Myocardial infarction, also called heart attack, is a leading cause of death in men and women worldwide. In the United States, the overall prevalence of heart attack is close to 3 percent of adults, which means someone in the country is experiencing a heart attack every 43 seconds.
The research effort in the University of Toledo laboratory of Dr. Jiang Tian focuses on reducing destructive heart damage after a heart attack. Our goal is to slow down or prevent heart failure after surviving a heart attack.
Heart attacks occur when a coronary artery, which feeds the muscle oxygen and nutrients, is blocked and is not quickly unblocked by clinical intervention. The cells within the heart muscle supplied by the blocked artery die because of the lack of oxygen and nutrients.
After a heart attack, those dead heart cells are replaced by scar tissue instead of new heart cells. Research has discovered that over time, healthy heart cells also are affected even in unblocked areas of the heart because they grow larger to compensate for the nonfunctional scar tissue. Unfortunately, enlarged heart cells lead to more heart cell death and formation of more scar tissue even in healthy areas of the heart. Together, these changes are called heart remodeling and can eventually lead to overall heart failure and death.
Our research lab is studying a possible way to reduce heart remodeling after a heart attack by preventing capillary loss in healthy heart muscle.
Capillaries are the smallest artery branches in the heart that directly provide blood to each individual heart muscle cell. By studying these very small arteries after heart attacks in mouse models, we have observed that even in unblocked and unharmed areas of the heart, the number of capillaries is decreased after a heart attack. We believe that decreased number of capillaries in otherwise healthy areas of the heart is part of the process that causes scar tissue formation in these areas.
We have discovered recently that the addition of a specialized nutrient that combines different cell growth factors to the heart blood vessels can improve overall heart function in our mouse model. Further studies in our lab demonstrate that these additional nutrients appear to increase the number of capillaries and therefore decrease scar tissue in undamaged areas of the heart after a heart attack.
Our research indicates that the beneficial effects of the specialized nutrients could result either from activation of existing endothelial cells or activation of a small population of cells in the heart called heart stem cells, which can grow into endothelial cells after a heart attack. These endothelial cells are specialized cells lining blood vessels that are essential for the development of new blood vessels and maintenance of older blood vessels, including capillaries feeding individual heart cells.
These activated or new endothelial cells would then form new capillaries in the heart, providing oxygen and nutrients that prevent destructive heart remodeling.
A deeper understanding of all of these mechanisms will eventually help to reduce long-term negative consequences of heart attacks and save lives.
Xiaoming Fan is a graduate student in the department of medicine at the University of Toledo College of Medicine, formerly the Medical College of Ohio. Xiaoming is doing his research in the laboratory of Dr. Jiang Tian. For more information, contact xiaoming.fan@rockets.utoledo.edu.
First Published September 5, 2016, 4:00 a.m.