Key result
Hypoxia training significantly improved left ventricular ejection fraction (54.39, P<0.05) and reduced left ventricular dimensions compared to myocardial infarction alone in rabbits.
Why the study?
Does hypoxia training improve left ventricular remodeling and function in a rabbit model of myocardial infarction?
RCT
Randomly divided
Does hypoxia training improve left ventricular remodeling and function in a rabbit model of myocardial infarction?
Hypoxia training attenuates left ventricular remodeling and improves ejection fraction in a rabbit model of myocardial infarction, potentially via angiogenesis.
Hypothesis-generating for hypoxia training post-MI remodeling; human trials needed before clinical consideration.
OBJECTIVE: Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myocardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. METHODS: ADULT MALE RABBITS WERE RANDOMLY DIVIDED INTO THREE GROUPS: group SO (sham operated), group MI (myocardial infarction only) and group MI-HT (myocardial infarction plus hypoxia training). Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber (having equivalent condition at an altitude of 4000 m, FiO214.9%) for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor (VEGF) in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were assessed by echocardiography. RESULTS: After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI (130.27 ± 18.58 pg/mL, P < 0.01) and MI-HT (181.93 ± 20.29 pg/mL, P < 0.01) were significantly increased. Infarct size in Group MI-HT (29.67% ± 7.73%) was deceased remarkably, while its capillary density (816.0 ± 122.2/mm(2)) was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic (15.86 ± 1.09 mm, P < 0.05) and end-systolic dimensions (12.10 ± 1.20 mm, P < 0.01) significantly and improved left ventricular ejection fraction (54.39 ± 12.74 mm, P < 0.05). CONCLUSION: Hypoxia training may improve left ventricular function and reduce remodeling via angiogenesis in rabbits with MI.
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Wan et al. (2014) conducted an RCT in Myocardial infarction. Hypoxia training vs. Myocardial infarction only and sham operated was evaluated on Left ventricular ejection fraction (p=<0.05). Hypoxia training significantly improved left ventricular ejection fraction (54.39, P<0.05) and reduced left ventricular dimensions compared to myocardial infarction alone in rabbits.
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