HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 294/4/H1651    most recent 00760.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kaufmann, B. A. Articles by Brunner-La Rocca, H. P. PubMed PubMed Citation Articles by Kaufmann, B. A. Articles by Brunner-La Rocca, H. P.

Evidence supportive of impaired myocardial blood flow reserve at high altitude in subjects developing high-altitude pulmonary edema

¹Department of Cardiology, University Hospital Basel; and ²Intensive Care Unit, Division of Internal Medicine, University Hospital, Zurich, Switzerland; ³Division of Cardiology, Oregon Health and Science University, Portland, Oregon; and ⁴Medical Clinic VII, Sports Medicine, University of Heidelberg, Heidelberg, Germany

Submitted 2 July 2007 ; accepted in final form 19 February 2008

An exaggerated increase in pulmonary arterial pressure is the hallmark of high-altitude pulmonary edema (HAPE) and is associated with endothelial dysfunction of the pulmonary vasculature. Whether the myocardial circulation is affected as well is not known. The aim of this study was, therefore, to investigate whether myocardial blood flow reserve (MBFr) is altered in mountaineers developing HAPE. Healthy mountaineers taking part in a trial of prophylactic treatment of HAPE were examined at low (490 m) and high altitude (4,559 m). MBFr was derived from low mechanical index contrast echocardiography, performed at rest and during submaximal exercise. Among 24 subjects evaluated for MBFr, 9 were HAPE-susceptible individuals on prophylactic treatment with dexamethasone or tadalafil, 6 were HAPE-susceptible individuals on placebo, and 9 persons without HAPE susceptibility served as controls. At low altitude, MBFr did not differ between groups. At high altitude, MBFr increased significantly in HAPE-susceptible individuals on treatment (from 2.2 ± 0.8 at low to 2.9 ± 1.0 at high altitude, P = 0.04) and in control persons (from 1.9 ± 0.8 to 2.8 ± 1.0, P = 0.02), but not in HAPE-susceptible individuals on placebo (2.5 ± 0.3 and 2.0 ± 1.3 at low and high altitude, respectively, P > 0.1). The response to high altitude was significantly different between the two groups (P = 0.01). There was a significant inverse relation between the increase in the pressure gradient across the tricuspid valve and the change in myocardial blood flow reserve. HAPE-susceptible individuals not taking prophylactic treatment exhibit a reduced MBFr compared with either treated HAPE-susceptible individuals or healthy controls at high altitude.

hypoxia; exercise; echocardiography