Capacity In Heart Failure Patients Research Articles

Right Ventricular Tissue Doppler Is Associated with Functional Capacity in Heart Failure Patients

Right Ventricular Tissue Doppler Is Associated with Functional Capacity in Heart Failure Patients

Immune activation is associated with reduced skeletal muscle mass and physical function in chronic heart failure

Background Chronic heart failure is characterized by immune activation and increased circulating levels of cytokines. Whether humoral factors contribute to the peripheral manifestations of the heart failure syndrome, such as muscle atrophy and reduced physical work capacity, however, is not clear. Methods We measured circulating cytokines (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)), their soluble receptors (sTNF-α RII, IL-6sR), markers of immune activation (C-reactive protein (CRP)), muscle mass, aerobic capacity and muscle strength in 10 patients with heart failure (mean ± S.E.; 63 ± 3 years) and 11 controls (70 ± 3 years). Results Heart failure patients exhibited decreased aerobic capacity ( P < 0.01) and leg muscle strength ( P < 0.05). Reduced muscle strength persisted in heart failure patients after statistical adjustment for differences in skeletal muscle size. All inflammatory markers were increased in heart failure patients ( P ≤ 0.05 to P < 0.01) compared to controls, with the exception of TNF-α. Despite no group differences in TNF-α, higher concentrations of this cytokine were correlated to lower skeletal muscle mass in the combined study population (range of r-values: − 0.436 to − 0.545; P < 0.05 to P < 0.02), as were IL-6 levels (range of r-values: − 0.438 to − 0.443; P < 0.05). TNF-α, sTNF-α RII, IL-6 and CRP showed strong negative relationships to aerobic capacity (range of r-values: − 0.579 to − 0.751; P < 0.01 to P < 0.001). In addition, elevated levels of IL-6 and TNF-α were associated with reduced leg and forearm skeletal muscle strength (range of r-values: − 0.440 to − 0.674; P < 0.05 to P < 0.01). Finally, correlations between cytokines and functional measures were present when heart failure patients were analyzed separately (range of r-values: − 0.646 to − 0.673; P < 0.05). Conclusions Our results suggest that circulating cytokines are related to both skeletal muscle mass and physical function. These findings provide further evidence to support the hypothesis that immune activation contributes to skeletal muscle atrophy and reduced functional capacity in heart failure patients.

Cardiac resynchronization therapy improves central sleep apnea and Cheyne-Stokes respiration in patients with chronic heart failure

ObjectivesWe studied the effects of cardiac resynchronization therapy (CRT) on heart failure (HF) patients with central sleep apnea (CSA). BackgroundPatients with advanced HF often suffer from CSA with Cheyne-Stokes respiration. Cardiac resynchronization therapy improves myocardial function and exercise capacity in HF patients with conduction disturbances. The relationship between CRT and CSA is currently unknown. MethodsTwenty-four patients (7 females; 62 ± 11 years) with HF, a reduced left ventricular ejection fraction (24 ± 6%), and left bundle branch block (QRS duration 173 ± 22 ms) received a CRT device. The number of apneas and hypopneas per hour (apnea-hypopnea index [AHI]) and minimal oxygen saturation (Sao2min) were quantified by cardiorespiratory polygraphy. Fourteen patients showed CSA (AHI >5/h), and 10 patients had an AHI <5/h without CSA. Subjective sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Data were evaluated before and after 17 ± 7 weeks of CRT. ResultsIn patients with CSA, CRT led to a significant decrease in AHI (19.2 ± 10.3 to 4.6 ± 4.4, p < 0.001) and PSQI (10.4 ± 1.6 to 3.9 ± 2.4, p < 0.001) without Cheyne-Stokes respiration and to a significant increase in Sao2min (84 ± 5% to 89 ± 2%, p < 0.001). There was no significant change in AHI (1.7 ± 0.7 to 1.5 ± 1.6), PSQI (2.4 ± 0.5 to 2.6 ± 0.9), and Sao2min (90 ± 2% to 91 ± 1%) in patients without CSA. ConclusionsCardiac resynchronization therapy leads to a reduction of CSA and to increased sleep quality in patients with HF and sleep-related breathing disorders. This may have prognostic implications in patients receiving CRT.

The Arg16Gly polymorphism of the β2-adrenergic receptor and left ventricular systolic function

Background β-Adrenergic receptors (ARs), including β1- and β2-AR, are involved in modulation of cardiac contractility and heart rate. Arg16Gly, a functional polymorphism in the β2-AR gene, has been reported to influence exercise capacity in heart failure patients. This study examined the association of the β2-AR Arg16Gly polymorphism with left ventricular (LV) systolic function in a biethnic population-based sample. Methods Echocardiograms and the β2-AR Arg16Gly polymorphism were analyzed in 267 normotensive (54% African Americans) and 252 severe hypertensive (53% African Americans) adults without coronary heart disease or diabetes. Results The frequencies of Gly16Gly16, Arg16Gly16, and Arg16Arg16 were 28.1%, 54.3%, and 17.6%, respectively, in normotensives, and 31.4%, 47.6%, and 21.0%, respectively, in hypertensives. In normotensives, the Gly16Gly16 homozygotes displayed greater fractional shortening (35.9% ± 4.3% v 34.1% ± 4.7% v 34.0% ± 3.9%, P = .01), ejection fraction (65.0% ± 5.8% v 62.5% ± 6.4% v 62.6% ± 5.4%, P = .01), midwall shortening (18.6% ± 1.6% v 17.9% ± 1.9% v 18.0% ± 1.6%, P = .02), and stress-corrected midwall shortening (110.1% ± 9.3% v 106.1% ± 10.6% v 108.1% ± 10.8%, P = .03) compared to the Arg16Gly16 and Arg16Arg16 groups. These associations were independent of age, sex, ethnicity, heart rate, body mass index, systolic blood pressure, LV end-diastolic dimension, and field center. No significant associations between the β2-AR Arg16Gly polymorphism and echocardiographic measures were found in hypertensives. Conclusions The Arg16Gly polymorphism of β2-AR may be a marker for LV chamber function and contractility in normotensive adults.

The beneficial effect of optimized neurohormonal therapy on exercise capacity in heart failure patients is associated with the restoration of endothelial function

The beneficial effect of optimized neurohormonal therapy on exercise capacity in heart failure patients is associated with the restoration of endothelial function

A practical guide to exercise training for heart failure patients

Background: Exercise training has been shown to improve exercise capacity in patients with heart failure. We sought to examine the optimal strategy of exercise training for patients with heart failure. Methods: Review of the published data on the characteristics of the training program, with comparison of physiologic markers of exercise capacity in heart failure patients and healthy individuals and comparison of the change in these characteristics after an exercise training program. Results: Many factors, including the duration, supervision, and venue of exercise training; the volume of working muscle; the delivery mode (eg, continuous vs. intermittent exercise), training intensity; and the concurrent effects of medical treatments may influence the results of exercise training in heart failure. Starting in an individually prescribed and safely monitored hospital-based program, followed by progression to an ongoing and progressive home program of exercise appears to be the best solution to the barriers of anxiety, adherence, and “ease of access” encountered by the heart failure patient. Conclusions: Various exercise training programs have been shown to improve exercise capacity and symptom status in heart failure, but these improvements may only be preserved with an ongoing maintenance program.

Sub‐maximal exercise capacity of heart failure patients with poor prognosis can be improved by ventricular resynchronization therapy

Sub‐maximal exercise capacity of heart failure patients with poor prognosis can be improved by ventricular resynchronization therapy

Prediction of exercise capacity in heart failure patients during pacing therapy using a new 2-D heart rate variability parameter

Prediction of exercise capacity in heart failure patients during pacing therapy using a new 2-D heart rate variability parameter

Exercise capacity in heart failure patients: relative importance of heart and skeletal muscle.

The knee extensor and the whole-body exercise capacities were measured in 11 chronic heart failure (CHF) patients and 11 healthy age- and sex-matched controls, and were related to ejection fraction and to biochemical and histochemical markers of the musculature. The CHF patients had a 39% lower maximal oxygen uptake measured on an ergometer cycle than the healthy controls (1.54 +/- 0.57 vs. 2.51 +/- 0.70 1 min-1, P < 0.001). The low exercise capacity was markedly related to the ejection fraction (r = 0.77, P < 0.001). The maximal strength of m. quadriceps femoris was 15% lower in the CHF patients than in the controls (P < 0.05). The cross-sectional area (CSA) of m. quadriceps femoris explained 55% (r = 0.74, P < 0.001) of the difference in strength between both groups. The endurance capacity of m. quadriceps femoris was 30% lower in CHF patients than in controls, partly as a result of the 25% lower capillary density (P < 0.05) and the 27% lower aerobic enzyme capacity (P < 0.05), as estimated by the citrate synthase activity, in the CHF patients. The citrate synthase activity correlated with the maximal oxygen uptake (r = 0.61, P < 0.05). Moreover, the ejection fraction, together with the CSA of m. quadriceps femoris, explained 75% (r = 0.86%, P < 0.01) of the difference in maximal oxygen uptake between CHF patients and controls. These results demonstrate that CHF patients have both a lower local and a lower whole-body work capacity than healthy controls. This is a function of a smaller leg muscle mass and a lower capillary density and mitochondrial enzyme capacity in the CHF patients; however, a lowered pump capacity of the heart is the factor which limits the exercise capacity the most.

Relation of the nine-minute self-powered treadmill test to maximal exercise capacity and skeletal muscle function in patients with congestive heart failure

The 9-minute self-powered treadmill test has been employed to evaluate submaximal exercise capacity in heart failure patients, but its relation to maximal exercise capacity and to indexes of skeletal muscle function has not been well defined. Two protocols were utilized. The first evaluated the relation of the peak oxygen uptake (VO 2) achieved on the self-powered treadmill to that during a symptom-limited treadmill protocol, and examined the reproducibility of this test. Thirteen patients (aged 62 ± 2 years, in New York Heart Association class I to III [2.3 ± 0.1], ejection fraction 23 ±2% [means ± SEM]) and 10 age-matched sedentary controls were studied. The second protocol, which involved 18 patients (aged 65 ± 2 years, in New York Heart Association class I to IV [2.4 ± 0.1], ejection fraction 23 ± 2%) and 10 age-matched controls evaluated the relation of performance on the self-powered treadmill to maximal systemic exercise capacity on a cycle ergometer and to indexes of skeletal muscle function. In the first protocol, the test was found to be highly reproducible. The proportion of self-powered treadmill to maximal treadmill peak VO 2 did not differ significantly between patients and controls (95 ± 5% vs 87 ± 6%). In the second protocol, patients achieved a lower peak VO 2 (15.6 ± 1.1 vs 25.6 ± 0.9 ml/kg/mm, p < 0.001), walked a shorter distance on the self-powered treadmill (367 ± 32 vs 667 ± 28 m, p < 0.001), and exhibited less knee extensor work capacity (1,075 ± 116 vs 1,390 ± 110 ft-lbs, p < 0.05). The self-powered treadmill distance correlated strongly with peak VO 2 in patients (r = 0.79, p < 0.001) and with total knee extensor work in both patients and controls (r = 0.62 and 0.80, respectively, both p < 0.01), but exhibited poor correlation with muscle strength and endurance. These results indicate that the self-powered treadmill test is a reproducible and convenient test that appears to be more of a measure of maximal than submaximal exercise tolerance in patients with congestive heart failure. Although it correlates relatively well with symptom status, it is poorly related to indexes of left ventricular function and muscle performance.

A patient-powered treadmill--a simple alternative means of assessing heart failure and treatment in family practice

A patient-powered treadmill was compared with the covered corridor walking test as assessments of exercise capacity in heart failure patients, and used to investigate their sensitivity in discriminating between the effects of xamoterol and placebo. The two methods were comparable, and sufficiently sensitive to demonstrate improvements in exercise capacity on xamoterol. The treadmill was more sensitive and could be useful as an assessment of treatment of heart failure in family practice.