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Tuberculosis & Respiratory Diseases

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Vol.69 No.6
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Long-Term Effects of ACE Inhibitors in Post-Tuberculosis Emphysema

Tuberculosis & Respiratory Diseases / Tuberculosis & Respiratory Diseases,
2010, v.69 no.6, pp.418-425
Myung A Kim (Seoul Metropolitan Boramae Medical Center, Seoul National University College of Medicine)
Chang-Hoon Lee (Seoul Metropolitan Boramae Medical Center, Seoul National University College of Medicine)
Deog Kyeom Kim (Seoul Metropolitan Boramae Medical Center, Seoul National University College of Medicine)
Hee Soon Chung (Seoul Metropolitan Boramae Medical Center, Seoul National University College of Medicine)
Myung, A. K. , Chang-Hoon, L. , Deog, K. K. , & Hee, S. C. (2010). Long-Term Effects of ACE Inhibitors in Post-Tuberculosis Emphysema. Tuberculosis & Respiratory Diseases, 69(6), 418-425.
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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.

keywords
Angiotensin-Converting Enzyme Inhibitors, Tuberculosis, Pulmonary Emphysema, Cardiac Output, Angiotensin-Converting Enzyme Inhibitors, Tuberculosis, Pulmonary Emphysema, Cardiac Output

Reference

1.

1. Kim MA, Kim SH, Zo JH, Hwangbo B, Lee JH, Chung HS. Right heart dysfunction in post-tuberculosis emphysema.Int J Tuberc Lung Dis 2004;8:1120-6.

2.

2. Nong Z, Stassen JM, Moons L, Collen D, Janssens S.Inhibition of tissue angiotensin-converting enzyme with quinapril reduces hypoxic pulmonary hypertension and pulmonary vascular remodeling. Circulation 1996;94:1941-7.

3.

3. Mancini GB, Etminan M, Zhang B, Levesque LE,FitzGerald JM, Brophy JM. Reduction of morbidity and mortality by statins, angiotensin-converting enzyme inhibitors,and angiotensin receptor blockers in patients with chronic obstructive pulmonary disease. J Am Coll Cardiol 2006;47:2554-60.

4.

4. Cazzola M, Matera MG, Rogliani P, Page C. Treating systemic effects of COPD. Trends Pharmacol Sci 2007;28:544-50.

5.

5. Mortensen EM, Copeland LA, Pugh MJ, Restrepo MI,de Molina RM, Nakashima B, et al. Impact of statins and ACE inhibitors on mortality after COPD exacerbations.Respir Res 2009;10:45.

6.

6. Schlueter DP, Immekus J, Stead WW. Relationship between maximal inspiratory pressure and total lung capacity (coefficient of retraction) in normal subjects and in patients with emphysema, asthma, and diffuse pulmonary infiltration. Am Rev Respir Dis 1967;96:656-65.

7.

7. Lung function testing: selection of reference values and interpretative strategies. American Thoracic Society. Am Rev Respir Dis 1991;144:1202-18.

8.

8. Poppius H. Airway obstruction in pulmonary tuberculosis.Scand J Respir Dis Suppl 1968;65:165-9.

9.

9. Birath G, Caro J, Malmberg R, Simonsson BG. Airways obstruction in pulmonary tuberculosis. Scand J Respir Dis 1966;47:27-36.

10.

10. Snider GL, Doctor L, Demas TA, Shaw AR. Obstructive airway disease in patients with treated pulmonary tuberculosis. Am Rev Respir Dis 1971;103:625-40.

11.

11. Global Initiative for Chronic Obstructive Lung Disease.Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease.Washington: Medical Communications Resources; 2009.

12.

12. Rubin LJ. Cardiovascular effects of vasodilator therapy for pulmonary arterial hypertension. Clin Chest Med 1983;4:309-19.

13.

13. Matthay RA, Arroliga AC, Wiedemann HP, Schulman DS, Mahler DA. Right ventricular function at rest and during exercise in chronic obstructive pulmonary disease. Chest 1992;101:255S-62S.

14.

14. Vizza CD, Lynch JP, Ochoa LL, Richardson G, Trulock EP. Right and left ventricular dysfunction in patients with severe pulmonary disease. Chest 1998;113:576-83.

15.

15. Schulman DS, Matthay RA. The right ventricle in pulmonary disease. Cardiol Clin 1992;10:111-35.

16.

16. Matthay RA, Niederman MS, Wiedemann HP. Cardiovascular-pulmonary interaction in chronic obstructive pulmonary disease with special reference to the pathogenesis and management of cor pulmonale. Med Clin North Am 1990;74:571-618.

17.

17. Willenheimer R, Rydberg E, Oberg L, Juul-Möller S,Erhardt L. ACE inhibition with ramipril improves left ventricular function at rest and post exercise in patients with stable ischaemic heart disease and preserved left ventricular systolic function. Eur Heart J 1999;20:1647-56.

18.

18. van Suylen RJ, Smits JF, Daemen MJ. Pulmonary artery remodeling differs in hypoxia- and monocrotaline-induced pulmonary hypertension. Am J Respir Crit Care Med 1998;157:1423-8.

19.

19. Dandona P, Dhindsa S, Ghanim H, Chaudhuri A.Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. J Hum Hypertens 2007;21:20-7.

20.

20. Busquets X, MacFarlane NG, Heine-Suñer D, Morlá M,Torres-Juan L, Iglesias A, et al. Angiotensin-converting-enzyme gene polymorphisms, smoking and chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis 2007;2:329-34.

21.

21. Barnes PJ. Future treatments for chronic obstructive pulmonary disease and its comorbidities. Proc Am Thorac Soc 2008;5:857-64.

22.

22. Klinger JR, Hill NS. Right ventricular dysfunction in chronic obstructive pulmonary disease. Evaluation and management. Chest 1991;99:715-23.

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