Heavily calcified coronary arteries seen on a CT scan of the heart. Research at the New York Institute of Technology will create blood flow modeling to show the impact of calcium in arteries as part of a project to develop treatments to remove calcium.
January 27, 2021 — A New York Institute of Technology research team has secured a five-year $1.8 million grant from the National Institutes of Health (NIH) National Heart, Lung, and Blood Institute for research to improve the understanding of atherosclerosis and deliver a new treatment for heart disease.
According to the Centers for Disease Control and Prevention (CDC), more than 30 million U.S. adults have been diagnosed with heart disease, which also causes one in every four deaths. Researchers have long believed that atherosclerosis is a risk factor in predicting heart disease-related illness and death. The buildup of calcium salts in blood vessel tissue, known as vascular calcification, is considered an atherosclerosis hallmark, but it is unclear whether calcification causes atherosclerosis or is simply a byproduct. If it is a risk factor, treatments targeting calcification may prevent millions of future heart disease cases and fatalities.
The team, led by Olga V. Savinova, Ph.D., assistant professor of biomedical sciences at New York Institute of Technology College of Osteopathic Medicine (NYITCOM), will use mouse and computer models to investigate whether vascular calcification contributes to the development of atherosclerosis and, if so, whether a decalcification treatment can correct and prevent it.
"Our overarching goal is to gain a better understanding of how calcification impacts the onset, progression, and treatment of atherosclerosis," said Savinova, who also received a 2018 NIH grant to examine vascular calcification in chronic kidney disease. "We believe calcification is a risk factor for atherosclerosis and one that can be corrected. By inhibiting vascular calcification caused by overactive phosphatase, we may be able to provide a therapy for atherosclerosis."
Savinova's team has collected data that suggests the enzyme phosphatase is responsible for vascular calcification. Their research shows that when a surplus of phosphatase exists in combination with high lipid levels, lipids are retained in the blood vessels, accelerating vessel hardening. Consequently, if the overactive gene responsible for the surplus can be "turned down," preventing its ability to cause calcification, atherosclerosis may also be treated.
Computational models will map the blood flow impact of increased calcification in mice with high lipid levels. After administering an inhibitor to mitigate excess enzyme activity, the team will monitor for reduced arterial stress. If their approach is successful, it could also prevent harmful changes in the area of the heart containing the aortic valve, which is critical for proper circulation.
An example of computational fluid dynamics modeling of blood flow inside an artery. Image from the British Cardiology Society.
Other New York Tech contributors include Dorinamaria Carka, Ph.D., assistant professor of mechanical engineering, who will lead computer simulations studies on blood flow dynamics, Brian Beatty, Ph.D., associate professor of anatomy, and Maria Plummer, M.D., pathologist and associate professor of clinical specialties. Jose Luis Millan, Ph.D., human genetics professor at the Sanford Burnham Prebys Medical Discovery Institute, is also involved.
The NIH, part of the U.S. Department of Health and Human Services, is the largest biomedical research agency in the world. The grant was supported by the NIH National Heart, Lung, and Blood Institute under Award Number R01HL149864. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.