Improvement of Alveolar–Capillary Membrane Diffusing Capacity With Enalapril in Chronic Heart Failure and Counteracting Effect of Aspirin

Circulation ◽  
1997 ◽  
Vol 95 (7) ◽  
pp. 1930-1936 ◽  
Author(s):  
Marco Guazzi ◽  
Giancarlo Marenzi ◽  
Marina Alimento ◽  
Mauro Contini ◽  
Piergiuseppe Agostoni
Circulation ◽  
1995 ◽  
Vol 91 (11) ◽  
pp. 2769-2774 ◽  
Author(s):  
Sundeep Puri ◽  
B. Leigh Baker ◽  
David P. Dutka ◽  
Celia M. Oakley ◽  
J. Michael B. Hughes ◽  
...  

Author(s):  
Caitlin C. Fermoyle ◽  
Glenn M. Stewart ◽  
Barry A. Borlaug ◽  
Bruce D. Johnson

Background Hemodynamic perturbations in heart failure with preserved ejection fraction (HFpEF) may alter the distribution of blood in the lungs, impair gas transfer from the alveoli into the pulmonary capillaries, and reduce lung diffusing capacity. We hypothesized that impairments in lung diffusing capacity for carbon monoxide (DL CO ) in HFpEF would be associated with high mean pulmonary capillary wedge pressures during exercise. Methods and Results Rebreathe DL CO and invasive hemodynamics were measured simultaneously during exercise in patients with exertional dyspnea. Pulmonary pressure waveforms and breath‐by‐breath pulmonary gas exchange were recorded at rest, 20 W, and symptom‐limited maximal exercise. Patients with HFpEF (n=20; 15 women, aged 65±11 years, body mass index 36±8 kg/m 2 ) achieved a lower symptom‐limited maximal workload (52±27 W versus 106±42 W) compared with controls with noncardiac dyspnea (n=10; 7 women, aged 55±10 years, body mass index 30±5 kg/m 2 ). DL CO was lower in patients with HFpEF compared with controls at rest (DL CO 10.4±2.9 mL/min per mm Hg versus 16.4±6.9 mL/min per mm Hg, P <0.01) and symptom‐limited maximal exercise (DL CO 14.6±4.7 mL/min per mm Hg versus 23.8±10.8 mL/min per mm Hg, P <0.01) because of a lower alveolar‐capillary membrane conductance in HFpEF (rest 16.8±6.6 mL/min per mm Hg versus 28.4±11.8 mL/min per mm Hg, P <0.01; symptom‐limited maximal exercise 25.0±6.7 mL/min per mm Hg versus 45.5±22.2 mL/min per mm Hg, P <0.01). DL CO was lower in HFpEF for a given mean pulmonary artery pressure, mean pulmonary capillary wedge pressure, pulmonary arterial compliance, and transpulmonary gradient. Conclusions Lung diffusing capacity is lower at rest and during exercise in HFpEF due to impaired gas conductance across the alveolar‐capillary membrane. DL CO is impaired for a given pulmonary capillary wedge pressure and pulmonary arterial compliance. These data provide new insight into the complex relationships between hemodynamic perturbations and gas exchange abnormalities in HFpEF.


2000 ◽  
Vol 98 (6) ◽  
pp. 633-641 ◽  
Author(s):  
Marco GUAZZI

Chronic heart failure (CHF) disturbs the alveolar–capillary interface and increases the resistance to gas transfer. Alveolar–capillary membrane conductance (DM) and capillary blood volume (Vc) are subcomponents of the lung diffusion capacity. Elevation of the capillary pressure causes alveolar–capillary membrane stress failure (i.e. increase in capillary permeability to water and ions, and disruption of local regulatory mechanisms for gas exchange), leading to a decrease in DM, an increase in Vc and subsequent impairment of diffusion capacity. Renewed recent interest in abnormalities in lung diffusion in patients with CHF has brought about new pathophysiological insights. A significant contribution of the altered gas transfer to the pathogenesis of exercise limitation and ventilatory abnormalities has been reported, and DM has been identified as the best lung function predictor of oxygen uptake at peak exercise. This review examines the pathophysiological and clinical significance of assessing lung diffusion capacity in patients with CHF.


Heart ◽  
1994 ◽  
Vol 72 (2) ◽  
pp. 140-144 ◽  
Author(s):  
S Puri ◽  
B L Baker ◽  
C M Oakley ◽  
J M Hughes ◽  
J G Cleland

1999 ◽  
Vol 96 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Marco GUAZZI ◽  
Piergiuseppe AGOSTONI

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLco). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLco. Angiotensin-converting enzyme inhibition improves DLco in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLco is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 ;h and 1 and 2 months after starting enalapril treatment (10 ;mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 ;mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 ;h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 ;h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLco despite a decrease in VC. In group 2 patients, nitrates failed to improve DLco and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.


1960 ◽  
Vol 15 (3) ◽  
pp. 372-376 ◽  
Author(s):  
J. E. Cotes ◽  
D. P. Snidal ◽  
R. H. Shepard

In one of two subjects studied in detail, using 0.1% carbon monoxide in the test gas and a 10-second breath-holding period, the alveolar capillary blood volume (Vc) was found to increase by nearly 100% when the intra-alveolar pressure was made negative during breath holding. This was accompanied by a reduction in venous pressure in the forearm. In both subjects Vc was increased on exercise. The diffusing capacity of the alveolar capillary membrane (Dm) remained relatively constant in spite of large changes in Vc. The findings suggest that stationary blood is present in some alveolar capillaries at rest. The implications of this finding and a likely mechanism for the increase in Vc with negative pressure are discussed. xsSubmitted on September 14, 1959


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