Acute changes in pulmonary artery pressures due to exercise and exposure to high altitude do not cause left ventricular diastolic dysfunction.
BACKGROUND
Altitude-induced pulmonary hypertension has been suggested to cause left ventricular (LV) diastolic dysfunction due to ventricular interaction. In this study, we evaluate the effects of exercise- and altitude-induced increase in pulmonary artery pressures on LV diastolic function in an interventional setting investigating high-altitude pulmonary edema (HAPE) prophylaxis.


METHODS
Among 39 subjects, 29 were HAPE susceptible (HAPE-S) and 10 served as control subjects. HAPE-S subjects were randomly assigned to prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo bid, starting 1 day before ascent. Doppler echocardiography at rest and during submaximal exercise was performed at low altitude (490 m) and high altitude (4,559 m). The ratio of early transmitral inflow peak velocity (E) to atrial transmitral inflow peak velocity (A), pulmonary venous flow parameters, and tissue velocity within the septal mitral annulus during early diastole (E') were used to assess LV diastolic properties. LV filling pressures were estimated by E/E'. Systolic right ventricular to atrial pressure gradients (RVPGs) were measured in order to estimate pulmonary artery pressures.


RESULTS
At 490 m, E/A decreased similarly with exercise in HAPE-S and control subjects (HAPE-S, 1.5 +/- 0.3 to 1.3 +/- 0.3; control, 1.7 +/- 0.4 to 1.3 +/- 0.3; p = 0.12 between groups) [mean +/- SD], whereas RVPG increased significantly more in HAPE-S subjects (20 +/- 5 to 43 +/- 9 mm Hg vs 18 +/- 3 to 28 +/- 3 mm Hg, p < 0.001). Changes in RVPG levels during exercise did not correlate with changes in E/A (p > 0.1). From 490 to 4,559 m, no correlations between changes in RVPG and changes in E/A or atrial reversal (both p > 0.1) were observed. Neither of the groups showed an increase in E/E' from 490 to 4,559 m.


CONCLUSIONS
Increased pulmonary artery pressure associated with exercise and acute exposure to 4,559 m appears not to cause LV diastolic dysfunction in healthy subjects. Therefore, ventricular interaction seems not to be of hemodynamic relevance in this setting.
Bernheim
Alain M
AM
Division of Cardiology, University Hospital, Petersgraben 4, 4031 Basel, Switzerland. bernheima@uhbs.ch
Kiencke
Stephanie
S
Fischler
Manuel
M
Dorschner
Lorenz
L
Debrunner
Johann
J
Mairbäurl
Heimo
H
Maggiorini
Marco
M
Brunner-La Rocca
Hans Peter
HP
D000328:Adult; D000531:Altitude; D001783:Blood Flow Velocity; D002243:Carbolines / Q000627:therapeutic use; D003907:Dexamethasone / Q000627:therapeutic use; D003971:Diastole; D015150:Echocardiography, Doppler; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D005500:Follow-Up Studies; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D009051:Mountaineering / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D011654:Pulmonary Edema / Q000209:etiology* / Q000503:physiopathology; D011669:Pulmonary Wedge Pressure / Q000502:physiology*; D012016:Reference Values; D012146:Rest / Q000502:physiology; D000068581:Tadalafil; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*
D002243:Carbolines; D005938:Glucocorticoids; D010726:Phosphodiesterase Inhibitors; D000068581:Tadalafil; D003907:Dexamethasone