Pulmonary function and respiratory muscle strength in chronic heart failure: comparison between ischaemic and idiopathic dilated cardiomyopathy

Daganou, Maria; Dimopoulou, Ioanna; Alivizatos, Peter A.; Tzelepis, George E.

doi:10.1136/hrt.81.6.618

Cited by 44 publications

(40 citation statements)

References 15 publications

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“…The mechanism for the loss of TLC in CHF remains controversial with factors such as changes in lung fluid balance, cardiomegaly, increased central blood volume, respiratory muscle weakness and airway remodeling being cited as potential causes. [20][21][22][23] However unlike Nannas et al 3 , we did not find that IC was an independent predictor of VO 2peak in CHF. After accounting for the variance due to LLCT, we found that adding IC did not significantly improve the model for determining VO 2peak .…”

Section: Discussioncontrasting

confidence: 92%

The Relationship Between Resting Lung-to-Lung Circulation Time and Peak Exercise Capacity in Chronic Heart Failure Patients

Morris

Snyder

Beck

et al. 2007

Journal of Cardiac Failure

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Background-Peak exercise capacity (VO 2peak ) is a measure of the severity of chronic heart failure (CHF), however few indices of resting cardiopulmonary function have been shown to predict VO 2peak . A prolonged circulation time has been suggested as an index of increased severity of CHF. The aim of this study was to investigate the relationship between resting lung-to-lung circulation time (LLCT) and VO 2peak in CHF.

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Section: Discussioncontrasting

confidence: 92%

The Relationship Between Resting Lung-to-Lung Circulation Time and Peak Exercise Capacity in Chronic Heart Failure Patients

Morris

Snyder

Beck

et al. 2007

Journal of Cardiac Failure

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“…Some of these data also suggest that the degree of impairment in respiratory muscle function parallels the severity of the cardiac dysfunction, its aetiology [115,[118][119][120][121], clinical prognosis [122] and, interestingly, increased peripheral chemosensitivity [123], a finding possibly related to an increase in sympathetic activation [124]. Importantly, some investigators have also reported on the relationship between the severity of respiratory muscle dysfunction and baseline dyspnoea [117], exertional dyspnoea [125], peak V′O 2 [119] and the abnormal V′E/V′CO 2 slope [121] in patients with heart failure.…”

Section: Alveolar-capillary Membrane Dysfunctionmentioning

confidence: 97%

Exertional dyspnoea in chronic heart failure: the role of the lung and respiratory mechanical factors

2016

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Exertional dyspnoea is among the dominant symptoms in patients with chronic heart failure and progresses relentlessly as the disease advances, leading to reduced ability to function and engage in activities of daily living. Effective management of this disabling symptom awaits a better understanding of its underlying physiology.Cardiovascular factors are believed to play a major role in dyspnoea in heart failure patients. However, despite pharmacological interventions, such as vasodilators or inotropes that improve central haemodynamics, patients with heart failure still complain of exertional dyspnoea. Clearly, dyspnoea is not determined by cardiac factors alone, but likely depends on complex, integrated cardio-pulmonary interactions.A growing body of evidence suggests that excessively increased ventilatory demand and abnormal "restrictive" constraints on tidal volume expansion with development of critical mechanical limitation of ventilation, contribute to exertional dyspnoea in heart failure. This article will offer new insights into the pathophysiological mechanisms of exertional dyspnoea in patients with chronic heart failure by exploring the potential role of the various constituents of the physiological response to exercise and particularly the role of abnormal ventilatory and respiratory mechanics responses to exercise in the perception of dyspnoea in patients with heart failure. @ERSpublications In heart failure, respiratory and peripheral factors play a significant role in exertional dyspnoea development

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“…Results from volitional as well as non-volitional tests using phrenic nerve stimulation have confirmed the decrease in inspiratory (mouth or transdiaphragmatic) pressure in CHF [31–33]. The inability to generate normal inspiratory pressure is independent of the etiology of disease [34,31,10,35]. Notably, the prevalence of this inspiratory dysfunction in CHF, defined arbitrarily as MIP < 70% predicted [35,36], does appear to depend on age.…”

Section: Evidence Of Inspiratory Dysfunction – Heart Failure and Amentioning

confidence: 97%

Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology

Kelley

Ferreira

2016

Heart Fail Rev

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Inspiratory function is essential for alveolar ventilation and expulsive behaviors that promote airway clearance (e.g., coughing and sneezing). Current evidence demonstrates that inspiratory dysfunction occurs during healthy aging and is accentuated by chronic heart failure (CHF). This inspiratory dysfunction contributes to key aspects of CHF and aging cardiovascular and pulmonary pathophysiology including: i) impaired airway clearance and predisposition to pneumonia; ii) inability to sustain ventilation during physical activity; iii) shallow breathing pattern that limits alveolar ventilation and gas exchange; and iv) sympathetic activation that causes cardiac arrhythmias and tissue vasoconstriction. The diaphragm is the primary inspiratory muscle, hence, its neuromuscular integrity is a main determinant of the adequacy of inspiratory function. Mechanistic work within animal and cellular models has revealed specific factors that may be responsible for diaphragm neuromuscular abnormalities in CHF and aging. These include phrenic nerve and neuromuscular junction alterations as well as intrinsic myocyte abnormalities, such as changes in the quantity and quality of contractile proteins, accelerated fiber atrophy, and shifts in fiber type distribution. CHF, aging, or CHF in the presence of aging disturbs the dynamics of circulating factors (e.g., cytokines and angiotensin II) and cell signaling involving sphingolipids, reactive oxygen species, and proteolytic pathways, thus leading to the previously listed abnormalities. Exercise-based rehabilitation combined with pharmacological therapies targeting the pathways reviewed herein hold promise to treat diaphragm abnormalities and inspiratory muscle dysfunction in CHF and aging.

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Pulmonary function and respiratory muscle strength in chronic heart failure: comparison between ischaemic and idiopathic dilated cardiomyopathy

Cited by 44 publications

References 15 publications

The Relationship Between Resting Lung-to-Lung Circulation Time and Peak Exercise Capacity in Chronic Heart Failure Patients

The Relationship Between Resting Lung-to-Lung Circulation Time and Peak Exercise Capacity in Chronic Heart Failure Patients

Exertional dyspnoea in chronic heart failure: the role of the lung and respiratory mechanical factors

Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology

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