Epicardial placement of human placental membrane protects from heart injury in a swine model of myocardial infarction.

Cardiac ischemic reperfusion injury (IRI) is paradoxically instigated by reestablishing blood-flow to ischemic myocardium typically from a myocardial infarction (MI). Although revascularization following MI remains the standard of care, effective strategies remain limited to prevent or attenuate IRI. We hypothesized that epicardial placement of human placental amnion/chorion (HPAC) grafts will protect against IRI.

Human Placental Allograft Membranes: Promising Role in Cardiac Surgery and Repair.

Despite the immense investment in research devoted to cardiovascular diseases, mechanisms of progression and potential treatments, it remains one of the leading causes of death in the world. Cellular based strategies have been explored for decades, having mixed results, while more recently inflammation and its role in healing, regeneration and disease progression has taken center stage. Placental membranes are immune privileged tissues whose native function is acting as a protective barrier during fetal development, a state which fosters regeneration and healing.

The effects of macrophages on cardiomyocyte calcium-handling function using in vitro culture models.

Following myocardial infarction (MI), myocardial inflammation plays a crucial role in the pathogenesis of MI injury and macrophages are among the key cells activated during the initial phases of the host response regulating the healing process. While macrophages have emerged as attractive effectors in tissue injury and repair, the contribution of macrophages on cardiac cell function and survival is not fully understood due to complexity of the in vivo inflammatory microenvironment. Understanding the key cells involved and how they communicate with one another is of paramount importance for the development of effective clinical treatments.