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Comando Brigata Alpina "Julia", Udine, Italy Ospedale di San Vito al Tagliamento, San Vito al Tagliamento, Italy
Correspondence to: Luca Mascitelli, MD, Comando Brigata Alpina "Julia," Sanitary Service, Via S Agostino, 8, Udine 33100, Italy
To the Editor:
Joppa et al (August 2006)1 have suggested that systemic inflammation might be related to pulmonary hypertension in patients with COPD. However, they did not mention whether patients in the studied population were being treated with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers.
ACE is present in very high concentrations in the lungs, and its activity is further increased by chronic hypoxia; it seems likely that angiotensin II may contribute to the development of chronic pulmonary hypertension via its vasoconstrictor effects or via action on vascular smooth muscle cell migration and growth.23 In fact, ACE inhibition has been shown to reduce hypoxic pulmonary hypertension and pulmonary vascular remodeling in rats.2 Furthermore, in patients with COPD lower activity of ACE may improve the efficiency of the peripheral use of oxygen and respiratory muscle function,45 and it has also been shown to be associated with lower exercise-induced pulmonary artery pressure.3 On the other hand, angiotensin II plays a significant role in the initiation and perpetuation of inflammatory processes; consequently, inhibition of the renin-angiotensin system may lead to a decrease in the concentration of markers of systemic inflammation.5
Therefore, we suggest that therapy with ACE inhibitors or angiotensin II type 1 receptor blockers should be recommended in most patients with COPD,5 especially those with pulmonary hypertension.
Footnotes
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
References
Safarik University, Kosice, Slovakia
Correspondence to: Ruzena Tkacova, MD, PhD, Louis Pasteur Teaching Hospital, Medical Faculty of PJ Safarik University, Department of Respiratory Medicine, Rastislavova 43, Kosice 041 90, Slovakia; e-mail: rtkacova{at}central.medic.upjs.sk
To the Editor:
We would like to thank Mascitelli and Pezzetta for raising the interesting aspect of renin-angiotensin system inhibition in patients with COPD, and its potential effects on the relationships between systemic inflammation and pulmonary artery pressures observed in our recent article in CHEST (August 2006).1 Indeed, since the sympathetic nervous system and the renin-angiotensin system are activated in patients with COPD,2 the potential effects of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 (AT1) receptor blockers on pulmonary artery pressure deserve deeper consideration. In our study, 6 of 19 patients with pulmonary hypertension and 8 of 24 patients without pulmonary hypertension were receiving therapy with ACE inhibitors or AT1 receptor blockers to treat their systemic hypertension. Therefore, the two studied groups of COPD patients were well matched for the use of this therapy. It should be emphasized that our study was not aimed at elucidating the effects ACE inhibition on pulmonary artery pressure in COPD patients.
However, two recent studies34 addressed this issue. Andreas et al3 recently studied the effects of angiotensin II blockers on COPD patients in a randomized controlled trial and did not notice a significant effect of this therapy on right ventricular dimensions. In another 12-month pilot study,4 losartan had no statistically significant beneficial effect on tricuspid pressure gradient in patients with pulmonary hypertension secondary to COPD. In addition, the renin-angiotensin system is unlikely to be a major determinant of pulmonary vascular pathology in therapeutic trials.5
Taken together, the current data provide little if any support for the suggestion that therapy with ACE inhibitors or AT1 receptor blockers should be recommended in most patients with COPD, as alluded to by Mascitelli and Pezzetta. Nevertheless, we value the suggestion to assess the effects of ACE inhibitors or AT1 receptor blockers in further therapeutic studies in patients with COPD.
References
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