Left ventricular adaptation to acute hypoxia: a speckle-tracking echocardiography study.

BACKGROUND

Hypoxia depresses myocardial contractility in vitro but does not affect or may even improve indices of myocardial performance in vivo, possibly through associated changes in autonomic nervous system tone. The aim of this study was to explore the effects of hypoxic breathing on speckle-tracking echocardiographic indices of left ventricular function, with and without β1-adrenergic inhibition.

METHODS

Speckle-tracking echocardiography was performed in 21 healthy volunteers in normoxia and after 30 min of hypoxic breathing (fraction of inspired oxygen, 0.12). Measurements were also obtained after the administration of atropine in normoxia (n = 21) and after bisoprolol intake in normoxia (n = 6) and in hypoxia (n = 10).

RESULTS

Hypoxia increased heart rate (from 68 ± 11 to 74 ± 9 beats/min, P = .001), without changing mean blood pressure (P = NS), and decreased total peripheral resistance (P = .003). Myocardial deformation magnitude increased (circumferential strain, -19.6 ± 1.9% vs -21.2 ± 2.5%; radial strain, 19.2 ± 3.7% vs 22.6 ± 4.1%, P < .05; longitudinal and circumferential strain rate, -0.88 ± 0.11 vs -0.99 ± 0.15 sec(-1) and -1.03 ± 0.16 vs -1.18 ± 0.18 sec(-1), respectively, P < .05 for both; peak twist, 8.98 ± 3.2° vs 11.1 ± 2.9°, P < .05). Except for peak twist, these deformation parameters were correlated with total peripheral resistance (P < .05). Atropine increased only longitudinal strain rate magnitude (-0.88 ± 0.11 vs -0.97 ± 0.14 sec(-1), P < .05). The increased magnitude of myocardial deformation persisted in hypoxia under bisoprolol (P < .05). In normoxia, bisoprolol decreased heart rate (73 ± 10 vs 54 ± 7 beats/min, P = .0005), mean blood pressure (88 ± 7 vs 81 ± 4 mm Hg, P = .0027), without altering deformation.

CONCLUSIONS

Hypoxic breathing increases left ventricular deformation magnitude in normal subjects, and this effect may not be attributed to hypoxia-induced tachycardia or β1-adrenergic pathway changes but to hypoxia-induced systemic vasodilation.