Significance of Changes in the Pulmonary Diffusing Capacity in Mitral Stenosis

Aber, Clive P.; Campbell, John

doi:10.1136/thx.20.2.135

Cited by 26 publications

(17 citation statements)

References 33 publications

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“…12 The reduction in DLCO and DM in this patient group correlates with NYHA functional class 12 and the severity of histological lung damage. 13 Moreover, pulmonary gas transfer may remain abnormal for up to 8 years after mitral valve replacement, 14 further supporting the hypothesis that a reduction of DM may reflect structural damage of the alveolar-capillary interface.…”

mentioning

confidence: 63%

Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Puri¹,

Dutka²,

Baker³

et al. 1999

Circulation

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Background-Impaired alveolar-capillary membrane conductance is the major cause for the reduction in pulmonary diffusing capacity for carbon monoxide (DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmonary microvascular damage, or is variable is unknown. The aim of this study was to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects of volume loading on airflow rates. Methods and Results-Ten patients with left ventricular dysfunction (LVD) and 8 healthy volunteers were studied. DM and Vc were determined by the Roughton and Forster method. The forced expiratory volume in 1 second (FEV 1 ), vital capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL ⅐ kg

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confidence: 63%

Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Puri¹,

Dutka²,

Baker³

et al. 1999

Circulation

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“…These specimens also showed that lymphatic vessels undergo compensatory changes including dilation and occasionally muscularization due to chronically increased edema clearance. [14][15][16][17][18][19] Other mechanisms have also been proposed that are adaptive to increased hydrostatic pressure and prevent pulmonary edema. 20 It is probable that several of these mechanisms occur in different degrees…”

Section: Resultsmentioning

confidence: 99%

Mediastinal Lymphadenopathy in Patients Undergoing Cardiac Transplant Evaluation

Pastis

Bakel

Brand

et al. 2011

Chest

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Mediastinal lymphadenopathy (MLA) is not commonly recognized as associated with congestive heart failure (CHF). However, recent case series have reported a 35% to 81% incidence of MLA in different patient populations with CHF. [1][2][3][4] However, the true incidence remains unknown as these reports analyzed different heart failure populations.The lymphatic circulation is primarily responsible for regulating pulmonary fl uid homeostasis. The lymphatic system is highly recruitable and, with time to adapt, can increase clearance of pulmonary edema fl uid by . 10-fold. This system enables low-pressure drainage of excessive fl uid from the interstitium through lymph nodes (LNs) and into collecting ducts. Lymphatic Abbreviations: CHF 5 congestive heart failure; CO 5 cardiac output; EBUS 5 endobronchial ultrasound; EF 5 ejection fraction; EUS 5 endoscopic ultrasound; HT 5 heart transplantation; LN 5 lymph node; MLA 5 mediastinal lymphadenopathy; MPAP 5 mean pulmonary artery pressure; MR 5 mitral regurgitation; MUGA 5 multigated acquisition scan; PCWP 5 pulmonary capillary wedge pressure; RAP 5 right atrial pressure; RVG 5 radionuclide ventriculography; TR 5 tricuspid regurgitation

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“…13 In non-valvular HF, a small amount of animal and human data regarding pulmonary changes exist. A murine model demonstrated increased collagen formation and myofibroblast activity following myocardial infarct induced HF.…”

Section: Pathological Changes In Hfmentioning

confidence: 99%

Heart Failure and the Lung

Kee

Naughton

2010

Circ J

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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

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Significance of Changes in the Pulmonary Diffusing Capacity in Mitral Stenosis

Cited by 26 publications

References 33 publications

Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Mediastinal Lymphadenopathy in Patients Undergoing Cardiac Transplant Evaluation

Heart Failure and the Lung

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