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

B. A. Kaufmann, A. M. Bernheim, S. Kiencke, M. Fischler, Jiri Sklenar, H. Mairbäurl, M. Maggiorini, H. P. Brunner-La Rocca

    Research output: Contribution to journalArticle

    6 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish (US)
    JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
    Volume294
    Issue number4
    DOIs
    StatePublished - Apr 2008

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    Pulmonary Edema
    Placebos
    Lung
    Tricuspid Valve
    Therapeutics
    Dexamethasone

    Keywords

    • Echocardiography
    • Exercise
    • Hypoxia

    ASJC Scopus subject areas

    • Physiology

    Cite this

    Evidence supportive of impaired myocardial blood flow reserve at high altitude in subjects developing high-altitude pulmonary edema. / Kaufmann, B. A.; Bernheim, A. M.; Kiencke, S.; Fischler, M.; Sklenar, Jiri; Mairbäurl, H.; Maggiorini, M.; Brunner-La Rocca, H. P.

    In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 294, No. 4, 04.2008.

    Research output: Contribution to journalArticle

    Kaufmann, B. A. ; Bernheim, A. M. ; Kiencke, S. ; Fischler, M. ; Sklenar, Jiri ; Mairbäurl, H. ; Maggiorini, M. ; Brunner-La Rocca, H. P. / Evidence supportive of impaired myocardial blood flow reserve at high altitude in subjects developing high-altitude pulmonary edema. In: American Journal of Physiology - Heart and Circulatory Physiology. 2008 ; Vol. 294, No. 4.
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    abstract = "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.",
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    AU - Kaufmann, B. A.

    AU - Bernheim, A. M.

    AU - Kiencke, S.

    AU - Fischler, M.

    AU - Sklenar, Jiri

    AU - Mairbäurl, H.

    AU - Maggiorini, M.

    AU - Brunner-La Rocca, H. P.

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    AB - 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.

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    KW - Exercise

    KW - Hypoxia

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