Abstract
Myocardial infarction (MI) remains the leading cause of cardiovascular death worldwide and a major cause of heart failure. Recent studies have suggested that cell-based therapies with bone marrow stem cells (BMSC) and human amniotic membrane (hAM) would recover the ventricular function after MI; however, the mechanisms underlying these effects are still controversial. Herein, we aimed to compare the effects of BMSC and hAM in a rat model of heart failure. MI was induced through coronary occlusion, and animals with an ejection fraction (EF) < 50% were included and randomized into three groups: control, BMSC, and hAM. The BMSC and hAM groups were implanted on the anterior ventricular wall seven days after MI, and a new echocardiographic analysis was performed on the 30th day, followed by euthanasia. The echocardiographic results after 30 days showed significant improvements on EF and left-ventricular end-sistolic and end-diastolic volumes in both BMSC and hAM groups, without significant benefits in the control group. New blood vessels, desmine-positive cells and connexin-43 expression were also elevated in both BMSC and hAM groups. These results suggest a recovery of global cardiac function with the therapeutic use of both BMSC and hAM, associated with angiogenesis and cardiomyocyte regeneration after 30 days.
Highlights
Acute myocardial infarction (AMI) is the most common cause of death globally, accounting for 32% of deaths worldwide in 2013 [1]
Data from the American Heart Association estimated a prevalence of 5.1 million individuals with heart failure (HF) in the United States in 2012, with projections of a 46% increase by 2030, resulting in more than 8 million people being affected by this complication [7,8,9]
03 animals of the human amniotic membrane (hAM) group and 02 animals of the control group died, related to postoperative complications, leaving 27 animals that were included in the final analysis: control (n = 08), bone marrow stem cells (BMSC) (n = 11) and hAM (n = 08)
Summary
Acute myocardial infarction (AMI) is the most common cause of death globally, accounting for 32% of deaths worldwide in 2013 [1]. The ventricular dysfunction is a major cause of heart failure (HF). Data from the American Heart Association estimated a prevalence of 5.1 million individuals with HF in the United States in 2012, with projections of a 46% increase by 2030, resulting in more than 8 million people being affected by this complication [7,8,9]. HF is the main cause of hospitalization worldwide in individuals older than 65 years, generating an annual cost of 26 billion USD in the United States [7]
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