Restrictive Ventilatory Pattern in Precapillary Pulmonary Hypertension

Horn, Matthew; Ries, Andrew L.; Neveu, Connie; Moser, Kenneth Μ.

doi:10.1164/arrd.1983.128.1.163

Cited by 54 publications

(16 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…While thoracotomy was associated with lung restriction, sternotomy was not, which is in keeping with previous studies 14. However, patients who had not had previous cardiothoracic surgery also had lower lung volumes than predicted values, suggesting that the presence of APAH may have a separate effect on lung restriction in keeping with lung restriction that has been described in IPAH patients 8, 9, 13, 44, 45…”

Section: Discussionsupporting

confidence: 87%

Lung Function, Inflammation, and Endothelin‐1 in Congenital Heart Disease–Associated Pulmonary Arterial Hypertension

Low

George

Howard

et al. 2018

JAHA

View full text Add to dashboard Cite

BackgroundBreathlessness is the most common symptom in people with pulmonary arterial hypertension and congenital heart disease (CHD‐APAH), previously thought to be caused by worsening PAH, but perhaps also by inflammation and abnormalities of lung function. We studied lung function and airway inflammation in patients with CHD‐APAH and compared the results with controls.Methods and ResultsSixty people were recruited into the study: 20 CHD‐APAH, 20 CHD controls, and 20 healthy controls. Spirometry, gas transfer, whole body plethysmography and lung clearance index, 6‐minute walk distance, and medical research council dyspnea scoring were performed. Inflammatory markers and endothelin‐1 levels were determined in blood and induced sputum. The CHD‐APAH group had abnormal lung function with lung restriction, airway obstruction, and ventilation heterogeneity. Inverse correlations were shown for CHD‐APAH between medical research council dyspnea score and percent predicted peak expiratory flow (r=−0.5383, P=0.0174), percent predicted forced expiratory flow rate at 50% of forced vital capacity (r=−0.5316, P=0.0192), as well as for percent predicted forced expiratory volume in 1 s (r=−0.6662, P=0.0018) and percent predicted forced vital capacity (r=−0.5536, P=0.0186). The CHD‐APAH patients were more breathless with lower 6‐minute walk distance (360 m versus 558 m versus 622 m, P=0.00001). Endothelin‐1, interleukin (IL)‐β, IL‐6, IL‐8, tumor necrosis factor α, and vascular endothelial growth factor were significantly higher in CHD‐APAH than controls. Serum endothelin‐1 for CHD‐APAH correlated with airflow obstruction with significant negative correlations with percent predicted forced expiratory flow rate at 75% of forced vital capacity (r=−0.5858, P=0.0135).ConclusionsRaised biomarkers for inflammation were found in CHD‐APAH. Significant abnormalities in airway physiology may contribute to the dyspnea but are not driven by inflammation as assessed by circulating and sputum cytokines. A relationship between increased serum endothelin‐1 and airway dysfunction may relate to its bronchoconstrictive properties.

show abstract

Section: Discussionsupporting

confidence: 87%

Lung Function, Inflammation, and Endothelin‐1 in Congenital Heart Disease–Associated Pulmonary Arterial Hypertension

Low

George

Howard

et al. 2018

JAHA

View full text Add to dashboard Cite

show abstract

“…A low DL,CO is also seen in patients with chronic pulmonary embolism, primary pulmonary hypertension [148], and other pulmonary vascular diseases. These patients may or may not also have restriction of lung volumes [149].…”

Section: Dlco Interpretationmentioning

confidence: 99%

Interpretative strategies for lung function tests

Pellegrino¹

2005

Eur Respir J

4,996

4,636

View full text Add to dashboard Cite

“…Additional specific causes of gas volume displacement include: 1) pulmonary oedema [58]; 2) inflammatory fluids and tissue in the alveoli or interstitium, as occurs in pneumonia [58] or an inflammatory interstitial process; 3) interstitial fibrosis; 4) engorgement of the pulmonary vascular bed and cardiomegaly as seen in congestive heart failure (CHF); 5) hypertrophy, hyperplasia, and fibrosis of the pulmonary vascular bed as has been reported in chronic pulmonary hypertension [59]; 6) tumours either within the lungs or impinging on the lungs from the pleura or mediastinum; 7) large pleural fluid accumulation; and 8) pneumothorax.…”

Section: Gas Volume Displacementmentioning

confidence: 99%

“…In addition, reductions in lung volumes have been attributed to reduced distensibility of the pulmonary vascular bed in patients with chronic pulmonary hypertension and resultant reduction in lung distensibility [59]. Finally, neuromuscular disease can be associated with reductions in lung distensibility [80]; the specific mechanisms may include microatelectasis or the effects of reduced alveolar size on surface tension [5].…”

Section: Decreases In Lung Compliance Increases In Lung Recoilmentioning

confidence: 99%

Pathophysiology of changes in absolute lung volumes

Bancalari

Clausen

1998

Eur Respir J

View full text Add to dashboard Cite

Changes in absolute lung volumes are common in lung disease and result in significant impacts on gas exchange, respiratory muscle function, the sensation of dyspnoea, and limitations to maximal exercise. Though our knowledge regarding the magnitude and determinants of changes in lung volumes in health and disease has increased in the past 20 years, a number of important questions remain unanswered. Consideration of the limitations of specific methods for measuring lung volumes is essential when analysing published studies regarding absolute lung volumes in infants, children and adults. Though functional residual capacity is most commonly measured in children and adults with the subject awake and at rest, increasingly attention is being directed to making these measurements under clinically more relevant conditions (e.g. during exercise, sleep, anesthesia, or mechanical ventilation). The relationships between dynamic changes in functional residual capacity, flow limitation during tidal breaths, sensation of dyspnoea and exercise limitation are important to understand, and are the focus of current and future research. Improved understanding of these relationships may lead to improvements in therapy of patients with acute and chronic lung disease and are likely to be particularly important for evaluating the efficacy of and optimal patient selection for new modes of therapy, such as lung volume reduction surgery.

show abstract

Restrictive Ventilatory Pattern in Precapillary Pulmonary Hypertension

Cited by 54 publications

References 0 publications

Lung Function, Inflammation, and Endothelin‐1 in Congenital Heart Disease–Associated Pulmonary Arterial Hypertension

Lung Function, Inflammation, and Endothelin‐1 in Congenital Heart Disease–Associated Pulmonary Arterial Hypertension

Interpretative strategies for lung function tests

Pathophysiology of changes in absolute lung volumes

Contact Info

Product

Resources

About