Cardiovascular health research identifies menopause risks and new plaque development drivers

Medical research is highlighting critical vulnerabilities in cardiovascular health, particularly regarding the physiological shifts during menopause and the cellular mechanisms of plaque development.

For menopausal women, the decline of estrogen levels alters vascular function, lipid metabolism, and blood pressure regulation. This transition can lead to endothelial dysfunction, systemic inflammation, and increased central adiposity. Clinical data indicates that cardiovascular diseases, including stroke and ischemic heart disease, are the primary causes of mortality and long-term disability among women, surpassing the mortality rates of breast, ovarian, and uterine cancers combined. Additionally, the loss of hormonal protection is linked to acute events like takotsubo cardiomyopathy, or ‘broken heart syndrome,’ which affects approximately 90 percent of patients over age 50.

In a separate study, researchers at the University of Virginia Health have identified potential drivers of coronary artery disease. By examining smooth muscle cells from heart transplant donors, a team led by Dr. Mete Civelek and doctoral student Noah Perry found that the way these cells process nitrogen and glycogen may influence their behavior. When these processes change, smooth muscle cells may transition from protecting against plaque rupture to behaving in ways that promote plaque growth. The researchers also identified mannose, a simple sugar, as a potential factor in this process, offering a new avenue for potential preventative treatments.