Tuberc Respir Dis.  2010 Dec;69(6):418-425.

Long-Term Effects of ACE Inhibitors in Post-Tuberculosis Emphysema

Affiliations
  • 1Department of Internal Medicine, Seoul Metropolitan Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea. heechung@snu.ac.kr

Abstract

BACKGROUND
Little is known about the long-term effects of angiotensin-converting enzyme (ACE) treatment on post-tuberculosis emphysema. This study evaluated the effects of ACE inhibition on cardiac function and gas exchange in patients with post-tuberculosis emphysema.
METHODS
At baseline and at 6 months after initiation of ACE inhibition therapy, patients underwent pulmonary function testing, arterial blood gas analysis, and echocardiography, both at rest and post exercise. Cardiac output (CO) and right ventricular ejection fraction (RVEF) were measured at those time points as well.
RESULTS
After ACE inhibition; resting and post-exercise RVEF (Mean+/-SEM, 61.5+/-1.0, 67.6+/-1.2%, respectively) were higher than at baseline (56.9+/-1.2, 53.5+/-1.7%). Resting and post-exercise CO (6.37+/-0.24, 8.27+/-0.34 L/min) were higher than at baseline (5.42+/-0.22, 6.72+/-0.24 L/min). Resting and post-exercise PaO2 (83.8+/-1.6, 74.0+/-1.2 mmHg, respectively) were also higher than at baseline (74.2+/-1.9, 66.6+/-1.6 mmHg). Post-exercise PaCO2 (46.3+/-1.1 mmHg) was higher than at baseline (44.9+/-1.1; Resting 42.8+/-0.8 vs. 42.4+/-0.9 mmHg). Resting and post-exercise A-a O2 gradient (12.4+/-1.4, 17.8+/-1.5 mmHg) were lower than at baseline (22.5+/-1.5, 26.9+/-1.6 mmHg).
CONCLUSION
In post-tuberculosis emphysema, RVEF and CO were augmented with a resultant increase in peripheral oxygen delivery after ACE inhibition. These findings suggest that an ACE inhibitor may have the potential to alleviate co-morbid cardiac conditions and benefit the patients with post-tuberculosis emphysema.

Keyword

Angiotensin-Converting Enzyme Inhibitors; Tuberculosis; Pulmonary Emphysema; Cardiac Output

MeSH Terms

Angiotensin-Converting Enzyme Inhibitors
Blood Gas Analysis
Cardiac Output
Echocardiography
Emphysema
Humans
Oxygen
Pulmonary Emphysema
Respiratory Function Tests
Stroke Volume
Tuberculosis
Angiotensin-Converting Enzyme Inhibitors
Oxygen

Figure

  • Figure 1 Changes in arterial blood gases after long-term ACE inhibition in post-tuberculosis emphysema. After ACE inhibition, resting and post-exercise PaO2 increased by ca. 10 mm Hg (each p<0.01), whereas resting PaCO2 did not change (p=0.524) and post-exercise PaCO2 increased by about 1 mm Hg (p<0.01).

  • Figure 2 Changes in A-a O2 gradient and right ventricular ejection fraction (RVEF) after long-term ACE inhibition in post-tuberculosis emphysema. After ACE inhibition, resting and post-exercise A-a O2 gradient reduced by approximately 10 mm Hg (each p<0.01). RVEF at rest was augmented by 5% after ACE inhibition and increased further with exercise-loading (each p<0.01), while RVEF at baseline was reduced by exercise-loading, without significance (p=0.055).

  • Figure 3 Changes in cardiac output (CO) and left ventricular ejection fraction (LVEF) after long-term ACE inhibition in post-tuberculosis emphysema. After ACE inhibition, resting and post-exercise CO increased by 1 to 1.5 L/min (approximately 20%; each p<0.01), and LVEF increased by 3 to 4% both at rest and after exercise (each p<0.05).


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