Stress-Induced Pulmonary Systolic Hypertension in Patients With Scleroderma: Response

Abstract

To the Editor:We appreciate the remarks of Callejas et al concerning our recent article in CHEST (July 2006).1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar The prevalence of a pulmonary artery systolic pressure of > 40 mm Hg in our patients was similar to that in the population described. In order to qualify as a positive response, we agree that patients should produce a minimum value of 40 mm Hg + right atrial pressure during exercise; a less robust response most often indicates pulmonary venous hypertension. For now, we believe it prudent to study all patients whose resting pulmonary artery pressure is normal and whose exercise pressure exceeds 40 mm Hg + right atrial pressure. Currently, we repeat the exercise echocardiogram every 3 to 6 months in those patients.As noted,1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar several of our patients ultimately progressed to resting pulmonary hypertension. Both of the markers for such disease progression, and the mechanism for stress-induced pulmonary hypertension remain the subject of intense interest and ongoing investigation. To the Editor:We appreciate the remarks of Callejas et al concerning our recent article in CHEST (July 2006).1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar The prevalence of a pulmonary artery systolic pressure of > 40 mm Hg in our patients was similar to that in the population described. In order to qualify as a positive response, we agree that patients should produce a minimum value of 40 mm Hg + right atrial pressure during exercise; a less robust response most often indicates pulmonary venous hypertension. For now, we believe it prudent to study all patients whose resting pulmonary artery pressure is normal and whose exercise pressure exceeds 40 mm Hg + right atrial pressure. Currently, we repeat the exercise echocardiogram every 3 to 6 months in those patients.As noted,1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar several of our patients ultimately progressed to resting pulmonary hypertension. Both of the markers for such disease progression, and the mechanism for stress-induced pulmonary hypertension remain the subject of intense interest and ongoing investigation. We appreciate the remarks of Callejas et al concerning our recent article in CHEST (July 2006).1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar The prevalence of a pulmonary artery systolic pressure of > 40 mm Hg in our patients was similar to that in the population described. In order to qualify as a positive response, we agree that patients should produce a minimum value of 40 mm Hg + right atrial pressure during exercise; a less robust response most often indicates pulmonary venous hypertension. For now, we believe it prudent to study all patients whose resting pulmonary artery pressure is normal and whose exercise pressure exceeds 40 mm Hg + right atrial pressure. Currently, we repeat the exercise echocardiogram every 3 to 6 months in those patients. As noted,1Alkotob ML Soltani P Sheatt MA et al.Reduced exercise capacity and stress-induced pulmonary hypertension in patients with scleroderma.Chest. 2006; 130: 176-181Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar several of our patients ultimately progressed to resting pulmonary hypertension. Both of the markers for such disease progression, and the mechanism for stress-induced pulmonary hypertension remain the subject of intense interest and ongoing investigation. Stress-Induced Pulmonary Systolic Hypertension in Patients With SclerodermaCHESTVol. 131Issue 4PreviewWe read with great interest the study of Alkotob et al (July 2006)1 on pulmonary hypertension (PHTN) in patients with scleroderma. They demonstrate that stress-induced pulmonary systolic hypertension in patients with scleroderma is highly prevalent, 46%, defined by an abnormal rise in pulmonary artery systolic pressure (PASP) > 40 mm Hg during exercise. The question is: are really all these patients a risk population of PHTN? Full-Text PDF