Heart Failure and the Lung

Abstract

Heart failure (HF) is a highly prevalent disease that leads to significant morbidity and mortality. There is increasing evidence that the symptoms of HF are exacerbated by its deleterious effects on lung function. HF appears to cause airway obstruction acutely and leads to impaired gas diffusing capacity and pulmonary hypertension in the longer term. It is postulated that this is the result of recurrent episodes of elevated pulmonary capillary pressure leading to pulmonary oedema and pulmonary capillary stress fracture, which produces lung fibrosis. It is likely that impaired lung function impairs the functional status of HF patients and makes them more prone to central sleep apnoea. (Circ J 2010; 74: 2507 - 2516

Using the Lower Limit of Normal Instead of the Conventional Cutoff Values to Define Predictors of Pulmonary Function Impairment in Subjects With Chronic Heart Failure

“…33 Restriction has been linked to cardiomegaly, pleural effusion, respiratory muscle weakness, coronary artery bypass grafting, fibrosis from chronic congestion, and reduced lung compliance due to chronic vascular engorgement, interstitial/alveolar fluid accumulation, and chronic remodeling of the pulmonary vasculature due to elevated left atrial pressure. 1,[4][5][6]13,34,35 In line with expectations, we found lung volumes to be lower in subjects with pulmonary congestion, pleural effusion, cardiomegaly, and a history of coronary artery bypass grafting.…”

“…[4][5][6][7]13 Diffusion impairment has been thought to be related to the thickening of the alveolar-capillary membrane due to hydrostatic mechanical injury, interstitial edema, remodeling, and fibrosis. 1,2,[4][5][6]27 Because heart transplantation does not affect or may even worsen pulmonary diffusing capacity despite an improvement in hemodynamic status and lung volumes, 28 it has been suggested that reduced diffusing capacity in chronic heart failure may be related to permanent damage to the alveolar-capillary membrane. 2 Other possible causes of diffusion impairment in heart failure include reduced lung and pulmonary capillary blood volumes, ventilation-perfusion mismatch, recurrent pulmonary emboli, smoking, and cardiopulmonary bypass.…”

“…Isolated or combined pulmonary function abnormalities, such as restriction, diffusion impairment, and to a lesser extent airway obstruction are common in patients with chronic heart failure [1][2][3][4][5][6][7] and can contribute to the perception of dyspnea 8 and exercise intolerance. [8][9][10][11][12] Several factors have been implied to play a role in the etiology of pulmonary function impairment in patients with heart failure, including the effects of heart failure itself on pulmo-nary function in addition to (previously undiagnosed) underlying pulmonary disease and confounding influences, such as smoking, coronary artery bypass grafting, and obesity.…”

Extrapulmonary comorbidities in chronic obstructive pulmonary disease: state of the art

“…It is well described that lung function is reduced in chronic and acute-on-chronic heart failure, and may reflect interstitial changes in those with long-standing disease (reviewed in [40]). Direct pathophysiological links between heart failure and COPD are not well established and it is more likely to be indirectly mediated through other comorbidities such as IHD and hypertension in most patients.…”

Effects of Autologous Bone Marrow Mononuclear Cells Implantation in Canine Model of Pulmonary Hypertension

“…10, 43 On the other hand, studies have shown that bone marrow-derived mesenchymal stem cells (BMSCs) produce growth factors such VEGF that promote neovascularization, which participates in BMSCs-based therapies for PH. 20 In fact, our qRT-PCR results demonstrated that the relative expression concentration of VEGF (2.06±0.43) in the lungs was significantly improved in the ABM-MNCs group (4.53±0.75), and the histological results showed that the density of pulmonary arterioles was significantly increased in the ABM-MNCs group compared with the PH group. However, red fluorescent-positive cells stained negative for SP-C, suggesting intratracheally injected ABM-MNCs are able to differentiate into vascular endothelial cells, but not lung cells, in vivo.…”