LETTER TO THE EDITOR
Reply
Richard A. Krasuski, MDa and
Thomas M. Bashore, MDa
a Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
thomas.bashore{at}duke.edu
We appreciate the comments of Drs. Robbins, Barst, Channick and Rubin. They are pioneers within the field of pulmonary hypertension, and their studies and reviews have laid the groundwork for present and future research. However, we would like to reiterate our published response rates to inhaled nitric oxide (NO) in primary pulmonary hypertension (PPH) and pulmonary hypertension from secondary causes (SPH). We agree that the definition of a positive response to vasodilators is not uniform throughout the literature, and for this reason we included a table in our publication examining our results using different definitions (1). This allows the reader to compare our results with those of our colleagues at different institutions.
Although Robbins and colleagues correctly state that most previous studies of vasodilators in PPH have response rates lower than our series, other series, particularly Atz et al. (2), have shown up to an 88% positive response rate to vasodilators. Why should such a wide discrepancy exist between studies? We agree that this is very disconcerting at first glance. But even within the Robbins et al. series of three institutions, a nearly threefold difference in response was seen between the investigators at the University of California at San Diego (UCSD) and the investigators at Columbia University. Should a twofold difference between the investigators at Columbia and our group be so surprising? A more thorough description of baseline hemodynamics in each patient group may help explain the difference in response rates. The majority of patients in our study were undergoing initial right heart catheterization for assessment of vasoreactivity. This would imply an earlier stage of disease, when the abnormalities at the vascular level may still be reversible. The higher response rates in children (3) may imply a difference in the pathophysiology of PPH in children, but it is more likely a result of earlier diagnosis and testing in this population. A young, active individual may notice a subtle limitation in physical endurance earlier and be brought to medical attention.
In our study, right ventricular dysfunction was more common in patients unresponsive to vasodilators. This was likely a result of more advanced disease. To date, no patient we have tested experienced a  20 mm Hg drop in pulmonary artery pressure if their baseline right ventricular end-diastolic pressure was >20 mm Hg. We have recently reviewed the echocardiograms of these patients and found that right ventricular (RV) systolic dysfunction correlates strongly with vasodilator response. In our population, significant RV dysfunction was rare (<20%), implying a fairly healthy population.
Present-day determination of vasoreactivity should occur in a cardiac catheterization laboratory with careful attention to hemodynamic measurements. We have not observed any hemodynamic instability during testing, and we have not found it necessary to repeat baseline measurements between escalating doses of NO.
In conclusion, we have presented the results of vasodilator testing at Duke University Medical Center for the express purpose of comparing response rates of SPH patients with those of PPH patients. We have observed similar degrees of vasoreactivity in both groups, and we have proposed that further studies be conducted. We also stated that assessment of vasoreactivity would be an essential first step in determining whether treatment with calcium channel blockers would be feasible and safe in these patients. We agree with Robbins and colleagues that empiric treatment of patients with SPH or PPH without safety data is dangerous in these patients, particularly if RV dysfunction is already present. Larger studies will be useful in sorting out the variability in response rates documented at different centers.
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References
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1. Krasuski RA, Warner JJ, Wang A, Harrison JK, Tapson VF, Bashore TM. Inhaled nitric oxide selectively dilates pulmonary vasculature in adult patients with pulmonary hypertension, irrespective of etiology. J Am Coll Cardiol. 2000;36:2204–2211[Abstract/Free Full Text]
2. Atz AM, Adatia I, Lock JE, Wessel DL. Combined effects of nitric oxide and oxygen during acute pulmonary vasodilator testing. J Am Coll Cardiol. 1999;33:813–819[Abstract/Free Full Text]
3. Barst RJ, Maislin G, Fishman AP. Vasodilator therapy for primary pulmonary hypertension in children. Circulation. 1999;99:1197–1208[Abstract/Free Full Text]
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