Submitted on July 2, 2007
Accepted on February 19, 2008
EVIDENCE SUPPORTIVE OF IMPAIRED MYOCARDIAL BLOOD FLOW RESERVE AT HIGH ALTITUDE IN SUBJECTS DEVELOPING HIGH ALTITUDE PULMONARY EDEMA
Beat A. Kaufmann1, Alain M Bernheim1, Stephanie Kiencke1, Manuel Fischler2, Jiri Sklenar3, Heimo Mairbaeurl4, Marco Maggiorini5, and Hanspeter Brunner-La Rocca1*
1 Cardiology, University Hospital Basel, Basel, Switzerland
2 Intensive Care Unit, University Hospital Zurich, Zurich, Switzerland
3 Cardiology, Oregon Health and Science University, Portland, Oregon, United States
4 Sports Medicine, University of Heidelberg, Heidelberg, Germany
5 Intersive care unit, University hospital Zurich, Zurich, Switzerland
* To whom correspondence should be addressed. E-mail: brunnerh{at}uhbs.ch.
Aims: An exaggerated increase in pulmonary artery pressure is the hallmark of 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 high altitude pulmonary edema (HAPE).
Methods and Results: Healthy mountaineers taking part in a trial of prophylactic treatment of HAPE were examined at low (490m) and high altitude (4559m). 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 indivuduals 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.
Conclusions: HAPE-susceptible individuals not taking prophylactic treatment exhibit a reduced MBFr compared to either treated HAPE-susceptible individuals or healthy controls at high altitude.
