Exercise Intolerance in Patients with Heart Failure: Role of Diastolic Dysfunction

1994 ◽  
pp. 295-302
Author(s):  
Dalane W. Kitzman ◽  
Martin J. Sullivan
2015 ◽  
Vol 9 ◽  
pp. CMC.S21372 ◽  
Author(s):  
Muhammad Asrar Ul Haq ◽  
Cheng Yee Goh ◽  
Itamar Levinger ◽  
Chiew Wong ◽  
David L. Hare

Reduced exercise tolerance is an independent predictor of hospital readmission and mortality in patients with heart failure (HF). Exercise training for HF patients is well established as an adjunct therapy, and there is sufficient evidence to support the favorable role of exercise training programs for HF patients over and above the optimal medical therapy. Some of the documented benefits include improved functional capacity, quality of life (QoL), fatigue, and dyspnea. Major trials to assess exercise training in HF have, however, focused on heart failure with reduced ejection fraction (HFREF). At least half of the patients presenting with HF have heart failure with preserved ejection fraction (HFPEF) and experience similar symptoms of exercise intolerance, dyspnea, and early fatigue, and similar mortality risk and rehospitalization rates. The role of exercise training in the management of HFPEF remains less clear. This article provides a brief overview of pathophysiology of reduced exercise tolerance in HFREF and heart failure with preserved ejection fraction (HFPEF), and summarizes the evidence and mechanisms by which exercise training can improve symptoms and HF. Clinical and practical aspects of exercise training prescription are also discussed.


Kardiologiia ◽  
2019 ◽  
Vol 59 (8S) ◽  
pp. 4-14
Author(s):  
A. G. Ovchinnikov ◽  
A. V. Potekhina ◽  
N. M. Ibragimova ◽  
E. A. Barabanova ◽  
E. N. Yushchyuk ◽  
...  

The main clinical manifestation of heart failure with preserved ejection fraction is poor exercise tolerance. In addi-tion to the dysfunction of the left heart chambers, which were presented in the first part of this review, many other disorders are involved in poor exercise tolerance in such patients: impairments of the right heart, vascular system and skeletal muscle. The second part of this review presents the mechanisms for the development of these disorders, as well as possible ways to correct them.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Galli ◽  
Y Bouali ◽  
C Laurin ◽  
A Gallard ◽  
A Hubert ◽  
...  

Abstract Background The non-invasive assessment of myocardial work (MW) by pressure-strain loops analysis (PSL) is a relative new tool for the evaluation of myocardial performance. Sacubitril/Valsartan is a treatment for heart failure with reduced ejection fraction (HFrEF) which has a spectacular effect on the reduction of cardiovascular events (MACEs). Purposes of this study were to evaluate 1) the short and medium term effect of Sacubitril/Valsartan treatment on MW parameters; 2) the prognostic value of MW in this specific group of patients. Methods 79 patients with HFrEF (mean age: 66±12 years; LV ejection fraction: 28±9%) were prospectively included in the study and treated with Sacubitril/Valsartan. Echocardiographic examination was performed at baseline, and after 6- and 12-month of therapy with Sacubitril/Valsartan. Results Sacubitril/Valsartan significantly increased global myocardial constructive work (CW) (1023±449 vs 1424±484 mmHg%, p<0.0001) and myocardial work efficiency (WE) [87 (78–90) vs 90 (86–95), p<0.0001]. During FU (2.6±0.9 years), MACEs occurred in 13 (16%) patients. After correction for LV size, LVEF and WE, CW was the only predictor of MACEs (Table 1). A CW<910 mmHg (AUC=0.81, p<0.0001, Figure 1A) identified patients at particularly increase risk of MACEs [HR 11.09 (1.45–98.94), p=0.002, log-rank test p<0.0001] (Figure 1 B). Conclusions In patients with HFrEF who receive a comprehensive background beta-blocker and mineral-corticoid receptor antagonist therapy, Sacubitril/Valsartan induces a significant improvement of myocardial CW and WE. In this population, the estimation of CW before the initiation of Sacubitril/Valsartan therapy allows the prediction of MACEs. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 10 (3) ◽  
pp. 504
Author(s):  
Marina Povar-Echeverría ◽  
Pablo Esteban Auquilla-Clavijo ◽  
Emmanuel Andrès ◽  
Francisco Javier Martin-Sánchez ◽  
María Victoria Laguna-Calle ◽  
...  

Introduction: Inflammation is a fundamental phenomenon in heart failure, but the prognostic or therapeutic role of markers such as interleukin-6 (IL-6) has not yet been clarified. The objective of this study is to describe the clinical profile of patients with elevated IL-6 and determine if they have worse clinical outcomes. Methods: A retrospective c.ohort observational study including 78 patients with heart failure followed up at the Heart Failure Outpatient Clinic of the Internal Medicine Department. IL-6 was determined in all patients, who were then assigned into two groups according to IL-6 level (normal or high). Clinical and prognostic data were collected to determine the differences in both groups. Results: The average age was 79 years, 60% female. A total of 53.8% of the patients had elevated IL-6 (group 2). Patients with elevated IL-6 presented more frequently with anemia mellitus (64.3% vs. 41.7%; p = 0.046), atrial fibrillation (83.3% vs. 61.9% p = 0.036), dyslipidemia (76.2% vs. 58.2%; p = 0.03), higher creatinine levels (1.35 mg/dL vs. 1.08 mg/dL; p = 0.024), lower glomerular filtration rate (43.6 mL/min/m2 vs. 59.9 mL/min/m2; p = 0.007), and anemia 25% vs. 52.4% p = 0.014. The factors independently associated with the increase in IL-6 were anemia 3.513 (1.163–10.607) and renal failure 0.963 (0.936–0.991), p < 0.05. Mortality was higher in the group with elevated IL-6 levels (16% vs. 2%; p = 0.044) with a log-rank p = 0.027 in the Kaplan–Meier curve. Conclusion: Patients with heart failure and elevated IL-6 most often have atrial fibrillation, diabetes mellitus, dyslipidemia, anemia, and renal failure. In addition, mortality was higher and a tendency of higher hospital admission was observed in stable HF patients with elevated IL-6.


2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests “peripheral,” i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.


2021 ◽  
Author(s):  
Susanne Bauer ◽  
Christina Strack ◽  
Ekrem Ücer ◽  
Stefan Wallner ◽  
Ute Hubauer ◽  
...  

Aim: We assessed the 10-year prognostic role of 11 biomarkers with different pathophysiological backgrounds. Materials & methods/results: Blood samples from 144 patients with heart failure were analyzed. After 10 years of follow-up (median follow-up was 104 months), data regarding all-cause mortality were acquired. Regarding Kaplan–Meier analysis, all markers, except TIMP-1 and GDF-15, were significant predictors for all-cause mortality. We created a multimarker model with nt-proBNP, hsTnT and IGF-BP7 and found that patients in whom all three markers were elevated had a significantly worse long-time-prognosis than patients without elevated markers. Conclusion: In a 10-year follow-up, a combination of three biomarkers (NT-proBNP, hs-TnT, IGF-BP7) identified patients with a high risk of mortality.


Open Heart ◽  
2017 ◽  
Vol 4 (2) ◽  
pp. e000632 ◽  
Author(s):  
Jodi McCoy ◽  
Matthew Bates ◽  
Christopher Eggett ◽  
Mario Siervo ◽  
Sophie Cassidy ◽  
...  

2017 ◽  
Vol 7 (3) ◽  
pp. 43-50 ◽  
Author(s):  
Nastaran Mansoreye ◽  
Hamid Poursharifi ◽  
Mohammad Reza Taban Sadegi ◽  
Mohammad Reza Seirafi ◽  
◽  
...  

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