Exercise-resembling effects of periodic somatosensory stimulation in heart failure.

BACKGROUND: The mechanism of the beneficial effects of exercise training on autonomic derangement and neurohumoral activation in chronic heart failure (CHF) is largely unexplained. In our here-presented hypothesis-generating study we propose that part of these effects is mediated by the exercise-accompanying somatosensory nerve traffic. To demonstrate this, we compared the effects of periodic electrical somatosensory stimulation in patients with CHF with the effects of exercise training and with usual care. METHODS: In a randomized controlled study we measured, in CHF patients, changes in blood pressure, baroreflex sensitivity (BRS), neurohormones, exercise capacity and quality of life (QOL) in response to periodic somatosensory stimulation in the form of 2 Hz transcutaneous electrical nerve stimulation (TENS) at both feet, in response to conventional exercise training (EXTR) and, as control (CTRL), in patients with usual care only. RESULTS: Group sizes were N=31 (TENS group), N=25 (EXTR group) and N=30 (CTRL group), respectively. Practically all improvements in BRS, neurohormone concentrations, exercise capacity and QOL in the TENS group were comparable to, or sometimes even better than in the EXTR group. These improvements were not observed in the CTRL group. CONCLUSIONS: This study demonstrates that periodic electrical somatosensory stimulation is as effective as exercise training in improving BRS, neurohormone concentrations, exercise capacity and QOL in CHF patients. These results encourage exploration of exercise modalities that concentrate on rhythm rather than on effort, with the purpose to normalize autonomic derangement and neurohumoral activation in CHF.

Biventricular pacing-induced acute response in baroreflex sensitivity has predictive value for midterm response to cardiac resynchronization therapy.

In a previous study we demonstrated that the institution of biventricular pacing in chronic heart failure (CHF) acutely facilitates the arterial baroreflex. The arterial baroreflex has important prognostic value in CHF. We hypothesized that the acute response in baroreflex sensitivity (BRS) after the institution of cardiac resynchronization therapy (CRT) has predictive value for midterm response. One day after implantation of a CRT device in 33 CHF patients (27 male/6 female; age, 66.5 +/- 9.5 yr; left ventricular ejection fraction, 28 +/- 7%) we measured noninvasive BRS and heart rate variability (HRV) in two conditions: CRT device switched on and switched off (on/off order randomized). Echocardiography was performed before implantation (baseline) and 6 mo after implantation (follow-up). CRT responders were defined as patients in whom left ventricular end-systolic volume at follow-up had decreased by > or =15%. Responders (69.7%) and nonresponders (30.3%) had similar baseline characteristics. In responders, CRT increased BRS by 30% (P = 0.03); this differed significantly (P = 0.02) from the average BRS change (-2%) in the nonresponders. CRT also increased HRV by 30% in responders (P = 0.02), but there was no significant difference found compared with the increase in HRV (8%) in the nonresponders. Receiver-operating characteristic curve analysis revealed that the percent BRS increase had predictive value for the discrimination of responders and nonresponders (area under the curve, 0.69; 95% confidence interval, 0.51-0.87; maximal accuracy, 0.70). Our study demonstrates that a CRT-induced acute BRS increase has predictive value for the echocardiographic response to CRT. This finding suggests that the autonomic nervous system is actively involved in CRT-related reverse remodeling.

Biventricular pacing in chronic heart failure acutely facilitates the arterial baroreflex.

Metabolic and mechanical stress in the failing heart activates the cardiac sympathetic afferent reflex (CSAR). It has been demonstrated that cardiac resynchronization therapy (CRT) acutely reduces MSNA in clinical responders. Mechanistically, this beneficial effect might be explained by acute deactivation of the CSAR. In addition to sympathoexcitation, CSAR inhibits the arterial baroreflex at the level of the nucleus tractus solitarii. Hence, in responders, CRT is likely to remove/reduce this inhibition. Therefore, we hypothesized that CRT acutely facilitates the arterial baroreflex. One day after implantation of a CRT device in 32 patients with chronic heart failure (LVEF; 27 +/- 6%), we measured noninvasive baroreflex sensitivity (BRS) and heart rate variability (HRV) in two conditions: CRT device switched on and switched off (on/off order randomized). BRS changes were correlated with the difference in unpaced/paced LVEF, a measure of acute mechanical response to CRT. CRT increased BRS by 35% from 2.96 to 3.79 ms/mmHg (P < 0.02) and increased HRV (standard deviation of the intervals between normal beats) from 18.5 to 24.0 ms (P < 0.01). The CRT-induced relative change in BRS correlated with the change in LVEF (r = 0.44; P < 0.01). In conclusion, CRT acutely increases BRS and HRV. This favorable response of the autonomic nervous system might be caused by CRT-induced CSAR deactivation. Follow-up studies should verify the mechanism of the acute response and the possible predictive value of an acute positive BRS response.

Exercise training increases oxygen uptake efficiency slope in chronic heart failure.

BACKGROUND AND AIM: The oxygen uptake efficiency slope (OUES) is a novel measure of cardiopulmonary reserve. OUES is measured during an exercise test, but it is independent of the maximally achieved exercise intensity. It has a higher prognostic value in chronic heart failure (CHF) than other exercise test-derived variables such as(Equation is included in full-text article.)or(Equation is included in full-text article.)slope. Exercise training improves(Equation is included in full-text article.)and(Equation is included in full-text article.)in CHF patients. We hypothesized that exercise training also improves OUES. METHODS AND RESULTS: We studied 34 New York Heart Association (NYHA) class II-III CHF patients who constituted an exercise training group T (N=20; 19 men/1 woman; age 60+/-9 years; left ventricular ejection fraction 34+/-5%) and a control group C (N=14; 13 men/one woman; age 63+/-10 years; left ventricular ejection fraction 34+/-7%). A symptom-limited exercise test was performed at baseline and repeated after 4 weeks (C) or after completion of the training program (T). Exercise training increased NYHA class from 2.6 to 2.0 (P<0.05),(Equation is included in full-text article.)by 14% [P(TvsC)<0.01], and OUES by 19% [P(TvsC)<0.01]. Exercise training decreased(Equation is included in full-text article.)by 14% [P(TvsC)<0.05]. CONCLUSION: Exercise training improved NYHA class,(Equation is included in full-text article.)and also OUES. This finding is of great potential interest as OUES is insensitive for peak load. Follow-up studies are needed to demonstrate whether OUES improvements induced by exercise training are associated with improved prognosis.