Abstract 12906: Insights into the Mechanisms of Myocardial Contractility Enhancement in Acute Hypoxia: A Speckle Tracking Imaging Study
Hypoxic exposure in vivo has been reported to increase cardiac output, and in some studies, the ratio of left ventricular (LV) peak systolic pressure to end-systolic volume, suggesting enhanced contractility. However, in vitro studies indicate that hypoxia either depresses or does not affect isolated myocardial fiber contractility. Part of these discrepancies between in vivo and in vitro studies could be explained by hypoxia-induced sympathetic nervous system activation. We therefore explored the effects of hypoxia on echocardiographic measurements of LV function, with speckle tracking measurements, in healthy volunteers with and without intake of the beta-blocker bisoprolol. Methods. Echocardiography and speckle tracking (Qlab 7.1, Philips) were performed in 21 subjects in normoxia and after 30 minutes of hypoxia (12% oxygen), and in 10 subjects in normoxia and after 2 days of bisoprolol (5 mg once daily) in hypoxia (mean age: 27±7 years). Among the 10 subjects, 6 were also studied in normoxia following bisoprolol to assess the role of the drug-induced decrease in blood pressure (BP). Results (table 1). Hypoxia was associated with a decreased arterial saturation (from 97±1 to 76± 8%, p=0.0001) and an increased LV strain and twist. In normoxia, bisoprolol decreased heart rate (HR, 76±12 vs 63±8 bpm, p=0.001) and mean BP (88±7 vs 77±5mmHg, p<0.05). Following bisoprolol intake, hypoxic breathing decreased oxygen saturation from 97±2 to 83±4% (p<0.0001), increased HR (from 63±8 bpm to 76±9 bpm, p<0.0001), and did not alter mean blood pressure (from 77±5 to 74±8 to mmHg, p= NS).The lack of increase in strain parameters under bisoprolol (in normoxia) suggests that the decrease in BP does not explain the increased strain observed in hypoxia. Conclusions. The increase in LV contractility in hypoxia after β-adrenergic inhibition is independent of the bisoprolol-induced decrease in BP, and allows hypothesizing an intrinsic mechanism unrelated to catecholergic activation.
- © 2012 by American Heart Association, Inc.