Development Of Exercise Intolerance Research Articles

Correlation between ventricular function as assessed by echocardiography and six-minute walk test as a surrogate of functional capacity in patients with chronic obstructive pulmonary disease

BackgroundExercise intolerance is common in patients with chronic obstructive pulmonary disease (COPD), which has multiple mechanisms underlying its progression. Ventricular dysfunction may play a role in the development of exercise incapacity in patients with COPD.AimTo investigate the possible contribution of left ventricular (LV) and right ventricular (RV) dysfunction (either systolic or diastolic) in development of exercise intolerance in patients with COPD.Patients and methodsA total of 60 patients with diagnosis of COPD were categorized according to GOLD spirometric stage into two groups (group 1: mild to moderate COPD, and group 2: severe to very severe COPD). Both groups were evaluated by spirometry, ECG, chest radiography, routine laboratory investigation, 6-min walk test, and echocardiography including tissue Doppler imaging.ResultsThe average age in the whole study group was 56.63 ±10.33 years. Male patients in the study were 46 (76.7%) and female patients were 14 (23.3%). Mean maximum walk distance among the whole group was 342.75±54.85 m. There was a significant correlation between 6-min walk distance and transtricuspid E velocity, tricuspid E/A, and transtricuspid deceleration time (P=0.011, 0.015, and 0.021, respectively). There was no significant correlation between 6-min walk distance and parameters of LV diastolic dysfunction. Prevalence of ventricular dysfunction was as follow: LV systolic dysfunction 3.3%, LV diastolic dysfunction 30%, RV systolic dysfunction 21%, and RV diastolic dysfunction 46%.ConclusionRV diastolic dysfunction may be a contributing factor in the progression of exercise intolerance in COPD. Although LV diastolic dysfunction may not be associated with exercise intolerance, it is still prevalent in COPD and must be assessed and managed through the course of the disease and especially during exacerbation.

Cardiac Rehabilitation in Heart Failure. Part I, Mechanism

Introduction Diagnosis and treatment issues among heart failure (HF) patients are becoming one of the most important points in public health of developed countries, largely due to the aging of population and the fact that HF affects mainly the elderly. In this review we would like to focus on pathophysiology of exercise intolerance in patients with heart failure and potential benefits of cardiac rehabilitation (CR). Material and Methods Analysis of articles in the EBSCO database using keywords: heart failure, cardiac rehabilitation, exercise training, pathophysiology. Results HF can be described as a composite syndrome which results from structural or functional impairment of ventricular filling or blood ejection. Patients have variety of symptoms which usually are nonspecific. The most frequently occurring symptoms of HF are dyspnea and fatigue, which may restrict exercise capacity, and fluid retention. There are many possible pathophysiological factors involved in the development of exercise intolerance. Based on the available literature pathological changes in central hemodynamic function, pulmonary system, skeletal muscles, endothelial function and neurohumoral system can be distinguished. They play a crucial role in the pathogenesis of HF symptoms and represent a potential curative object. Conclusions HF patients are characterized by diminished functional performance. Exercise training has many potential profits in patients with heart failure, including an increase in peak oxygen uptake, improvement in central hemodynamics, peripheral vascular and skeletal muscle function and has become part of evidence-based clinical therapy in these patients.

Diaphragm Muscle Dysfunction in Patients With Heart Failure

BackgroundInspiratory muscle weakness is associated with the development of exercise intolerance in patients with heart failure (HF). Ultrasound assessment of the diaphragm is used to evaluate respiratory muscle function, but its application in patients with HF remains undefined. We examined the relationship of diaphragm function as assessed by ultrasonography with inspiratory muscle strength and exercise tolerance in HF. Methods and ResultsSeventy-seven patients hospitalized with HF were enrolled. Impaired diaphragm muscle function was defined as a diaphragm thickness at end-inspiration of less than the median value of 4.0 mm, which represents diaphragm muscle loss and reduced contraction. Compared with patients with preserved diaphragm muscle function, those with impaired diaphragm muscle function were older; had significantly lower vital capacity, handgrip strength, and inspiratory muscle strength as assessed by the maximum inspiratory pressure; and had a significantly shorter 6-minute walk distance (6MWD; P < .05). Although low handgrip strength was also associated with a short 6MWD, the relationship between impaired diaphragm muscle function and short 6MWD was independent from age, vital capacity, and handgrip strength. ConclusionDiaphragm dysfunction as assessed by ultrasonography represents inspiratory muscle weakness and predicts exercise intolerance independently from comorbid pulmonary dysfunction and dynapenia in patients with HF.

Cardiac rehabilitation in heart failure

Heart failure is amalignant disorder with increasing prevalence and ahigh socioeconomic impact. Sceletal muscle myopathy seems to play akey role in the development of exercise intolerance. Cardiac rehabilitation for heart failure mainly adresses training, namely moderate continuous endurance training or interval training in combination with resistance training, and is highly recommended in the current ESC-guidelines. Following amultimodal concept cardiac rehabilitation also implements optimisation of neurohumoral therapy, education and counselling to empower self-care as well as psychosocial support.

Increased Left Ventricular Stiffness Impairs Exercise Capacity in Patients with Heart Failure Symptoms Despite Normal Left Ventricular Ejection Fraction

Aims. Several mechanisms can be involved in the development of exercise intolerance in patients with heart failure despite normal left ventricular ejection fraction (HFNEF) and may include impairment of left ventricular (LV) stiffness. We therefore investigated the influence of LV stiffness, determined by pressure-volume loop analysis obtained by conductance catheterization, on exercise capacity in HFNEF. Methods and Results. 27 HFNEF patients who showed LV diastolic dysfunction in pressure-volume (PV) loop analysis performed symptom-limited cardiopulmonary exercise testing (CPET) and were compared with 12 patients who did not show diastolic dysfunction in PV loop analysis. HFNEF patients revealed a lower peak performance (P = .046), breathing reserve (P = .006), and ventilation equivalent for carbon dioxide production at rest (P = .002). LV stiffness correlated with peak oxygen uptake (r = −0.636, P < .001), peak oxygen uptake at ventilatory threshold (r = −0.500, P = .009), and ventilation equivalent for carbon dioxide production at ventilatory threshold (r = 0.529, P = .005). Conclusions. CPET parameters such as peak oxygen uptake, peak oxygen uptake at ventilatory threshold, and ventilation equivalent for carbon dioxide production at ventilatory threshold correlate with LV stiffness. Increased LV stiffness impairs exercise capacity in HFNEF.

Abstract 2199: Left Ventricular Diastolic Function Impacts Age Based Differences in Exercise Capacity

Limited information exists regarding the echocardiographic and clinical predictors of exercise capacity and their effects on exercise with advancing age or by sex. We hypothesized that LV diastolic function (DF) impacts exercise capacity to a greater degree with advancing age. This was a prospective cohort study of consecutive patients undergoing routine exercise echocardiography with the Bruce protocol (n=2955). DF assessments at rest and exercise were performed. Those with echocardiographic exercise-induced ischemia and significant valvular disease were excluded. Univariate and multivariate analyses were conducted to determine the strongest echocardiographic and clinical predictors of exercise capacity (METs). Results were reported as unstandardized β coefficient (Standard Error) as outlined beside each variable. Age and sex interactions of these predictors with exercise capacity were determined. The strongest independent multivariate predictors of exercise capacity were female vs. male sex [−1.98 (0.07), p&lt;0.0001], body mass index &gt;30 kg/m 2 [−1.24 (0.08), p&lt;0.0001], age per 10 year increment [−0.85 (0.01), p&lt;0.0001], mild resting diastolic dysfunction vs. normal [−0.70 (0.10), p&lt;0.0001], and moderate/severe resting diastolic dysfunction vs. normal [−1.3 (0.13), p&lt;0.0001]. LV filling pressures measured by a resting E/e’ ≥ 15 [−0.42 (0.14), p=0.004] or exercise E/e’≥ 15 [−0.31 (0.14), p&lt;0.0001] similarly predicted a reduction in exercise capacity, each in separate multivariate analyses. The impact of impaired relaxation and left ventricular filling pressures on exercise capacity increased with advancing age (p&lt;0.001 and p=0.02 respectively), and was most marked after age 50. These predictors had a similar negative effect on exercise capacity among men and women (p=NS). In conclusion, in this large population referred for exercise echocardiography and not limited by ischemia, resting DF and resting/exercise LV filling pressures independently predicted exercise capacity. The increasingly potent effect of impaired relaxation and exercise LV filling pressures with advancing age suggest that DF plays an important role in the development of exercise intolerance in the elderly.

Use of peak Doppler gradient across ventricular septal defect leads to underestimation of right-sided pressures in a patient with M-shaped Doppler signal: A case report

CASE REPORT A 4-year-old girl with a history of complex congenital heart disease consisting of pulmonary atresia, ventricular septal defect (VSD), hypoplastic central pulmonary artery (PA), and multiple systemic to PA collaterals was brought to the cardiac catheterization laboratory for evaluation of the caliber and pressure of her PAs and the gradient across her VSD. She has been clinically stable without development of exercise intolerance. Her first surgical procedure was a central systemic to PA shunt as an infant. Subsequently, she had coil embolization of systemic to PA collateral vessels. She then underwent complete repair with a right ventricular (RV) outflow tract patch with a Gore-Tex monocusp valve (Gore and Associates, Flagstaff, Ariz) and a fenestrated VSD closure at 18 months of age. Because of recurrent branch PA stenoses, she had undergone cardiac catheterization with balloon angioplasty of multiple branch PA obstructions on the right and left side. Since her surgical repair at 18 months, her electrocardiogram had shown a right bundle branch block. While the patient was sedated and anesthetized, RV and left ventricular (LV) pressures were measured and recorded simultaneously during cardiac catheterization. To avoid dampening or delay artifacts as seen with standard fluid-filled catheters, two 2F microtip catheter pressure transducers were used (Millar SPC-320, Millar Instruments Inc, Houston, Tex). These transducers were placed at the end of the catheters to record the pressure directly within the cardiac chamber. Simultaneously, an echocardiography machine (Sequoia, Siemens Co, Mountain View, Calif) was used to obtain the Doppler signal across the VSD. The transthoracic transducer was placed in a position to obtain the maximal Doppler velocity. The spectral Doppler gain settings were adjusted to obtain the clearest signal. Electrocardiographic tracings were recorded simultaneously. The ventricular tracings and simultaneous echocardiographic gradients are displayed in Figure 1.

Skeletal muscle oxidative capacity and exercise tolerance in rats with heart failure.

Past research has shown the development of exercise intolerance after myocardial infarction (MI). The purpose of this study was to test the hypothesis that reductions in oxidative enzyme activity, in a variety of skeletal muscles, coincide with the development of exercise intolerance in a rat model of chronic heart failure (CHF) induced by MI. The animals were initially divided into two groups: sham-operated controls (Sham) and animals in which a MI was surgically induced. MI rats were then subdivided into two groups according to left ventricular end-diastolic pressure (LVEDP): <20 mm Hg [small MI (SMI)] and > 20 mm Hg [large MI (LMI)]. Exercise tolerance was measured by performing a progressive run to fatigue test (RTF). Citrate synthase (CS), 3-hydroxyacyl CoA dehydrogenase (HADH), and malate dehydrogenase (MDH) activities were measured in six hindlimb muscles. After approximately 6 wk of recovery, LVEDP differed among groups (P < 0.05): Sham (1 +/- 1 mm Hg, N = 7), SMI (7 +/- 2 mm Hg, N = 7), and LMI (30 +/- 2 mm Hg, N = 6). RTF was 20 +/- 1 min for Sham, 25 +/- 3 min for SMI, and 11 +/- 2 min for LMI (P < 0.05 for LMI vs Sham, SMI). Significant reductions in enzyme activity were found for all three enzymes in the red portion of the gastrocnemius muscles of LMI. However, no significant correlation was found between RTF and CS, HADH, or MDH in any muscle of the three groups of animals. The results of the present study demonstrate that severe left ventricular dysfunction is associated with reductions in exercise tolerance and modest decreases in oxidative enzyme activities in selected muscles. It does not appear, however, that the development of exercise intolerance in CHF and oxidative enzyme activities are mechanistically related to one another.