Abstract
Background We hypothesized that daily administration of a potent antioxidant (α-lipoic acid: ALA) would protect the heart against both acute myocardial infarction (AMI) and left ventricular remodeling (LVR) post-AMI. Methods and Results Two separate studies were conducted. In the AMI study, C57Bl/6 mice were fed ALA daily for 7 d prior to a 45-minute occlusion of the left coronary artery (LCA). Mean infarct size in control mice (fed water) was 60 ± 2%. Mean infarct size in ALA-treated mice was 42 ± 3% in the 15 mg/kg·d group and 39 ± 3% in the 75 mg/kg·d group (both P < 0.05 vs. control). In the LVR study, AMI increased LV end-systolic volume (LVESV) and reduced LV ejection fraction (LVEF) to a similar extent in both groups when assessed by cardiac MRI 1 day after a 2-hour LCA occlusion. Treatment with ALA (75 mg/kg·d) or H2O was initiated 1 day post-AMI and continued until study's end. Both LVESV and LVEF in ALA-treated mice were significantly improved over control when assessed 28 or 56 days post-AMI. Furthermore, the survival rate in ALA-treated mice was 63% better than in control mice by 56 days post-AMI. Conclusions Daily oral ingestion of ALA not only protects mice against AMI but also attenuates LVR and preserves contractile function in the months that follow.
Highlights
It has long been known that reactive oxygen species (ROS) play a key role in the pathophysiology of acute myocardial infarction (AMI) [1,2,3]
Recent studies indicate that oxidative stress persists in the myocardium after AMI [4,5,6,7,8] and secondary prevention trials of antioxidant vitamins such as vitamin E and β-carotene have yielded encouraging results [9]
Unlike vitamin E and β-carotene, alpha-lipoic acid (ALA) is a relatively potent antioxidant with a broad spectrum of antioxidant properties [10] that may make it more efficacious in disease states where oxidative stress contributes to cardiovascular pathophysiology [11,12,13]
Summary
It has long been known that reactive oxygen species (ROS) play a key role in the pathophysiology of acute myocardial infarction (AMI) [1,2,3]. Recent studies indicate that oxidative stress persists in the myocardium after AMI [4,5,6,7,8] and secondary prevention trials of antioxidant vitamins such as vitamin E and β-carotene have yielded encouraging results [9]. These same clinical trials failed to demonstrate a reduction in the risk of fatal coronary events, perhaps because the antioxidant vitamins under investigation were intrinsically weak and/or provided a limited spectrum of antioxidant protection. Oral ingestion of ALA protects mice against AMI and attenuates LVR and preserves contractile function in the months that follow
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