Correspondence |


Michael A. Mathier, MD
Author and Funding Information

University of Pittsburgh Pittsburgh, PA

Correspondence to: Michael A. Mathier, MD, University of Pittsburgh, Cardiology, 200 Lothrop St, Scaife Hall S 559, Pittsburgh, PA 15213; e-mail: mathierm@upmc.edu

Dr. Mathier received consulting fees from Actelion, Gilead, and United Therapeutics; grant support from Actelion; and speakers bureau fees from Actelion, Gilead, GlaxoSmithKline, and United Therapeutics.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

Chest. 2008;134(3):670-671. doi:10.1378/chest.08-1518
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To the Editor:

Diaz-Lobato et al, in addressing our recent report in CHEST (March 2008),1 outlined the many complexities inherent in the diagnosis and management of the morbidly obese patient with pulmonary hypertension. We appreciate their comments. They have raised a number of questions about our patient that we would like to clarify.

Regarding the question of obesity-hypoventilation syndrome, our patient underwent a single arterial blood gas analysis at the time of the initial diagnosis and was not hypercarbic. Regarding the question of sleep apnea, as stated in the report: “Obstructive sleep apnea had been diagnosed years earlier, and continued to be treated successfully with positive airway pressure.” Diaz-Lobato et al suggested that hypoxemia could completely explain the presence of pulmonary arterial hypertension (PAH) in our patient. We would stress again, however, that nocturnal hypoxemia was corrected with therapy with continuous positive airway pressure and oxygen for several years prior to the diagnosis of PAH. Furthermore, daytime hypoxemia was not present until 1 year prior to the patient undergoing bariatric surgery, and supplemental oxygen therapy was initiated at that time. Thus, it is difficult to ascribe our patient's PAH to hypoxemia.

Diaz-Lobato et al also suggested that PAH therapy should not have been administered to our patient because of the presence of diastolic heart failure. Yet, our patient's pulmonary artery balloon occlusion pressure was normal or minimally elevated throughout the course of his treatment, suggesting very mild, if any, diastolic heart failure. Nevertheless, we acknowledged all of these issues in the report, stating “… while a contribution of left ventricular diastolic dysfunction or obesity hypoventilation syndrome could not be definitively excluded, the patient appeared to have idiopathic PAH.” Following a full diagnostic evaluation, there was no evidence of hepatic, renal, or thyroid disease, or any other established cause of PAH. While our patient's pulmonary pressures were higher while receiving bosentan therapy, this was found 3 years after therapy with the agent was initiated; it is more likely that this represented the expected progression of the disease rather than an adverse effect of bosentan.

We fully agree that there are no clear criteria for the use of combination therapy for patients with PAH. As indicated in the report,1 we initially recommended therapy with epoprostenol. When our patient refused this, yet wished to pursue bariatric surgery, we felt that a combination of the other available therapies was the best way to achieve sufficient hemodynamic improvement to allow for surgery. As can be seen in Table 1 in our article, there was indeed a stepwise improvement in hemodynamics (most notably cardiac output and pulmonary vascular resistance) with each added therapy leading up to surgery.

We agree that the improvement in functional status experienced by our patient following bariatric surgery was likely related to weight loss. As we stated in the original report, “the mechanism of the observed improvement is uncertain…” That it was not related to the resolution of PAH is indicated by the findings of the follow-up echocardiogram and a recent right heart catheterization that revealed ongoing severe PAH with normal pulmonary artery balloon occlusion pressure and preserved cardiac output. Despite this, the patient's functional status remains markedly better than it had been before surgery; while mild sleep apnea persists (and treatment of it continues), daytime hypoxemia has resolved.

Mathier MA, Zhang J, Ramanathan RC. Dramatic functional improvement following bariatric surgery in a patient with pulmonary arterial hypertension and morbid obesity. Chest. 2008;133:789-792. [PubMed] [CrossRef]




Mathier MA, Zhang J, Ramanathan RC. Dramatic functional improvement following bariatric surgery in a patient with pulmonary arterial hypertension and morbid obesity. Chest. 2008;133:789-792. [PubMed] [CrossRef]
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