Characterization of exercise limitations by evaluating individual cardiac output patterns: a prospective cohort study in patients with chronic heart failure (original) (raw)
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Journal of Cardiopulmonary Rehabilitation and Prevention, 2020
H eart failure (HF) is a major health care problem associated with high morbidity and mortality. 1 Currently, >6 million Americans ≥20 y of age have HF, and its prevalence is expected to increase by 46% by 2030. 1,2 Nearly half of all HF patients have preserved left ventricular (LV) ejection fraction (heart failure with preserved ejection fraction [HF-pEF]) and this phenotype is more common in older individuals, women, and those with a history of hypertension, obesity, and anemia. 1,3 Decreased exercise tolerance is a hallmark feature in clinically stable HFpEF patients and is associated with reduced quality of life (QoL). 4,5 Given the relationship between cardiorespiratory fitness (CRF; ie, peak oxygen uptake, • Vo 2peak) and survival, 6,7 an important goal of therapy should be to improve CRF in HFpEF patients. 8-12 Currently, exercise training is the only proven effective intervention to improve • Vo 2peak , aerobic endurance, and QoL in HFpEF patients. 4,10 Several recent meta-analyses have reported that endurance exercise training, performed alone or combined with resistance training, improves • Vo 2peak and 6-min walk test distance by 2.2 mL/kg/min and 33 m, respectively. 4,13,14 Accordingly, understanding the mechanisms responsible for reduced • Vo 2peak and its improvement with exercise training is critical to optimally improve functional capacity and QoL in HFpEF patients. In this brief review, the pathophysiology of exercise intolerance and the role of exercise training to improve • Vo 2peak in clinically stable patients with HFpEF are discussed. Further discussion of the mechanisms responsible for the exercise training-mediated increase in • Vo 2peak is provided, along with evidence-based exercise prescription guidelines for clinically stable HFpEF patients participating in an exercise-based cardiac rehabilitation (CR) program. PATHOPHYSIOLOGY OF EXERCISE INTOLERANCE IN HFpEF Appreciating the Fick principle for • Vo 2 is fundamental to understanding the pathophysiology of exercise intolerance in patients with HFpEF. Specifically, the Fick principle dictates that • Vo 2 = cardiac output (Q) × arterial-venous O 2 content difference (a-vO 2 Diff), with Q and the a-vO 2 Diff each having their own modulating factors that ultimately drive the highest achievable • Vo 2 at peak exercise (Figure). ROLE OF CARDIAC FUNCTION ON EXERCISE LIMITATIONS IN HFpEF The reduction in • Vo 2peak observed in patients with HFpEF is due, in part, to a reduction in cardiac function during exercise. Several independent laboratories have demonstrated that peak Q is 30-40% lower in patients with HF-pEF compared with control subjects. 16-19 Evidence to date suggests that chronotropic incompetence rather than stroke volume (SV) is a fundamental concern for the blunted Q response to peak exercise in patients with HFpEF. 16-18,20-22 Indeed, significant relationships between Q (independent of major reductions in SV) 18 and heart rate (HR) 20 with • Vo 2peak have previously been reported, even when matched for important comorbidities, 21 supporting that underlying chronotropic incompetence is a major contributor to reduced Q and subsequent reductions in • Vo 2peak in HFpEF. Despite the major role that HR plays on the severely reduced peak exercise • Vo 2 in patients with HFpEF, several impairments in left ventricular function have also been reported (Figure). Normally, LV relaxation is augmented during exercise to compensate for the reduction in filling
2010
OBJECTIVES We studied whether direct assessment of the hemodynamic response to exercise could improve the prognostic evaluation of patients with heart failure (HF) and identify those in whom the main cause of the reduced functional capacity is related to extracardiac factors. BACKGROUND Peak exercise oxygen consumption (VO 2) is one of the main prognostic variables in patients with HF, but it is influenced also by many extracardiac factors. METHODS Bicycle cardiopulmonary exercise testing with hemodynamic monitoring was performed, in addition to clinical evaluation and radionuclide ventriculography, in 219 consecutive patients with chronic HF (left ventricular ejection fraction, 22 Ϯ 7%; peak VO 2 , 14.2 Ϯ 4.4 ml/kg/min). RESULTS During a follow-up of 19 Ϯ 25 months, 32 patients died and 6 underwent urgent transplantation with a 71% cumulative major event-free 2-year survival. Peak exercise stroke work index (SWI) was the most powerful prognostic variable selected by Cox multivariate analysis, followed by serum sodium and left ventricular ejection fraction, for one-year survival, and peak VO 2 and serum sodium for two-year survival. Two-year survival was 54% in the patients with peak exercise SWI Յ30 g⅐m/m 2 versus 91% in those with a SWI Ͼ30 g⅐m/m 2 (p Ͻ 0.0001). A significant percentage of patients (41%) had a normal cardiac output response to exercise with an excellent two-year survival (87% vs. 58% in the others) despite a relatively low peak VO 2 (15.1 Ϯ 4.7 ml/kg/min). CONCLUSIONS Direct assessment of exercise hemodynamics in patients with HF provides additive independent prognostic information, compared to traditional noninvasive data.
Circulation, 1985
We evaluated the hemodynamic effects of isometric exercise in 53 patients with congestive heart failure (CHF) and compared them with those found in 10 normal subjects. In both groups, isometric exercise increased heart rate and blood pressure. Systemic resistance increased in patients with CHF (1862 + 520 vs 2126 ± 642 dyne-sec-cm-5; p < .001) but not in normal subjects (1359 + 268 vs 1380 ± 252 dyne-sec-cm-5). Cardiac index and stroke volume index increased mildly but not significantly in the normal subjects (2.8 0.5 vs 3. 1 ± 0.7 liters/min/m2 and 46 + 8 vs 47 ± 7 mI/M2) and showed a significant fall in the patients with CHF (2.1 ± 0.6 to 1.9 ± 0.6 liters/min/m2, p < .01 and 23 ± 7 vs 20 + 7 ml/m2, p < .01). Mean pulmonary arterial wedge pressure increased in patients with CHF from 26 ± 7 to 30 ± 8 mm Hg (p < .001). Although no significant change was found in mean value for stroke work index (21 ± 9 vs 20 + 9 g-m/m2), the individual changes were variable, with marked decrease (>15%) in 17 of the patients. This hemodynamic deterioration could not be predicted from resting hemodynamics, left ventricular ejection fraction, or functional classification. Isometric exercise resulted in no significant change in circulatory catecholamine levels or plasma renin concentration in our 10 normal subjects. In the patients with CHF renin (measured in 12 patients) and epinephrine (measured in 16 patients) also did not change during isometric exercise, but norepinephrine levels (measured in 16 patients) increased significantly. No correlation was found between changes in hormonal levels and any of the hemodynamic changes during static exercise. We conclude that in patients with chronic CHF, isometric exercise can lead to a significant increase in left ventricular outflow resistance and filling pressure and to a fall in cardiac performance. In the presence of CHF, this form of exercise results in a consistent elevation in norepinephrine levels, but there is no correlation between changes in its plasma level and in hemodynamic values. There is considerable individual variation in the hemodynamic response, with a significant deterioration in cardiac performance in some patients, which cannot be separated by resting hemodynamic values, left ventricular ejection fraction, or clinical status. Circulation 72, No. 5, 975-981, 1985. Patients with CHF. Hemodynamic effects of isometric exercise were evaluated in 53 patients who were admitted to the University of Southern California/Los Angeles County Medical Center for inadequate control of chronic CHF. There were 39 men and 14 women, ranging in age from 20 to 80 years (mean ± SD 51 + 6 years). The cause of CHF was coronary artery disease in 14 patients and congestive cardiomyopathy in 39 patients. Thirty-two of the patients were classified on admission into the NYHA functional class 111 and 21 were class IV. The diagnosis of left ventricular systolic dysfunction was confirmed by cardiac catheterization in 26 patients, by radionuclide ventriculography in 22 patients, and by echocardiography in five 975 by guest on October 5, 2017
Exercise limitation in chronic heart failure: Central role of the periphery
Journal of the American College of Cardiology, 1996
The symptoms of chronic heart failure (CHF) are predominantly shortness of breath and fatigue during exercise and reduced exercise capacity. Disturbances of central hemodynamic function are no longer considered to be the major determinants of exercise capacity. The two symptoms of fatigue and breathlessness are often considered in isolation. A pulmonary abnormality is usually considered to be the cause of abnormal ventilation, and increased dead space ventilation has come to be accepted as a major cause of the increased ventilation relative to carbon dioxide production seen in CHF. Rather than decreased skeletal muscle perfusion, an intrinsic muscle abnormality is considered to be responsible for fatigue. Another abnormality seen in CHF is persistent sympathetic nervous system activation, which is difli.
Journal of Clinical Medicine, 2022
Background: The association between right ventricular function and exercise capacity in patients with chronic heart failure remains uncertain. Several studies very recently mentioned the association between right ventricular reserve and exercise capacity, whereas the implication of tricuspid annular plane systolic excursion (TAPSE) remains uninvestigated. We aimed to assess the impact of TAPSE on exercise capacity in cardiac rehabilitation candidates. Methods: Data from patients with chronic heart failure who received cardiopulmonary exercise tests and transthoracic echocardiography prior to cardiac rehabilitation were retrospectively collected, and their association was investigated. Results: A total of 169 patients with chronic heart failure (70.3 ± 11.7 years old, 74.6% men) were included. Tertiled tricuspid annular plane systolic excursion significantly stratified anaerobic threshold (10.2 ± 2.2, 11.4 ± 2.2, and 12.2 ± 2.8 mm; p < 0.01) and peak oxygen consumption (15.9 ± 4.5...