Air pollution and chronic cough in China.

We are grateful for the thoughtful commentary by Dr Medford relating to our recent article in CHEST . 1 We agree that because procedural risk in patients with idiopathic pulmonary arterial hypertension (IPAH) is high, pretest suspicion for a more ominous diagnosis is warranted prior to invasive studies of associated mediastinal lymphadenopathy (MLAD). Specifi cally, exclusion of malignancy (lymphoma, lung primary, metastatic primary, and so forth) should be the only immediate justifi cation for invasive assessment in this setting. Unfortunately, few studies have commented on MLAD associated with pulmonary hypertension. Our observed frequency of close to one in fi ve patients with IPAH (18%) involved a selected cohort with both right-sided heart catheterization and chest CT scan for the purposes of correlating lymphadenopathy with severity of cardiac hemodynamics. This may underestimate the true prevalence of MLAD in all patients with IPAH. We did fi nd a similar dis tribu tion and size of abnormal lymph nodes when compared with left-sided congestive adenopathy, 2 and, although others have shown resolution or improvement in adenopathy following heart failure treatment, 3 only one of nine patients with MLAD and follow-up CT scanning in our study had regression, despite receiving therapy. These specifi c fi ndings from our study contribute to the clinical understanding of MLAD associated with pulmonary hypertension and may be applicable to MLAD with pulmonary hypertension from other causes. As Dr Medford noted, enlarged nodes of , 2 cm on short axis with known leftor right-sided heart disease may justify observation with directed heart failure management for 1 to 3 months prior to invasive assessment. This approach appears reasonable for MLAD and pulmonary hypertension from most causes. For Andrew R. L. Medford , MD, FCCP Westbury-on-Trym, Bristol, England