedure we used could be applied in reliability studies concerning other CoP-based variables or other biological variables in the field of physical medicine and rehabilitation.

Abstract-Sympathetic activation contributes to both the initiation and progression of heart failure. The role of anemia in determining sympathetic overactivity in chronic heart failure (CHF) patients is unknown. We tested the hypothesis that, in CHF patients, anemia could lead to increased sympathetic activity through tonic activation of excitatory chemoreceptor afferents. We conducted a double-blind, randomized, vehicle-controlled study to examine the effect of chemoreflex deactivation on muscle sympathetic nerve activity in CHF patients with and without anemia. We compared the effect of breathing 100% oxygen for 15 minutes in 18 stable CHF patients with anemia and 18 control CHF patients matched for age, sex, blood pressure, and body mass index. Baseline muscle sympathetic nerve activity was significantly elevated in CHF patients with anemia compared with patients with CHF alone (56.0Ϯ3.2 versus 45.5Ϯ3.1 bursts per minute; PϽ0.0237). Administration of 100% oxygen led to a significant decrease in muscle sympathetic nerve activity in CHF patients with anemia (from 56.0Ϯ3.4 to 50.9Ϯ3.2 bursts per minute; PϽ0.0019). In contrast, neither room air nor 100% oxygen changed muscle sympathetic nerve activity or hemodynamics in patients with CHF alone. We report for the first time direct evidence of increased sympathetic nerve traffic in patients with CHF-related anemia. Sympathetic hyperactivity in patients with CHF and anemia is partially chemoreflex mediated and could explain how anemia contributes to the progression of CHF and increases morbidity and mortality in these patients. (Hypertension. 2010;55:1012-1017.)