hronic congestive heart failure (CHF) is a complex metabolic syndrome resulting from global hypoperfusion and neurohumoral activation. Sympathoadrenergic hyperactivity and stimulation of the reninangiotensin -aldosterone cascade promote endothelial dysfunction in the macro-and microcirculation, and thus influence the distribution of the terminal blood flow. The increased total peripheral resistance, reduction of blood supply and impaired peripheral vascular dilatation in response to vasodilator stimuli result in atrophy of skeletal muscle and decreased oxidative activity. Physical training could reverse the pathologic changes in patients with CHF and there have been many reports during the past decade that clearly demonstrate the benefits of exercise on functional capacity, ventilation, metabolic status, autonomic control of heart rate (HR) variability and other parameCirculation Journal Vol. 70, January 2006 ters, 1-5 including skeletal muscle performance and impaired endothelial function. 6,7 However, most of the actual training protocols are based on systemic exercise requiring increased cardiac output, which cannot be achieved by all patients, and in general are only suitable for patients with a moderately advanced grade of CHF; less attention has been paid to the development of safe and efficient training programs for patients with severe grades of the disease. Background This study was designed to evaluate the effects of low-frequency electrical stimulation (LFES) on muscle strength and blood flow in patients with advanced chronic heart failure (CHF). Methods and ResultsPatients with CHF (n=15; age 56.5±5.2 years; New York Heart Association III -IV; ejection fraction 18.7±3.3%) were examined before and after 6 weeks of LFES (10 Hz) of the quadriceps and calf muscles of both legs (1 h/day, 7 days/week). Dynamometry was performed weekly to determine maximal muscle strength (Fmax; N) and isokinetic peak torque (PTmax; Nm); blood flow velocity (BFV) was measured at baseline and after 6 weeks of LFES using pulsed-wave Doppler velocimetry of the right femoral artery.

To obtain a physiological response by a total artificial heart (TAH), while eliminating the hemodynamic abnormalities commonly observed with its use, we proposed the use of a conductance- and arterial pressure-based method (1/R control) to determine TAH cardiac output. In this study, we endeavored to make use of a variable more closely tied to central nervous system (CNS) efferents, systemic conductance, to provide the CNS with more direct control over the output of the TAH. The control equation that calculates the target cardiac output of the TAH was constructed on the basis of measurement of blood pressures and TAH flow. The 1/R control method was tested in TAH-recipient goats with an automatic method by using a microcomputer. In 1/R control animals, the typical TAH pathologies, such as mild arterial hypertension and substantial systemic venous hypertension, did not occur. Cardiac output varied according to daily activity level and exercise in a manner similar to that observed in natural heart goats. These results indicate that we have determined a control method for the TAH that avoids hemodynamic abnormalities exhibited by other TAH control systems and that exhibits physiological responses to exercise and daily activities under the conditions tested. The stability of the control and the complete lack of inappropriate excursions in cardiac output is suggestive of CNS involvement in stabilizing the system.

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SUMMARYThe aim of this study was to investigate whether electrical stimulation of skeletal muscles could represent a rehabilitation alternative for patients with chronic heart failure (CHF). Thirty patients with CHF and NYHA class II-III were randomly assigned to a rehabilitation program using either electrical stimulation of skeletal muscles or bicycle training. Patients in the first group (n = 15) had 8 weeks of home-based low-frequency electrical stimulation (LFES) applied simultaneously to the quadriceps and calf muscles of both legs (1 h/day for 7 days/week); patients in the second group (n = 15) underwent 8 weeks of 40 minute aerobic exercise (3 times a week). After the 8-week period significant increases in several functional parameters were observed in both groups: maximal VO 2 uptake (LFES group: from 17.5 ± 4.4 mL/kg/min to 18.3 ± 4.2 mL/kg/min, P < 0.05; bicycle group: from 18.1 ± 3.9 mL/kg/min to 19.3 ± 4.1 mL/kg/min, P < 0.01), maximal workload (LFES group: from 84.3 ± 15.2 W to 95.9 ± 9.8 W, P < 0.05; bicycle group: from 91.2 ± 13.4 W to 112.9 ± 10.8 W, P < 0.01), distance walked in 6 minutes (LFES group: from 398 ± 105 m to 435 ± 112 m, P < 0.05; bicycle group: from 425 ± 118 m to 483 ± 120 m, P < 0.03), and exercise duration (LFES group: from 488 ± 45 seconds to 568 ± 120 seconds, P < 0.05; bicycle group: from 510 ± 90 seconds to 611 ± 112 seconds, P < 0.03). These results demonstrate that an improvement of exercise capacities can be achieved either by classical exercise training or by home-based electrical stimulation. LFES should be considered as a valuable alternative to classical exercise training in patients with CHF. (Int Heart J 2006; 47: 441-453)

This study has three purposes, as follows. The first is to develop a microscopic system to observe the microcirculation of animals implanted with an artificial heart. The second is to investigate the influence of flow pattern change from pulsatile to nonpulsatile on the microcirculation. The third is to study the effects of pulsatility in blood flow on endothelium-derived nitric oxide release in the microvasculature. When the flow pattern was changed from pulsatile to nonpulsatile, the velocity of erythrocytes in many capillaries dropped and remained at a low level, and the number of perfused capillaries decreased. After the flow pattern was returned to pulsatile, the velocity of erythrocytes recovered to the initial level. In many cases, the flow of nonperfused capillaries recovered to the initial level as well. Also, the pulsatile flow enhances the basal and flow-stimulated endothelium-derived nitric oxide release in microvessels.